ClickCease
+1-915-850-0900 spinedoctors@gmail.com
Select Page

Ketogenic Diet Explained

Back Clinic Ketogenic Diet Explained. A ketogenic diet, or keto diet, is a diet, which turns your system into a fat-burning machine. It has some initial side effects on health and functionality and many advantages for weight loss.
A ketogenic diet is comparable to other rigorous low-carb diets, like the Atkins diet plan or LCHF (low carb, higher fat). However, these diets wind up being ketogenic more or less by accident. The main difference between LCHF and keto is that protein is restricted in the latter.

A keto diet plan is made specifically to lead to ketosis. It’s possible to measure and adapt to optimal ketone amounts for wellness or bodily and psychological performance. Below, you can learn how to use keto to achieve your personal goals. We cover and explain the concept for a clear understanding. El Paso Chiropractor explains and gives insight into this cryptic and confusing diet. Science is changing daily. I hope and pray that the post gives you insight.


Podcast: Nutrition and Fitness During These Times

 

PODCAST: Dr. Alex Jimenez, Kenna Vaughn, Lizette Ortiz, and Daniel “Danny” Alvarado discuss nutrition and fitness during these times. During quarantine, people have become more interested in improving their overall health and wellness by following a proper diet and participating in exercise. The panel of experts in the following podcast offers a variety of tips and tricks on how you can improve your well-being. Moreover, Lizette Ortiz and Danny Alvarado discuss how they’ve been helping their clients achieve their optimal well-being during these COVID times. From eating fruits, vegetables, lean meats, good fats, and complex carbohydrates to avoiding sugars and simple carbohydrates like white pasta and bread, following a proper diet and participating in exercise and physical activity is a great way to continue to promote your overall health and wellness. – Podcast Insight

 


 

[00:00:00] You know, Lizette we have been working with patients for a long, long time. And I want to ask you a little bit about what got you into fitness. OK. So start from kind of the beginning of, like what got you into this, let the people know what it is that, who you are and what it’s about. What was the reason? Yeah. Your story. So it really makes it real easy for us to kind of get it going. [00:00:30][20.8]

 

[00:00:31] OK, I’ll try to make it short. [00:00:33][2.3]

 

[00:00:40] OK. So basically, I’m originally from Juarez. So I’m originally Mexican. And I grew up over there and I went all the way through high school. And then I moved to El Paso to go to UTEP and get a degree in psychology. So my whole life growing up, my mom’s been struggling with weight. She’s always struggled with weight because my mom’s family tends to be overweight. They even suffer from, like, you know, heart disease and other diseases that just come with it. And so I grew up with that. Like, my mom was always on a diet. She was always exercising. She always had exercise tapes. [00:01:18][37.5]

 

[00:01:18] So I guess it was ingrained in me to not be in that situation, but it still didn’t stop me from gaining a lot of weight. Did you get heavy? [00:01:27][9.1]

 

[00:01:29] Yes, of course. Of course. Because I didn’t have the tools, you know, I didn’t know any better. So I was eating like we all normally do, you know, like when you don’t know about things, just a lot of bread and sweets. Soda. I didn’t really drink water like water, water daily until I was sixteen. Yeah. My drinks were always Coca-Cola, it was the family drink. The family beverage and then maybe like Kool-Aid and things like that. Yes. And so I didn’t start drinking water until I had to be on treatment for a UTI or something. When I was 16, and that’s when I learned my first lesson was, OK, well, you’re on treatment so you can’t eat like acidic things. So I couldn’t even eat lime, but I couldn’t eat candies either, so I couldn’t eat sugar. I loved tamarind candies. I couldn’t eat that. I couldn’t eat sugar, no chocolate, no coffee, no cream. Like, they cut a lot of things. And I had to drink only water. Like the first time that I had to drink a glass of water. I thought I was going to throw up like that bad like that’s how bad it was. [00:02:35][66.5]

 

[00:02:36] And so then a month of this treatment, I lost like 15 pounds and I felt amazing. And this is I’m 16. I’m like, oh, my God, this feels great. I lost all this weight. Of course, that’s all I was focusing on at that point because that’s, I was 16. Right. So it’s like, oh, my God, I lost all this weight. I look great. [00:02:54][18.2]

 

[00:02:55] And so I started exercising more with the focus of being more fit. And so little by little that happened. So that happened the rest of my high school. Then I came to the U.S., I started college and I gained like 30 pounds. Right. Like you do like one does, right? Yeah. And then I didn’t really care. I did care. I did care. But I didn’t care. Like, I wasn’t doing anything about it. But it did depress me. And it caused me a lot of inner turmoil and anxiety and just depression and things, among other things. [00:03:25][29.7]

 

[00:03:26] And so I started exercising. I always kept active. [00:03:28][2.4]

 

[00:03:29] Is what’s interesting because I grew up with my mom, like having the videotapes and stuff. I always was on and off exercising. And so then I started doing more research. And that’s when I started kind of teaching myself, you know, like, look up, exercises, look up. But luckily, we already had the Internet and things. So I learned a lot about that. And I started doing my own workouts and I started watching what I ate. And I started like eating every three hours because supposedly that accelerated metabolism, which now we know is not the case. But I started doing that. So that actually shrunk my portions and I learned how that helps, too. Mm-hmm. And then I was going to move to L.A. because that’s what I always wanted to do when I went to go over there and pursue a career. [00:04:09][39.9]

 

[00:04:09] At what age did you go to L.A.? [00:04:10][0.9]

 

[00:04:11] When I graduated from college, I was. Twenty four. Yeah. Twenty four. So I was twenty-four when I moved and. But before I moved I was like, well I can’t go to L.A. to want to be an actress and have 30 extra pounds. Because when I see TV, that’s not, you know, you’re sold this image, this image of I need to look like this and this and this. And of course, I never filled out any of the requirements, but I still wanted to do it. And so I really focused on this. Not in a healthy way, though, you know, like I was really not eating well enough. I was probably exercising too much and not eating the right things because while I was losing weight, I wasn’t necessarily feeling any better. And so once I moved to L.A., I continued to work out and study and learn and then I studied nutrition. When I was over there in the university, not the university, the city college. And so that’s when I learned and that was my next big lesson was when I learned about nutrition, how like certain foods and the like, too much of this, too little of that, the wrong balance of things, the importance of vegetables and fruits, which I’ve always loved. But you see the difference between filling up on vegetables and fruits instead of filling up on pasta and bread. Yeah. And the repercussions that that has on your health, not only on the way that you look like we were mentioning earlier, right, not only in the way that you look but also the way that you feel and just learning that changed my life completely. I remember one day when we learned about additives in foods and dyes. We talked about Red 40 and like how, you know, like all these additives can have repercussions. You know, they build up in your system. Kids usually get hyperactive more because of the mix of dyes and additives than they do because of the sugar. Because if you eat like a lot of honey, you don’t get hyper necessarily. But if you eat a bunch of like Skittles, maybe because it has a bunch of other things in it. And so we learned about that. And like oh red 40 and then I get home and my husband had like this three-pound thing of red vines and I’m like, oh, red vines? [00:06:17][126.0]

 

[00:06:17] What are those? Those like Twizzlers? [00:06:19][2.3]

 

[00:06:20] Oh, no, no. Three pounds, literally three pounds. Yeah. Yeah. [00:06:25][5.2]

 

[00:06:26] Oh, we can’t eat that. Like, I just learned all this. And so every time I learned something about something, it’s like a new epiphany and a new item that I didn’t keep on my shelf anymore. And you know, I was like this fluffy white bread that’s delicious on sandwiches has zero nutrition for me. I need to get something that’s more whole grains, you know, like if I’m going to do a PB & J, I need to find my peanut butter. [00:06:50][24.5]

 

[00:06:50] That’s just peanuts and my bread. That is like sprouted grains and whole grains. And if I’m really going to stick to the bread, I at least need to do it right. And so that really, like, just that knowledge changed everything for me. And then I decided to… [00:07:05][14.4]

 

[00:07:08] Get certified as a personal trainer, because I kept being told by people at the gym that I should. As they would come, I was like on my training and I was like, oh, we should exercise together or whatever. And they would see how I would exercise and push myself. And they’re like, have you ever thought of being a trainer? And I was asked that so many times. I was like, no, no, I just. [00:07:27][19.8]

 

[00:07:28] You’re crazy like no. [00:07:30][1.5]

 

[00:07:31] Of course not. Like, I just had that, I was told that by several trainers over the course of maybe five years. And I was like, you know what, maybe I should, because then people would ask me, hey, how do you do this? How come you’re fit? How come you’re this, well, OK, all right, I’ll do it. [00:07:47][16.1]

 

[00:07:48] But I also wanted to live in Japan. That was another dream that I was waiting to fulfill while I was in L.A. I went in the meantime while because, as I said, I’m from Mexico, but to go teach English in Japan, I needed to be an American citizen and my mom’s American. But I was a resident. I had to wait until I had my citizenship to apply to go to Japan. So in the meantime, I went to L.A. and I did acting and modeling there. And then I was like, OK, but let me go to Japan first. But what if I don’t get in? So I got my certification before I left. I did get in. I went to Japan for two years. [00:08:17][29.7]

 

[00:08:18] I taught PE classes in Japanese high school and it was super fun. I was an English teacher. But, you know, they have you get involved with the students. And it was just really, really fun because I taught them, I did three different ones and one was just all cardio, like high-intensity interval training then the other one was just yoga. And then the other one was strength training. And so, like, I kicked their little butts, but, you know, like it was awesome. [00:08:42][23.5]

 

[00:08:42] And then the teachers were, how old were they? How old were the kids? [00:08:44][1.8]

 

[00:08:44] They were high school. [00:08:45][0.4]

 

[00:08:45] The last three years of high school, because they do years like in Mexico, where it’s like three middle school, three high school. So they were between 15 and 18. [00:08:52][7.0]

 

[00:08:53] Wow. Yeah. Yeah. No, that sounds familiar. How did you begin. How did you begin your fitness stuff. [00:08:57][4.4]

 

[00:08:58] Oh, my mom’s always been super active. We come from a super active family just because my mom has like crazy amounts of energy, she’s always like, yeah, she’s like, let’s go hiking, let’s do something. [00:09:11][12.3]

 

[00:09:11] Let’s do this. Like, we never just watched TV or did anything. [00:09:14][2.6]

 

[00:09:14] So I just grew up exercising. And in sports, it was just always a thing. So yeah, I just continued it and then in high school joined high school sports. And then once I got to college, I wasn’t in any sports. And I just felt weird. Like once you have been active for so long, you can’t just sit around. So I kept working out, kept doing that. And then, you know, I really loved watching your body change. It’s fascinating. It’s so. Yeah, it’s so. I just watch my own body change and not even that, like you said, how you feel. You’re like, oh, I have so much energy, I’m sleeping great, I’m doing better in school. Like, everything just starts to come together. So I just changed my major. I originally wanted to do physical therapy because I wanted to help people. But then I realized that I wanted to help them in more ways than just that. And so I switched it to exercise science where it’s more focused around nutritional aspects and things like that, where I could kind of do almost I felt a little bit more with it for where I wanted to go in life. So then I switched into that and then we ended up moving to El Paso. And now we’re here and I’m oh, we love it. And we’re still working out when I have a son. So he’s always busy, always playing, and we’re always looking up like what’s the youngest soccer league that they have, like something to get them interested. I also think if you give people tools early on, it also helps so much then they don’t have to have that same struggle that you had, because even though my mom was always active, she was still always like on a diet. She was wanting to look how TV looks. And it’s not always realistic for us, you know. [00:10:56][101.2]

 

[00:10:57] Right. So and she never really went about it the healthy way because she was uneducated. So she was just kind of, sorry… [00:11:04][7.4]

 

[00:11:05] Mom, she just didn’t know about it. [00:11:11][5.7]

 

[00:11:12] She doesn’t know about fitness and how carbs and everything actually work in your body. She just sees Pinterest and she’s like, oh, same as how you were talking about earlier. Well, this keto works for them, so I’m gonna do it. But if you don’t know what’s actually happening in your body, you don’t know the results because you’re not doing it correctly, you’re not following everything, there’s so much misinformation. So I love that you love to spread information and teach our clients like real-life skills that they’re going to use and implement. [00:11:44][32.6]

 

[00:11:44] Lizette what kind of other clients do you have? What kind of clients do you like to train? What’s your thing that you enjoy the most? [00:11:49][4.5]

 

[00:11:49] My thing. Look, you know what? I enjoy all kinds. And I really have had all kinds of clients. [00:11:55][6.0]

 

[00:11:56] I’ve had everything from people who used to be athletes in school who now aren’t like they’ve only been out from being athletes for like six months. So they’re still super fit and they want to keep training, you know, so I can really push them really hard for that. [00:12:08][12.9]

 

[00:12:10] So that’s really fun because I get to play with them and really push them and have them do crazy things that I’d come up with. It’s like, OK, now let’s jump over that box. And then you’re gonna pick up this weight and then you’re going to do a clean & press and then you gonna turn around. Are you’re going to do it again? OK. Because they can. Right. [00:12:26][16.5]

 

[00:12:27] But then also something that I love is the people that are looking for transformation. They’re like, you know what? Like, I just feel sluggish. I feel tired. I just don’t feel good. I’m starting to feel the pounds adding up and I just have aches and pains. It’s like, OK, let’s start. I love seeing them progress. I love seeing a person who can do 10 squats and be dying. And then by the end of the month, they’re hitting out the 20 and by the 20, they’re dying. But they look so much stronger. They feel great. They already told me, I feel stronger, I can sleep better, you know. And that’s just so I feel like my favorite is probably the transformation. [00:13:11][44.1]

 

[00:13:13] Like seeing their aha moments almost when they realize that they’re like, I’m here is when I’m doing this is what I’ve wanted. And yeah, like you said, that progress. That you first start seeing that it gives them, you even motivation to help them even more. And it’s great. It just…� [00:13:29][15.9]

 

[00:13:29] Keeps going. Exactly like when people are like struggling to do a push up on their knees. And then the first time you see them do five off their knees and they’re so proud of themselves. Yes. [00:13:39][9.6]

 

[00:13:39] You’re so proud of them. It’s like, yes. Over like, oh, I didn’t have any cravings this week because they finally were able to put themselves through, you know, like cleaning out their eating. [00:13:52][13.1]

 

[00:13:52] And now they’re used to eating healthy and eating like the healthy versions of sweet things or whatever it is, you know, and just having them have their aha moment, having them feel and live the transformation and understand it and be like, I love this, I can do this and I want to do this forever. That’s my favorite. [00:14:10][18.1]

 

[00:14:11] That makes a big difference, you know. El Paso has been in the last couple of years. I’ve been here since 1991, so I’ve seen the transition. When I first came here, El Paso was really dilapidated. It was a different town. And I got to say that when I first, I came from South Florida, my background was a fitness person and we were all into exercise physiology in Florida and California when we came out. When I came out here in 91, it was, there was no one into fitness. It was hard. They didn’t understand what it was to diet. There were a lot of metabolic syndromes, a lot of issues with weight, you know, waist-hip ratios. It just wasn’t important at one point. As I mentioned before in a prior podcast says that El Paso was considered the fattest sweatiest town in the United States. At one point. So this is within about. Around 2000, I started seeing a migration of a lot of fitness people and a lot of people that really took to it. And it’s really cool to see you guys because you guys have a love for fitness. [00:15:07][56.4]

 

[00:15:09] That’s endemic everywhere in El Paso, where right now we’re inside of the Push Fitness Center. It’s a Crossfit type of fitness center. Daniel Alvarado owns it. And he’s the one that actually might be here in a few moments. But what I wanted to say was that the world has changed in terms of fitness and it’s got a lot of individuals like yourselves out there teaching people, showing people. Where do you teach people at? Where is your fitness center at? [00:15:33][24.4]

 

[00:15:34] Well, right now, at the moment, I am not at a fitness center, but when I do have a fitness center, where I have been is Matt’s personal training and wellness center, which is on Airport Road. And so I am one of the trainers that use those facilities. [00:15:51][16.5]

 

[00:15:52] Before that, I was working at Gold’s Gym. But right now the goal is to have my own small, just small gym for only personal training. Personal coaching. Yeah, yeah. I originally wanted to have like actually kind of like this, like the push fitness, you know, not necessarily Crossfit but like a small gym where anybody can come and do their workouts. And also I’d like hit, I like teaching like short 30 minute hit classes. [00:16:16][23.9]

 

[00:16:16] When you say hit, what do you do particularly in your hit classes? [00:16:18][2.1]

 

[00:16:19] My gosh, so many things. [00:16:22][3.2]

 

[00:16:24] So for hit, I enjoy anything that is a lot, enjoy is a very particular word because it’s like you kind of hate it at that moment, but then you feel so good afterward. [00:16:34][9.8]

 

[00:16:35] And it’s a lot of jumping. So a lot of plyo. Plyometrics. So a lot of jumping. A lot of like box jobs. Burpees, love the burpees. The best thing is the combos of burpees and something else. So for example, like a burpee to a clean & press, burpee, clean & press and then just do that like 10 times and then you do something else. A lot of slam ball. You know, I love doing those in a lot of compound movements. And I also like doing the HIRT, which is high-intensity resistance training. So it’s kind of like hit. But instead of so much jumping. Right, you’re doing more of the strength. So really pushing, pushing, pushing short sets. Repeat, repeat, repeat. Between four and six minutes. And then I give a break, maybe 45 seconds to a minute and then we keep going. [00:17:18][43.0]

 

[00:17:19] That’s awesome. You know, with the transition, with the people who are stuck at home. How have you adapted to that situation in terms of the COVID protocol? [00:17:27][8.4]

 

[00:17:27] No. Well, basically virtual. Just seeing everybody virtual. I live in a small apartment, but I have a space where I can move. So I just tell my clients, make sure you find a spot in your house, your backyard, wherever you can. Where you have enough room to do A, B, and C before we have our meeting. And then we meet up and on Zoom. Zoom. Uh-huh.[00:17:49][21.6]

 

[00:17:49] And basically I usually end up working out with my clients. I’m going to be honest with you. I can’t stand there watching you do push-ups. [00:17:58][8.1]

 

[00:17:58] You know what? That’s true. It’s true. It is a fitness individual. I don’t know the idea that the best workouts are when you do it with somebody. Right. So, you know, in terms of even as a young kid, I was involved in training individuals and it was not fun watching. You know, it’s like I’m wasting my life here watching you. Right. So you get in there with them, you know, and while you’re in there, you give them the right amount of time to rest. And it’s almost like back and forth. So it’s kind of in tune the same way. So I like that. What other things do you do in terms of the times? The time? [00:18:32][34.0]

 

[00:18:33] Well, besides that, because a lot of people don’t have equipment at home. So I am implementing a lot of my hit workouts with the people that can do it. But for example, my older clients, they can’t really be, you know, like jumping around and doing things like that. But we work more on balance and flexibility and just basic strength. So no equipment workouts, which honestly, you don’t necessarily need equipment to get a good workout. You can always kick your butt with nothing like you, just your own body weight. So I do a lot of body weight. If people happen to have a lot of us have equipment, you know, at home, like some of us have a couple of dumbbells or a band or something. So I just adapt to whatever they have at home, be that nothing or a full gym at home. You know, some people are lucky and they just have a full gym so I can go all out. [00:19:22][49.1]

 

[00:19:22] What do you think of this new movement with the rubber bands and people using, you know, elastic bands to be able to supplement? [00:19:27][4.7]

 

[00:19:27] I like it. I like it a lot because of several things. One, it’s cheaper, so it makes strength training more reachable for anybody. More approachable. [00:19:39][11.5]

 

[00:19:41] And you can take it anywhere so you can travel with them. You can keep your routine even if you travel. And another thing that I like as a trainer and fitness person, you know, you need variety both in what you eat and what you do activity-wise. So I think they also add a nice variety to what you can do with them. The only thing is you need to know, like with so many other things, you need to educate yourself or have someone educate you about how to properly use them because it’s so easy for a band, for example, to put it in the wrong place by your knees and put the pressure in the wrong place, and I’m sure as you know, you could mess up joints and things by not putting the right equipment in the right place. So if you’re using a band wrong, you could potentially maybe cause some damage if you don’t. Don’t know how to use it properly. [00:20:29][48.3]

 

[00:20:29] Yeah, we were, I was watching, my son, who he actually trains people and they got caught in Chicago and they were kind of held in the university and no gym. The gyms were closed and out there in Chicago as well. And they developed these kinds of rubber band techniques. [00:20:45][15.2]

 

[00:20:46] That are amazing. And he calls his group, the functional fitness fellows. But what they learn is with all those exercises that you guys do with the rubber bands, you know, it really helps out the joints because the rubber bands kind of glide in the direction of the body movement. And that’s not obvious until you go through it. You feel like, man, this feels good. This rubber band. And then you also get the negative joy out of it, too, because you’re holding it from snapping back. Right. So it’s really a really cool thing. So I think that’s cool. What are the, do you work on diets as well? [00:21:19][32.6]

 

[00:21:19] Yes. Yes, I actually do a lot of nutrition. So anybody that I train for fitness, I also coach them in their nutrition. Again, we were talking about how they go hand-in-hand. You can’t have one without the other. And so for diets, I usually, it depends on what people’s goals are. Most people, especially in El Paso, like we’re talking about, most people are looking to lose weight, get fit. Right. So first of all, to lose weight, we need to balance things out. I always, always suggest to everybody, just for health in general, is to balance your plate in a way that half of it, half to 75 percent of it, should be vegetables. [00:21:59][39.3]

 

[00:22:00] That’s what I just, makes me happy, you know. Yeah. And I think that’s the best. Why? Because they have fiber. They have vitamins, minerals. They have all the good stuff that we need. [00:22:08][8.6]

 

[00:22:09] Well, if you look at a food plate now, if you just Google like what a food plate should be. So much of it is grains and bread. And it’s not. It’s like the person who made it isn’t. They need more vegetables, you know. So that, yeah, we need more. [00:22:24][15.1]

 

[00:22:24] I struggle with that with clients precisely because they see that plate. And it’s like but here it says that I need to have bread every day. A quarter of my plate should be bread. Well, no though. Yeah. Especially not if you want to lose weight and especially not that bread. It’s like, you know. [00:22:42][17.7]

 

[00:22:42] And so basically I always recommend. You want weight loss. You want to feel better. Let’s cut out all the super processed grains first. First of all, no pasta, no bread, no cookies, no processed sugar, no added sugars. That’s my first step. [00:22:55][12.5]

 

[00:22:55] And what do you, what do they say when that happens? What are they going to get? [00:22:58][2.7]

 

[00:22:58] They get very sad. But it’s also like unknowing sadness. [00:23:06][8.0]

 

[00:23:07] Like I knew you were going to say that, you know, it’s kind of like they don’t say it, but you can see it in their eyes. And it’s like, I’m sorry. Like, I know everyone wants to hear magical. What do you call like a recipe, a magical recipe that just like snaps and I can eat and do whatever and just Netflix all day and eat chips and be skinny but and fit? But you can’t like. You can’t. Yeah. So, yeah, 50 to 75 percent veggies. The other quarter or half should be balanced between proteins and healthy fats and maybe a few carbs but whole grains. And I always suggest that whole grains and that type of starches and things are kept to a minimum. [00:23:49][42.0]

 

[00:23:49] I always recommend especially for weight loss, either just keep them out completely or two to three times a week. I would say no more than three times a week is what I recommend. And I usually recommend my clients to eat their grains, whole preferably, you know, brown rice or quinoa or buckwheat. Oh, my God, I’m loving buckwheat. I just started buying it and eating it. And I love it. [00:24:11][22.1]

 

[00:24:12] I mean, but it’s very little like you literally need half a cup. You know you don’t need a million pounds of this. You don’t need to fill up a bowl with rice or something and then put like three vegetables on it. [00:24:24][12.5]

 

[00:24:24] It’s the opposite. [00:24:25][0.3]

 

[00:24:25] So do you do the Zoom diets, too, as well. Do you help them out with their diet? [00:24:28][3.0]

 

[00:24:28] Yeah. Yeah, we do. So I do. For nutrition coaching we usually talk and kind of like this. [00:24:32][3.8]

 

[00:24:33] It’s basically a conversation, you know the first time I get to know my client, we talk about it. What are your needs? What do you do? What is your schedule? Do you like to cook? Do you have time to cook? [00:24:44][11.7]

 

[00:24:45] Because all of these are important things, you know, and. Yeah, and yeah cooking makes life easier. But at the same time, not everyone has the time or ability. [00:24:52][7.6]

 

[00:24:53] And you want to make a plan for them that they’ll stick to. [00:24:55][2.2]

 

[00:24:55] Yeah, exactly. And you want them to stick to it. So I always try to work with them in regards to. Okay. What do you have available this and this and this. I make a note. We talk about it. I give them the information we verbally. But then once we’re done, now that we’re doing it this way, once we’re done, I send an email that has all the knowledge that I have. So everything that we talk about portions, the plate, portion sizes. So, like, measure your proteins like this. Like, for example, your fist is good to measure your vegetables. And for example, for women, we want to eat at least four to six portions a day. [00:25:29][33.9]

 

[00:25:30] So it’s like that’s an easy way to eyeball it. [00:25:33][3.2]

 

[00:25:36] I’m not the best. Always, at getting four to six, but it’s a good number to have again. [00:25:41][5.5]

 

[00:25:43] Four to six is good. You know what? For many of the diets, you kind of try to figure out which diets can work for people. Sometimes we end up with like Mediterranean, low fat, low carbohydrate diets. These diets, they change. I’m finding that a lot of the, just for El Paso in general, from the Mediterranean to low fats to even the ketogenic diet and though there’s been a lot of talk about the ketogenic diet. Do you do that? Do you offer those or what kind of diets do you like working with an individual, with an individual? [00:26:12][29.8]

 

[00:26:13] It really again, it depends on the person, because you also have to take into account like vegan people, people who are vegan, who are vegetarian or who have certain allergies to certain things. And so you need to really take a lot of that into account. And so I don’t necessarily prefer those like very restrictive diets, like keto and things only because people have a really hard time sticking to them. [00:26:41][28.2]

 

[00:26:42] I don’t know anyone who can for a long time, no. It’s hard. [00:26:44][2.4]

 

[00:26:45] And then they always want to, like, kind of cheat. And it’s like, oh. But I had this, too. And it’s like, no, no, no. Like, if you’re doing keto, it’s so specific. [00:26:52][7.1]

 

[00:26:52] Like Kenna was talking about, if you don’t know what this process is doing in your body, like there’s a specific reason why you’re only supposed to eat A, B, and C, but not D, E, F, you know. And if you add a little bit of these other ones, you’re throwing the whole thing off balance and instead of losing weight and still feeling better, you’re going to actually ruin it. So I prefer to work on something that is sustainable, which would be just OK. Kind of like portioned yourself. Try aim for the plates. But I do like paleo. Yeah, I love paleo or like primal ish. Yes. I always say that my diet is kind of primal ish. How so? Because I stick mostly meats, vegetables, fruits, seeds, nuts, vegetables, fruits, meats. I don’t do a lot of byproducts like I’ll eat eggs for example that. But that’s something that you could have gotten, you know, primally. I do. And then the ish comes from the grain sometimes, you know. Mm-hmm. So my ish comes from grains, sometimes cooked potatoes which, obviously that wasn’t a thing that they were doing. And my added sugars, I guess, which I don’t do a lot of. And I use monk fruit and I use stevia. But for the most part, I try to eat as whole as possible. And I consider that primal ish. Because it’s mostly things that are the least processed possible, and that’s what I prefer to give people. [00:28:24][92.0]

 

[00:28:25] Do you give your clients like help in the grocery store? Like, I know I learned when I first went to college and I had to buy my own groceries, that if you stick to usually the outside of the grocery stores, you’re gonna be way healthier because once you start going in those aisles, that’s where you start. All of the bad stuff, all the additives, it all starts coming in. And a lot of people I didn’t even think about it until I was in that position. I was like, wow, that’s true. Yeah. So what kind of tips do you give your clients when it comes to grocery shopping and success and things like that? [00:28:57][32.6]

 

[00:28:58] Basically that. Exactly, yeah. When I first heard the saying I was already doing it, but I hadn’t thought about it. [00:29:04][5.8]

 

[00:29:05] And so when I heard shop the perimeter of the store is when I thought, oh, no wonder I never know where anything is inside, like in the middle. I always if I ever need a can of something. Yeah. I’m like I don’t know where they have that or like if I’m going to bake. And I actually need regular flour for something like I don’t know where that is because I always just like shop the perimeter of the store. So yes, that’s I would definitely do that when shopping. [00:29:31][26.1]

 

[00:29:32] Just stick to buying things that have the least amount of processing. [00:29:36][4.4]

 

[00:29:37] So if you go around the perimeter, you get all your vegetables, you get your meats, you get your animal products right. You have your eggs, your milk, your cheese, you have all those things. So I think that’s a really good idea. You also have your freezers, which while they do have all the bad frozen stuff, they also are frozen fruits and veggies, which, as we know sometimes can be better than buying fresh, because if the zucchini is sitting in your fridge for two weeks, it’s lost a lot of nutrition. [00:30:04][26.5]

 

[00:30:04] But if you buy some frozen stuff, you can actually, you know, it keeps its nutrients a little better so you can make smoothies, especially for people who don’t have a lot of time. [00:30:15][10.5]

 

[00:30:15] I recommend frozen fruits, for example, and just kind of like throw them in there for the smoothies, some yogurt and let’s go, you know, quick breakfast. [00:30:22][6.9]

 

[00:30:23] We’re big fans, big smoothie fans here. Yes, big fans. Because, as you said, they’re just so fast. Yes. And you just throw everything you need in there. You’ve got your fruit. You can do vegetables in there, too. [00:30:33][10.3]

 

[00:30:34] Lizette, we have Daniel here. Daniel, come on in. Have a seat, please. [00:30:40][6.8]

 

[00:31:30] Daniel. Just to turn to you for a little bit here. I’ve noticed that in the last couple of days this place gets really packed in terms of people looking for new fitness during these periods of time. How has it been during this COVID period of time for you in terms of the diets, in terms of fitness? [00:31:43][14.0]

 

[00:31:46] It’s been a lot of adaptabilities trying to make sure to make everybody feel as comfortable and safe as possible, so we have constant like screening in every single class as far as wiping things down and mopping the area. I mean, the cleaners, the gym has never been cleaner than ever before, which is. [00:32:03][16.3]

 

[00:32:03] And I can attest to that. I love this place. I really wanna eat in this place, man. I want to eat off the floor. [00:32:07][3.9]

 

[00:32:10] But with that and then with still the online training promos that we’re doing, that I’m sending online it still gives people the option of either coming into the gym or doing it at home. We were able to rent, lend some equipment so they can feel comfortable and so do it at home until they feel safe and coming back to the gym. But through all of that, what I’ve told people is that they have to make sure that the workouts have to be a little bit longer than here because they’re living more sedentary lifestyles so they can’t eat the same as they were before. Even if you were used to driving from point A to point B, up and down, and round, you’re still doing more activity than you were before, because now you’re just behind the computer, sitting down and you sit down and then you go to the sofa. And then when you’re on the sofa, you water the grass. Isn’t going to the refrigerator… [00:33:04][54.5]

 

[00:33:05] Exercise? Unless you put your refrigerator a mile away from your house. That’s a good idea. Come to your house. Everyone can eat it at your refrigerator. [00:33:15][10.7]

 

[00:33:16] Only. Ten burpees on your way to the fridge every time. [00:33:19][3.3]

 

[00:33:20] Yeah, that’s a good idea. Ten burpees on the way to the fridge. You know what? That makes it worthwhile. Just punishment for opening the door. Exactly. [00:33:28][8.1]

 

[00:33:29] So I’ve noticed that everyone’s doing a lot of people, as I was just speaking regarding that she does the I guess the telehealth over the phone, over the systems, and in the Internet. And Zoom, you found that to be very comfortable. I know you began that process when this COVID got really hard and heavy. [00:33:45][15.9]

 

[00:33:46] You were all over it, like just talking to people one on one on the Internet. How did that work out? [00:33:51][4.9]

 

[00:33:52] Danny oh, me? Yeah. Yeah. [00:33:56][3.6]

 

[00:33:57] You know, it was a little bit. It was a harder transition for me first. Took me about a week after we shut down. To actually get it going. Just because. First of all, I’m not the craziest about even face time, I don’t like looking at myself when I’m talking to someone it’s weird. So I would have to shut off the camera. But then it defeats the purpose. You know, some people want to see you. So we develop videos and it shows you how to whether it’s me or another instructor and how to do the workouts and things like that. And then all our app is messaging. So you can instantly message on the app. And now we send out motivational quotes, daily tips, you know, things like that to help them keep them going. This is a transition because I got used to, you know, interacting with people on a day to day basis. So seeing me on a computer, which I hadn’t done in a very long time since I was back in school. Yeah. Was different for me, but it was good. I mean, you have to adapt to survive, you know. [00:34:54][57.0]

 

[00:34:56] You know, I’ve seen the whole world go through a massive transition in terms of the fitness. She was talking about the diets and how do you help people with diets and tune in to diets during this period of time? [00:35:07][10.9]

 

[00:35:09] Initially, first I ask what their lifestyle was like. Obviously, if they love working in a warehouse trying to keep them on a low carb diet like that is probably not the most ideal. They’re sweating, losing electrolytes, things like that. So they’re gonna be grumpy and dehydrated at the end of the day, so once they get their lifestyle, then from there I can adapt to their cording needs. You know, if they only work out three times a week, will we adjust more carbs on those workout days, less carbs on the non-workout days? So everything’s just right. Yeah, balance and manageability according to what the individual’s lifestyle is like. [00:35:50][41.4]

 

[00:35:52] You know, it’s really a big thing. And let me ask you this, how are people adapting to coming out and especially during these times? How are they feeling when they come in? And with all the regulations and all the fear that is behind people? [00:36:05][13.1]

 

[00:36:06] Well, we ensure that if before they walk into a door, if our main focus is that they can smell bleach, OK, if they can smell bleach, then our gym facilities are clean. So we try to keep that and I know this sounds kind of dumb, but I do ask people, hey, how does it smell? I’m sure you can smell the cleaning from the parking lot. Cool. We’re good. So that’s what makes people feel initially comfortable. Obviously they’re not inhaling it. So don’t misconstrue my words. [00:36:37][30.9]

 

[00:36:38] Well, well, well. We do have a biochemist on the line here. OK. So the biochemist would be my son and he calls me up and he goes… [00:36:46][7.2]

 

[00:36:46] Hey, Dad, listen, I know that you like the smell of bleach and I go yeah, that means it’s clean. But I want you to know something, chlorine is odorless. [00:36:54][8.3]

 

[00:36:56] It’s a good point. So he says it’s when it binds to certain urea molecules. Right. Where the smell of the chlorine comes out. So actually, the smell at a pool and the smell in an area is the actual effect of it’s combining with human dynamics. Isn’t that interesting? [00:37:14][18.1]

 

[00:37:15] So I don’t know if I wanted to know. [00:37:16][1.4]

 

[00:37:17] Oh, yes. I don’t think you wanted to know. But hey, you know what? [00:37:19][2.2]

 

[00:37:19] I got to tell you, it lets you know that when it’s being used and you smell that combination, it’s doing its job, working and working. [00:37:27][7.3]

 

[00:37:27] It’s working because chlorine. [00:37:30][3.0]

 

[00:37:31] Oh yes. Well yeah. Well you know I don’t know. This a different kind of show. I mean. He just took it to far. Yeah. Thank you. You took it too well but thank you for coming by Danny. No, no, no. [00:37:44][13.1]

 

[00:37:44] So, we’re looking at it and it really, really is a big difference because we’ve seen a lot of people. And what I was surprised with Danny is knowing how many people are, Lizette, there’s a lot of people out there, you know, that need the fitness. Right. Are you finding a lot of people coming to and knocking on your door to asking for your kind of like, help me now? [00:38:01][16.1]

 

[00:38:01] Because this is a real big problem. A lot of people don’t know what to do and they need help. Do you see that there’s a lot of people outreaching towards you right now because of the situation? [00:38:10][9.2]

 

[00:38:10] Yes, yes. Yes. Now, especially now that it’s been months and people are seeing the effects of their change of lifestyle, you know, the less walking, the less activity and the improper eating. Yeah, I have actually over the last week even I was approached by like three people within two days. Yes. That’s like not normal. [00:38:34][23.9]

 

[00:38:35] Right. Right. Because I’m not even promoting right now and we promote via social media. [00:38:40][5.3]

 

[00:38:42] You know, it’s like. Oh. Oh, jeez. OK. Yeah. Yeah. [00:38:45][2.6]

 

[00:38:45] You know what? I get ready to see sometimes though the context through the push and I see people 3:00 in the morning, hey I need help at 2:00 in the morning. People all over the time just we need help. We need to have individuals out there that can help us and guide us. So it’s really cool to see what’s going on. Let me ask you this in terms of these times, nutritional tips. Tell me a little bit about like what kind of nutritional tips you tell people. Danny just mentioned some things about, you know, certain things to eat. How do you do it? [00:39:13][27.9]

 

[00:39:14] Well, along the lines of what Danny was saying is exactly like a great point is making sure that what you’re taking in matches what you’re doing during the day. So if you’re doing your workout that day and you have like really intense workout or really intense job, you can eat maybe your carbs that day, you know, like add some rice or some buckwheat or quinoa to your lunch. On the other days, if you’re not doing anything, you only maybe walked for 30 minutes or an hour and then went home and just chilled all day. Then good salad, some grilled veggies, some steamed veggies, some grilled proteins or alternatives would be good. So my biggest tip is cut out all the additives that you don’t need, like sugars and super processed foods. But make sure that if you are exercising the days that you are active, you are ingesting the right amount of food and the right types of foods too, you know, like just basically that just match your foods, your intake to what you’re doing and mostly stick to the veggies, stick to the lean proteins. And then when you’re active, you can have a little bit of the starches. [00:40:26][71.4]

 

[00:40:27] I’d like to ask both you these questions because I know what we can talk forever and we have some gifted communicators here. But let me ask you this, Danny, in terms of like a visual how to set up a kitchen, you know, in terms of for success. I was, you know, kind of questioning. How do you approach a person and say, this is how I want you to set up your kitchen so that you can be successful? This is the domain. Everything starts in the kitchen. It starts there and from there propagates. So how do you help them out in terms of preparing the philosophy or the way of thinking for their kitchen? [00:41:01][34.2]

 

[00:41:03] In, man, that can be designed in 100 or one different, it depends on the person. [00:41:08][5.3]

 

[00:41:09] But. What I tell people is if they’re going to lose weight. [00:41:13][4.0]

 

[00:41:14] And it’s not healthy. Don’t buy it. That’s probably the easiest thing. Chips. Obviously, don’t buy them. Candy. Don’t buy it. [00:41:24][10.2]

 

[00:41:27] That’s true. Yes. [00:41:28][0.6]

 

[00:41:28] It’s a realistic way. Because if you buy it, I don’t care who you are. Even me, there’s a bag of chips at home. I’ll open them up and start eating away. [00:41:37][8.9]

 

[00:41:38] Yeah. Actually, yes. [00:41:38][0.6]

 

[00:41:39] So I’m not gonna tell people, you know, willpower. Just say no to those chips. It’s dumb, you know? It’s just don’t buy it because obviously at 9:00 at night, you’re less likely to go out to the corner store and buy chips or candy or ice cream or something like that. So it’s better you don’t buy it. So if, for example, your cheat day is on a Saturday, then go out on a Saturday and go buy, go to the grocery store and buy like somalo kind of ice cream. Don’t buy a tub of ice cream because you know, you’re eating it. [00:42:14][34.6]

 

[00:42:14] Well, I mean, you might finish in a day, but don’t. [00:42:17][3.2]

 

[00:42:18] But at least you have a gauge as far as what to do and what not to do. And then you can also do it as far as. Right. All right. So I didn’t buy this amount of extra and I saved forty bucks. Why don’t you take that 40 bucks and put it into like an extra count, you add it up? That’s an extra 300 bucks a month. And use that to reward yourself. You could buy, I don’t know whatever you’re into, not necessarily new clothes, something for your cars and for your house, you know, but find other means of reward for yourself, because if you’re just looking for food as a reward, then you’re going to go into a constant cycle of never losing weight. [00:42:56][37.9]

 

[00:42:56] Danny, you mentioned something that was real, real important. And I think sometimes we need some weight up quarantine ourselves because we’ll be good if we’re quarantined. [00:43:04][7.5]

 

[00:43:05] And one of the things is through the budget, if you can take the budget and you can say, I want to you know, my family typically spends, let’s say, four hundred dollars on their food a week because it gets expensive. Right. How about just say, you know what, I am not going to allow me this myself to spend more than 300 dollars. Right. And in that three hundred dollars, you kind of make you got to shoot it. Perfect. In other words, you’re not going to get the extra junk. The ice creams and the stuff you’re gonna get them, the stuff that is healthy inside the diet. And if you can do that. I bet you say that if a family that eats 400 hours a week can say, I’m going to make my budget last for 250, 250, let’s say 250, start with 250, and bust yourself to work 250 in that store and make sure that you don’t put anything extra at that point. You’ve hit close to the market. And before, you know, your refrigerator starts looking good, it starts looking nutritional things and you don’t have the extra the bonbons, the sugary stuff, the chocolates, the cookies, all those things get that are really, really bad in our diets. If they are expensive, too. And that’s what you were alluding to, that you say, you know what? That’s extra money. But if we don’t know and what’s 100 bucks a week for food and for a family that’s four hundred dollars a month? Well, that’s four hundred dollars. That’s five thousand dollars a year. That’s five thousand dollars. So if we look at it, if you look at one hundred, you can save about two thousand dollars almost. If you want a hundred fifty dollars. What can you do with two thousand dollars a year? That’s just on the budget side of things. Right. So if you can contain it and say, you know, I want to stick to that, it may help people also guide and make the right choices because I don’t have the option to go ahead and buy the chips aisle. That’s expensive. And that’s the stuff that gets us, you know, kind of unhealthy. Well, the well-nourished is what they call it. That’s what I call it in the books. Well-nourished. So those are the cool things. So let me ask you this in terms of nutritional tips for people to kind of be left with today, because I know we can talk for three days here. Nutritional tips. What are the nutritional tips during these times? If you could give them Lizette. Tell us about your nutritional tips for people during these times that would help them out. [00:45:14][129.0]

 

[00:45:14] My nutritional tips. [00:45:15][0.8]

 

[00:45:15] Well, part of like with the kitchen set up one thing that I feel like it’s important that you can implement. Some of the suggestions that I’ve said before is having the right kind of equipment in the kitchen, for example, if you have, for example, good nonstick pans. [00:45:31][16.2]

 

[00:45:32] That’s going to reduce the amount of oil because so many people are like, oh, well, just so it doesn’t stick a million gallons of oil, it’s like no no no get a good nonstick pan. [00:45:41][8.8]

 

[00:45:42] And then one teaspoon of oil should be enough to give your food a good flavor and kind of like, you know, measure yourself basically, measure your oil and make sure you have the right equipment. Bake things. Make sure you have stuff in the kitchen to bake, to grill. Anything baked, anything grilled is much better than anything fried. Right. Of course. [00:46:02][19.7]

 

[00:46:03] And get an air fryer. You can have. Oh, my gosh. Yes. You can get fries. You can have wings. But not extra greasy. You know, like every now and then when you have your treat instead of a super greasy meal, you know, you can make it. [00:46:17][13.6]

 

[00:46:17] So basically, just make sure you have the resources to make healthy choices. Like Danny’s point is exactly something that I always say is don’t keep it. That’s also my number one, is don’t keep junk at home. Only get it when you want it at the weekend. Whenever you cheat day is get one for that day and that’s it. Other than that, fill up on veggies and lean proteins and save the starch and the carbs for either when you worked out really, really hard, or only two to three times a week and only wholegrain. [00:46:48][30.9]

 

[00:46:49] Those are amazing tips. I could totally see myself doing that. You got some tips, Danny, for people during these times. [00:46:54][5.8]

 

[00:47:04] Make sure you distinguish whether if you’re thirsty or you’re hungry. It’s a lot of times people will confuse that. And so if you drink eight, 16 ounces of water, even you can swing it with a little crystal light. I don’t always recommend that, but you can chug that first. And if you’re still hungry, then your body needs some nutritional value. [00:47:25][20.3]

 

[00:47:25] But if you get full after you get energized, like you should be good, you’re just thirsty, dehydrated. [00:47:30][5.0]

 

[00:47:31] And then another thing too, is moderation of fruits. You know, apples and strawberries, blueberries, things like that. Anything like mangoes, bananas, a little bit higher in sugar. So maybe you can stay away from those because they sometimes will make you hungrier because they’ll release, certain hormones and they’ll trick your body into thinking that it’s really hungrier when it’s not. So a lot people will confuse that when you eat carbs. You sometimes get full, you get full for a short amount of time, and then you’re hungry right away again. And then you think your metabolism is going. But it’s not necessarily true. It’s releasing hormones as tricking the mind and the body to thinking that it’s hungry and it’s not full. [00:48:12][40.6]

 

[00:48:12] But in reality, you like it. You’re not hungry. Yes. Yes. So distinguishing those two as part of those, the top two of them on top of. Well, as I just said, that would help you. Like I said, the more basic, the better. The more complex, the more options give yourself, the harder it’s going to be. Every. There’s so many diets out there and they’re all good in their own way as long as you stay consistent. Yes. Reason diets don’t work is because everybody stops after fourteen or fifteen days and then they have to start the loop all over again. Takes 21 days to create a habit. So if you break that before you got it, you have to start every single time. So it’s like drive yourself crazy. It’s insane. You know? Yeah. [00:49:00][47.9]

 

[00:49:00] Well, I tell you, I’ve learned a lot. I’ve learned. You know, I’ve learned about monk fruit. You have mentioned the monk fruit and tell me before. But before you go, what do you, what’s your theories on monk fruit? Lizette. [00:49:10][9.8]

 

[00:49:11] Well, for now. So far. Yeah. Remember when Splenda was good? [00:49:16][5.2]

 

[00:49:17] What I gotta tell you right now, Splenda is like they’re saying, hey, you know what? Even stevia. You mean even organic stevia. It’s already like, you know, it’s on the cutlist. [00:49:24][6.6]

 

[00:49:24] Now it’s my Alzheimer’s. That’s right, Bill. You’re gonna leave me with no options. [00:49:31][7.3]

 

[00:49:32] Well, so far for until. For now, it seems like monk fruit. It tastes a lot like sugar. So it helps you with that like craving. But it doesn’t have the like the effect that the fruits or the grains will give you where your insulin is going to drop and then you’re gonna be hungry again. Or you store it in. It turns into fat or anything like that. So far it looks like it doesn’t. I love it because it doesn’t have that bitter chemical aftertaste. [00:50:01][28.7]

 

[00:50:01] That maybe some stevias do. And I’ve gotten away with sneaking that into desserts for kids and other people that don’t know that’s in it and they don’t notice the difference. Yeah, and they’re cutting a ton of calories. You know, I love it so far. [00:50:17][15.8]

 

[00:50:18] It’s an amazing little dynamic option there, because one of the things is, is that with diseases now, the monster is insulin. And if we can stop the insulin reaction from occurring, that is the name of the game, whether it’s through periodic eating or limiting your time slots of eating, the whole thing is to stop Lipoprotein lipase from putting it into fat. And the thing that does that is insulin. And monk fruit seems to not stimulate an insulin response. So that becomes the biochemistry, from what I understand. [00:50:49][30.5]

 

[00:50:49] And like you said, as of today, right now we don’t know. [00:50:53][4.4]

 

[00:50:53] So we’ll talk about those things as we go. Listen, guys, I want to thank you guys up and down on the bottom. You’ll see the connection to everybody here and the links directly to their facilities. And I look forward to having that. So we’ll be able to talk about some more things in the future. Thank you, Kenna. Thank you Lizette. Danny, thank you. Thank you, me. We’re all here. And it was a pretty comfortable place and it was a really interesting dynamics. And we’re gonna be bring different topics in. And as we go through the times and discuss those issues that are important to our people in El Paso, it’s very important to be able to kind of understand the minds, to be in with our patients. It’s not about them and us. It’s about we. So when we work together, we look together for solutions and it’s not so mezocryptic when you realize that people like us are all really trying to help everybody here. So look forward to connecting again and look forward to hearing from you. So, thank you, guys. Thank you again. [00:51:44][51.0]

 

[2973.8]

 

Does the Brain Need Carbohydrates?

Does the Brain Need Carbohydrates?

Our brain is constantly working to help us make decisions, speak, read, and perform many other important functions. It’s also responsible for several involuntary processes, including breathing, regulating body temperature, and secreting hormones. The brain needs a consistent supply of energy in order to perform these essential functions. It mainly uses glucose as fuel for energy, however, does the brain really need glucose from carbohydrates to function properly?

 

What Happens When You Don’t Eat Carbohydrates?

 

According to healthcare professionals, the brain needs between 110 to 145 grams of glucose per day to function properly. Most people who follow a high-carb diet provide their brains with an abundant supply of glucose. However, what happens when you eat less than 110 grams of carbohydrates per day or even no carbs at all? Does your brain starve? Absolutely not! Our muscles and liver store glucose in the form of glycogen, a polysaccharide of glucose.

 

When you don’t eat carbs, glycogen in the liver is broken down into glucose and released into the bloodstream to prevent low blood glucose levels. While more glycogen is stored in the muscles than in the liver, it stays in the muscles to meet their demand for energy and it can’t be broken down and released into the bloodstream to prevent low blood glucose levels. After about 24 to 48 hours without eating carbohydrates, glycogen in the liver is depleted and insulin decreases.

 

The liver will then produce ketones, water-soluble compounds produced by the breakdown of fatty acids. Ketones are produced from the fats you eat or the movement of stored body fat. Ketones can penetrate the blood-brain barrier (BBB) and enter the bloodstream in order to reach the brain and provide additional energy. This ultimately means that ketones can also be used as fuel for energy when our body is running low on glucose from carbohydrates.

 

Can Your Brain Use Ketones Alone for Energy?

 

Our brain always needs some glucose for energy. However, healthcare professionals have shown that for several people following a ketogenic diet, ketones can be used to meet up to 70 percent of the brain�s energy needs. As for the rest of the brain�s energy needs, your liver can produce the glucose it needs through a process known as gluconeogenesis. Thus, the liver can meet the brain’s energy needs through stored glucose, the production of ketones, or gluconeogenesis.

 

Glucose Alone vs Glucose and Ketones for Energy

 

If you follow a moderate-carb to a high-carb diet, your brain may not be properly adapted to use ketones as fuel for energy. Therefore, glucose will be the main source of energy for your brain. However, when your body has adapted to following a low-carb or carb-free diet, the brain can easily use ketones to meet the brain’s energy needs and the liver can make as much glucose as it needs to meet the rest of the brain’s energy needs in order to function properly.

 

What are the Low-Carb and Ketogenic Diet?

 

While there is a lot of similarities between the low-carb and ketogenic diet, there are also several important differences. The differences between the low-carb and the ketogenic diet may include but are not limited to the following:

 

Ketogenic Diet

 

  • Carbohydrates are limited to 50 grams or less per day.
  • Protein is generally limited or restricted.
  • The main goal is to increase the production of ketones.

 

Low-Carb Diet

 

  • Carbohydrates can vary from 25 to 150 grams per day.
  • Protein is typically not limited or restricted.
  • Production of etones may or may not increase.

 

In conclusion, eating carbohydrates to use as fuel for the brain’s energy needs is an option, not a requirement. It�s true that the brain can�t depend on ketones alone as it always needs some glucose as well. It’s important to understand that your brain isn�t in any danger if you follow a low-carb or a ketogenic diet. However, before following any particular diet, always make sure to talk to a healthcare professional to determine if these nutritional guidelines are right for you.

 

For information regarding the effects of carbohydrates on the brain, please review the following article:

Effects of a Carbohydrate Supplement Upon Resting Brain Activity

 


 

 

Our brain is constantly working to perform many important functions. The brain needs a consistent supply of energy in order to perform these essential functions and while it mainly uses glucose as fuel for energy,� the brain doesn’t really need glucose from carbohydrates to function properly. Glycogen in the liver is broken down into glucose. The liver will then produce ketones, water-soluble compounds produced by the breakdown of fatty acids. Ketones are produced from the fats you eat or the movement of stored body fat. Ketones can penetrate the blood-brain barrier (BBB) and provide additional energy for the brain. However, our brain always needs some glucose for energy. Your liver can also produce the glucose it needs through a process known as gluconeogenesis. Thus, the liver can meet the brain’s energy needs through stored glucose, the production of ketones, or gluconeogenesis. A low-carb or a ketogenic diet can provide a variety of benefits. Always make sure to talk to a healthcare professional to determine if these nutritional guidelines are right for you.�- Dr. Alex Jimenez D.C., C.C.S.T. Insight

 


 

Image of zesty beet juice.

 

 

Zesty Beet Juice

Servings: 1
Cook time: 5-10 minutes

� 1 grapefruit, peeled and sliced
� 1 apple, washed and sliced
� 1 whole beet, and leaves if you have them, washed and sliced
� 1-inch knob of ginger, rinsed, peeled and chopped

Juice all ingredients in a high-quality juicer. Best served immediately.

 


 

Image of carrots.

 

Just one carrot gives you all of your daily vitamin A intake

 

Yes, eating just one boiled 80g (2�oz) carrot gives you enough beta carotene for your body to produce 1,480 micrograms (mcg) of vitamin A (necessary for skin cell renewal). That’s more than the recommended daily intake of vitamin A in the United States, which is about 900mcg. It’s best to eat carrots cooked, as this softens the cell walls allowing more beta carotene to be absorbed. Adding healthier foods into your diet is a great way to improve your overall health.

 


 

The scope of our information is limited to chiropractic, musculoskeletal, physical medicines, wellness, and sensitive health issues and/or functional medicine articles, topics, and discussions. We use functional health & wellness protocols to treat and support care for injuries or disorders of the musculoskeletal system. Our posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate and support directly or indirectly our clinical scope of practice.* Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. We understand that we cover matters that require an additional explanation as to how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900. The provider(s) Licensed in Texas*& New Mexico*�

 

Curated by Dr. Alex Jimenez D.C., C.C.S.T.

 

References:

 

  • Spritzler, Franziska. �Food for Thought: Does the Brain Need Carbs?� Diet Doctor, Diet Doctor Media, 17 Jan. 2019, www.dietdoctor.com/low-carb/does-the-brain-need-carbs.
  • Spritzler, Franziska. �How Low-Carb and Ketogenic Diets Boost Brain Health.� Healthline, Healthline Media, 26 Mar. 2016, www.healthline.com/nutrition/low-carb-ketogenic-diet-brain#section1.
  • Dowden, Angela. �Coffee Is a Fruit and Other Unbelievably True Food Facts.� MSN Lifestyle, 4 June 2020, www.msn.com/en-us/foodanddrink/did-you-know/coffee-is-a-fruit-and-other-unbelievably-true-food-facts/ss-BB152Q5q?li=BBnb7Kz&ocid=mailsignout#image=24.

 

Stubborn Weight: Genetics or Diet?

Stubborn Weight: Genetics or Diet?

Today, there can be a lot of confusion when it comes to diet. The information received can be contradicting, confusing, and leave individuals feeling lost. This can often result in giving up on the diet and being left with joint pain, inflammation, discomfort, headaches and more.

The reason why there is more than one diet out there is because the research is always advancing. We have come to realize that everyone’s body reacts to different food sources and diets differently.

Genetic Code

As more and more research is being done, the more we are realizing how the genetic factor of individual cells directly correlate to a patient’s weight, diet, and changes as they age. For years, as one would get older and start gaining weight, we would attribute it to age. Although age is a factor, what we are finding now is that the genes are actually changing as we age and that is what creates this weight gain.

Sure enough, there are also genes that will tell us if you are susceptible to snacking. These genes can detect if you have a predisposition for heightened snacking or satiety. Satiety is the feeling of fullness after a meal. If you have reduced satiety, you tend to snack more because you do not feel as full after the meals you eat.

Getting your genes tested will allow the treatment plans created to be more personal and more geared to see results! Believe it or not, your genes can tell us if you are genetically prone to obesity,� if you have weight loss resistance when it comes to carbohydrates, and how your body responds to exercise! Using the genes, we can see how many hours per week you will need for weight loss or to maintain your current weight.

Proven Methods

The best option is to know your genes so the diet plan can be geared more towards you directly. However, if that is not a possibility right away, there has been one diet that has been proven time and time again to work for almost everyone. This diet is referred to as the Ketogenic Diet.

In simple terms, the ketogenic diet is a low carb, high-fat diet. This diet works by sending the body into a state of ketosis which burns fat as fuel.

Research shows that those using a ketogenic diet demonstrated a higher percentage of weight loss and kept the weight off longer when compared to those who did a low-fat diet.

Available Resources

Considering the fact that there is misinformation about diets out there, proper education is going to be the key. As someone who has gone through dietary changes myself and figuring out what works best with my body with type 1 diabetes for optimal health, the right team is what made me successful.

Surround yourself with those who are continuously educating themselves and have a system in place. For example, we make sure our patients get one on one time with the doctor and a health coach. From here, the health coach and patient become connected through a virtual database allowing the patient’s food, weight, supplements, hydration, BMI, BIA, and activity to be tracked by the health coach. The health coach can then instant message or video chat the patient throughout the week to ensure they are staying on track, staying motivated, and answer any questions they may have!

Do not be left confused over diets anymore! Remember that your genetic code holds the key to the right diet for you.

The right diet has the ability to make individuals see the results they have been waiting for. It all comes down to the genes. As mentioned, genes change over time but they hold the code. If you are someone who has struggled with diets, feeling good, or are stuck at a certain weight, I highly recommend getting tested! The information you gain from this is so beneficial! I have seen the results first hand, and they are eye-opening. They let you know if you have the genetics that will hold onto fat. This knowledge can help us prevent health issues such as metabolic syndrome! – Kenna Vaughn, Senior Health Coach�

Dr. Alex Jimenez�s Blog Post DisclaimerThe scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.

 

REFERENCES
Bueno, Nassib Bezerra, et al. �Very-Low-Carbohydrate Ketogenic Diet v. Low-Fat Diet for Long-Term Weight Loss: a Meta-Analysis of Randomised Controlled Trials.� British Journal of Nutrition, vol. 110, no. 7, 2013, pp. 1178�1187., doi:10.1017/s0007114513000548.

 

Ketogenic Diet for Metabolic Syndrome

Ketogenic Diet for Metabolic Syndrome

The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.

 

What is the Ketogenic Diet?

As previously mentioned, the keto diet is a low-carb, high-fat diet similar to the Atkins diet, as well as other low-carbohydrate diets. The primary goal of the ketogenic diet is to considerably decrease the consumption of carbohydrates and replace them with “good” fats. Reducing carb intake will allow the body to enter a metabolic state, known as ketosis. During ketosis, the body becomes tremendously efficient at burning fat in order to turn it into energy for fuel. It will also produce ketones in the liver to be used as energy by the brain. The ketogenic diet can greatly improve high blood sugar levels and insulin resistance.

 

Metabolic syndrome is commonly characterized by 5 risk factors. People with 3 our of 5 risk factors may have metabolic syndrome, including:

 

  • Excess waist fat (> 40 inches in men, and > 35 inches in women)
  • High blood pressure (130/85 mm Hg)
  • Hight blood sugar or glucose levels (100 mg/dL or greater)
  • High triglyceride levels (150 mg/dL or greater)
  • Low HDL cholesterol (< 40 mg/dL in men or < 50 mg/dL in women)

 

Metabolic syndrome can increase the risk of a variety of health issues, including diabetes, stroke, and heart disease. Fortunately, the keto diet can help improve the risk factors associated with metabolic syndrome, such as increased HDL cholesterol as well as decreased blood pressure and blood sugar levels. In a controlled 12-week research study, people with metabolic syndrome following a calorie-restricted ketogenic diet lost 14 percent of their body fat. The research study also found that the participants had decreased triglycerides by more than 50 percent and experienced several other health benefits.

 

How the Keto Diet Helps Improve Metabolic Syndrome

The ketogenic diet has been demonstrated to help improve the risk factors associated with metabolic syndrome. As a low-carbohydrate, high- fat diet, the keto diet is effective in decreasing high blood sugar levels and improving insulin resistance by having the body break down body fat into ketones for energy. Metabolic syndrome is a cluster of signs that are associated with various health issues, including diabetes, stroke, and heart disease. The signs of metabolic syndrome include excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL or “good” cholesterol.

 

A research study conducted by researchers at Bethel University, Minnesota, USA, compared the health of three groups of adults with metabolic syndrome. The first group followed the ketogenic diet without exercise, the second group followed the standard American diet without exercise, and the third group followed the standard American diet with 30 minutes of exercise or physical activity for three to five days per week. The findings showed that the ketogenic diet without exercise was much more effective than the other groups at promoting weight loss, decreasing body fat and reducing HbA1c.

 

According to a variety of other research studies like the one above, the ketogenic diet may help improve a variety of other health issues, including:�

 

Type 2 Diabetes

Although there’s a variety of research studies on what is the best type of diet for people with type 2 diabetes to promote weight loss and improve insulin resistance, healthcare professionals recommend following the keto diet. The keto diet lowers carb intake which causes high blood glucose levels to drop, producing less insulin, burning fat, and potentially improving insulin sensitivity. Research studies suggest that the keto diet may be helpful for people with type 2 diabetes. Several hospitals have comprehensive programs dedicated to using the nutritional approach to help treat type 2 diabetes.

 

Obesity

Excess weight and obesity increase the risk of developing type 2 diabetes. A small research study published in December 2016 in the journal Endocrine involved 45 obese participants either on a very-low-calorie ketogenic diet or a standard low-calorie diet. After two years, the participants following the keto diet lost approximately 27 pounds on average compared with less than 10 pounds in the low-calorie participants. The participants following the keto diet also lost more belly fat. The ketogenic diet also helped keep lean body mass during weight loss which prevented a metabolic slowdown.

 

Metabolic Syndrome

 

Metabolic syndrome is a collection of risk factors, including excess waist fat, high blood pressure, high blood sugar, high triglyceride levels, and low HDL cholesterol, according to the American Heart Association. Improving insulin resistance may also reduce the risk of developing metabolic syndrome. One small research study on 30 adults found that adults with metabolic syndrome who followed the ketogenic diet for 10 weeks lost more weight and body fat as well as lowered their A1C levels compared with participants who followed a standard American diet, even with or without exercise.

 

Dr. Alex Jimenez Insights Image

About 23 percent of adults in the United States have metabolic syndrome. Although the risk factors for developing the collection of signs are significant, there are good news. Many of the risk factors associated with metabolic syndrome can be addressed through diet and lifestyle modifications, such as the ketogenic diet as well as exercise and physical activity. By making these changes, people can considerably reduce their risks of developing a variety of other health issues, including diabetes, stroke, and heart disease. Although metabolic syndrome can be a serious health issue, people can reduce their risks by reducing their weight; increasing exercise and physical activity; eating a heart-healthy diet that’s rich in fruits, vegetables, whole grains, and fish; as well as working with a healthcare professional to regulate blood pressure, blood sugar, blood cholesterol. In the following article, we will discuss how the ketogenic diet can help improve metabolic syndrome and its risk factors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

The ketogenic diet also referred to as the keto diet, is a low-carbohydrate, high-fat diet that has been demonstrated to have a variety of health benefits, especially for people with metabolic syndrome. Several research studies found that the ketogenic diet can help promote weight loss and improve overall wellness. Researchers also found that the keto diet may even be beneficial against diabetes, epilepsy, Alzheimer’s disease, and cancer, among others.

 

The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.�

 

Curated by Dr. Alex Jimenez

 

References:

  1. Mawer, Rudy. �The Ketogenic Diet: A Detailed Beginner’s Guide to Keto.� Healthline, Healthline Media, 30 July 2018, www.healthline.com/nutrition/ketogenic-diet-101#weight-loss.
  2. Spritzler, Franziska. �15 Health Conditions That May Benefit From a Ketogenic Diet.� Healthline, Healthline , 12 Sept. 2016, www.healthline.com/nutrition/15-conditions-benefit-ketogenic-diet.
  3. Editor. �Ketogenic Diet Improves Metabolic Syndrome in Multiple Ways.� Diabetes, Diabetes Media, 18 Dec. 2017, www.diabetes.co.uk/news/2017/dec/ketogenic-diet-improves-metabolic-syndrome-in-multiple-ways-99064712.html.
  4. Migala, Jessica. �Can Keto Cure You? 11 Conditions It May Help and 6 It Won’t: Everyday Health.� Everyday Health, Everyday Health Media, 28 Dec. 2018, www.everydayhealth.com/ketogenic-diet/diet/health-conditions-it-may-help-and-definitely-wont/.

 

Dr. Alex Jimenez Podcast: Metabolic Syndrome

 

Metabolic syndrome is a cluster of risk factors that can ultimately increase the risk of developing a variety of health issues, including heart disease, stroke, and diabetes, among other problems. Central obesity, high blood pressure, high blood sugar, high triglycerides, and low HDL or good cholesterol levels are the 5 risk factors associated with metabolic syndrome. Having at least three of the five risk factors may suggest the presence of metabolic syndrome. Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas explain the 5 risk factors associated with metabolic syndrome, in further detail, as they recommend diet and lifestyle modification advice and guidelines, such as the ketogenic diet or the keto diet, as well as demonstrate the biochemical and chemical pathways that the body goes through during ketosis to help people with metabolic syndrome improve their overall health and wellness. From eating good fats and staying hydrated to exercise and better sleep, Dr. Alex Jimenez, Alexander Jimenez, Truide Torres, Kenna Vaughn, and Astrid Ornelas discuss how diet and lifestyle modifications, such as the ketogenic diet or keto diet, can help improve the 5 risk factors associated with metabolic syndrome to prevent the risk of developing a variety of other health issues, including heart disease, stroke, and diabetes. – Podcast Insight

 


 

Neural Zoomer Plus for Neurological Disease

Neural Zoomer Plus | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.

 

Food Sensitivity for the IgG & IgA Immune Response

Food Sensitivity Zoomer | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate health issues associated with a variety of food sensitivities and intolerances. The Food Sensitivity ZoomerTM is an array of 180 commonly consumed food antigens that offers very specific antibody-to-antigen recognition. This panel measures an individual�s IgG and IgA sensitivity to food antigens. Being able to test IgA antibodies provides additional information to foods that may be causing mucosal damage. Additionally, this test is ideal for patients who might be suffering from delayed reactions to certain foods. Utilizing an antibody-based food sensitivity test can help prioritize the necessary foods to eliminate and create a customized diet plan around the patient�s specific needs.

 

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Gut Zoomer | El Paso, TX Chiropractor

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate gut health associated with small intestinal bacterial overgrowth (SIBO). The Vibrant Gut ZoomerTM offers a report that includes dietary recommendations and other natural supplementation like prebiotics, probiotics, and polyphenols. The gut microbiome is mainly found in the large intestine and it has more than 1000 species of bacteria that play a fundamental role in the human body, from shaping the immune system and affecting the metabolism of nutrients to strengthening the intestinal mucosal barrier (gut-barrier). It is essential to understand how the number of bacteria that symbiotically live in the human gastrointestinal (GI) tract influences gut health because imbalances in the gut microbiome may ultimately lead to gastrointestinal (GI) tract symptoms, skin conditions, autoimmune disorders, immune system imbalances, and multiple inflammatory disorders.

 


Dunwoody Labs: Comprehensive Stool with Parasitology | El Paso, TX Chiropractor


GI-MAP: GI Microbial Assay Plus | El Paso, TX Chiropractor


 

Formulas for Methylation Support

Xymogen Formulas - El Paso, TX

 

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

 

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

 

Please call our office in order for us to assign a doctor consultation for immediate access.

 

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

 

For your convenience and review of the XYMOGEN products please review the following link. *XYMOGEN-Catalog-Download

 

* All of the above XYMOGEN policies remain strictly in force.

 


 

 


 

Modern Integrated Medicine

The National University of Health Sciences is an institution that offers a variety of rewarding professions to attendees. Students can practice their passion for helping other people achieve overall health and wellness through the institution’s mission. The National University of Health Sciences prepares students to become leaders in the forefront of modern integrated medicine, including chiropractic care. Students have an opportunity to gain unparalleled experience at the National University of Health Sciences to help restore the natural integrity of the patient and define the future of modern integrated medicine.

 

 

What Is Metabolic Syndrome?

What Is Metabolic Syndrome?

Metabolic syndrome is caused by having more than one condition. Metabolic syndrome often leaves individuals with headaches, joint pain, fatigue, and more! Metabolic syndrome is an epidemic all over the world, but in the US, we are seeing this condition all too often.

 

Metabolic Syndrome can be defined as having two or more of the conditions listed below:

 

  • Women with abdominal fat or a waistline greater than 35
  • Men with abdominal fat or a waistline greater than 40
  • Individuals with high blood pressure ( 130/85 or higher)
  • Patients with triglycerides higher than 150
  • A fasting glucose of 100 or greater
  • Low HDL ( good cholesterol ) less than 40 in men and 50 for women

 

These symptoms are often associated with inflammation. Many people believe inflammation is just something that occurs in the joints and on the skin, but inflammation can occur to the organs inside the body and create havoc.

 

Metabolic syndrome does not target a specific population but can affect anyone who has an overlap of the factors listed above. Those who have an “apple” or “pear” body shape, are likely to have higher abdominal fat, and therefore are more at risk.

 

apple and pear body shape

 

As individuals age, their chances of developing metabolic syndrome increases. On top of age, previously having or having a history of diabetes in one’s family also increases their risk of developing metabolic syndrome.

 

Speaking from personal experience, and having Type 1 Diabetes myself, I can say that metabolic syndrome really takes a toll on one’s body. With experiencing these symptoms first hand, it can leave your body feeling exhausted. When the blood glucose level in the body rises, it causes the blood to become thick due to the excess sugar in the blood. This then causes the heart to work harder and raise the body’s blood pressure due to the effort needed to pump. From here, the body responds with a hard and heavy headache, nausea, occasional vomiting, increased thirst, increased urination, and blurred vision. Recovering from a day of high blood sugars can leave you feeling defeated and similar to feeling like you are recovering from the flu.

 

One of the things that occur within the body when an individual has metabolic syndrome is their insulin sensitivity decreases. Insulin is the hormone produced that helps to turn the food you eat into fuel for the body or store it as fat. When the insulin sensitivity becomes decreased, it means not enough glucose in the body is being absorbed.� Leading to high blood glucose levels and increases the risk for Type 2 Diabetes.

 

For those who are suffering from metabolic syndrome, or have one or more of the above risk factors there are ways to take charge. The benefits of taking charge and preventing metabolic syndrome from getting worse or returning means getting back the energy you thought was lost. By decreasing your symptoms and increasing your energy, you could be feeling better than you remembered.

 

The best diet to quickly gain control of blood sugars and raise HDL is the ketogenic diet. This diet works by eating low carb, high-fat foods. In turn, this makes the body burn fat as fuel rather than carbohydrates. It starts by burning the fat around the pancreas and liver and then starts to burn the intramuscular fat ( excess abdominal weight ). By eliminating most carbs and increasing water intake, individuals can see a decrease in depression, brain fog, their risk of stroke, and blood pressure. All while seeing an increase in sleep and energy.

 

One of the best ways to reach your goals and stay healthy is to work with a team who understands them and is willing to educate you. We provide 1:1 coaching, scales to track weight that also reports the water weight and BMI of the individual, wrist bands to track caloric activity, and education. The education will help you understand why you are following a specific diet or food guidelines, how that food is breaking down to help you, and what foods to avoid. We will never leave a patient confused or with unanswered questions.

 

Speaking from personal experience, it is best to get a handle on these symptoms before they cause permanent damage. There are ways and things to do to help reduce your risk. I highly recommend seeing us, or a local doctor to start to build your plan. We can create personalized plans that will help you reach your goals, lower your risk, and work with your lifestyle. Take it from me, you do not want to be stuck feeling the side effects metabolic syndrome comes with.� -Kenna Vaughn, Senior Health Coach

 

The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.

 

References:
Mayo Clinic Staff. �Metabolic Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 14 Mar. 2019, www.mayoclinic.org/diseases-conditions/metabolic-syndrome/symptoms-causes/syc-20351916.
Sherling, Dawn Harris, et al. �Metabolic Syndrome.� Journal of Cardiovascular Pharmacology and Therapeutics, vol. 22, no. 4, 2017, pp. 365�367., doi:10.1177/1074248416686187.

The Ketogenic Diet and What To Know | El Paso, TX.

The Ketogenic Diet and What To Know | El Paso, TX.

If you have been paying any attention to the latest diet trends, the ketogenic diet has probably come under your radar. The diet has been gaining popularity for a while now and may stay that way�as those who follow the diet are able to obtain some impressive weight loss and other health improvements. The main question about the ketogenic diet is whether it is sustainable or not. It is a challenging diet to maintain, which means you will need to be quite motivated over the long-term to make it a permanent lifestyle.

Understanding Ketosis

Under normal dietary conditions, the body burns glucose for energy. Glucose, which comes from carbohydrates, is easy to access and works well for fuel. But under the right dietary conditions, it is possible to put the body into a state of ketosis, where it starts to burn fat for energy.

11860 Vista Del Sol, Ste. 128 The Ketogenic Diet and What To Know | El Paso, TX.

How the Ketogenic Diet Works

The ketogenic diet is designed to put your body in a state of ketosis. Successful ketogenic dieters are able to burn fat at a relatively rapid rate. But reaching ketosis requires eating a lot differently than most people eat, especially those eating the Standard American Diet (SAD). In fact, it requires eliminating almost all carbs.

There is actually quite a history behind the ketogenic diet. It was developed over 100 years ago to help children suffering from seizures. There are definitely proven benefits to ketosis for at least the short term.

The average keto diet consists of 75% fat, 20% protein, and 5% carbohydrates. Achieving this ratio takes focus and persistence, but it does start getting results quickly. It only takes around 72 hours to start going into ketosis and burning your body�s fat for energy.

What do Ketogenic Dieters Eat?

Popular foods in the keto diet include:

  • Dairy that is high in fat�like butter, high-fat cream, and hard cheeses
  • All types of meat�including beef, lamb, chicken, turkey, pork
  • Eggs
  • Seeds and nuts�including walnuts, pecans, almonds, peanuts, macadamias, and sunflower seeds
  • Avocado
  • Berries
  • Broccoli and cauliflower
  • Leafy greens�like kale, spinach, lettuces
  • Coconut oil
  • Saturated fats

What do Ketogenic Dieters Avoid?

There are some foods that the keto diet definitely does not include:

  • All grains�including wheat, corn, rice, oats, etc.
  • Legumes�beans, peas, etc.
  • Fruit�bananas, apples, oranges, pears, plums, grapes, oranges, etc.
  • Tubers�yams, sweet potatoes, russet potatoes
  • Sugar for sweetening�agave, maple syrup, honey

What are the Challenges of the Ketogenic Diet?

Being a successful keto dieter requires a serious commitment to the task at hand. With the exception of perhaps the Inuit in the Arctic, it is difficult to think of a culture that does not eat any grains, fruit or tubers. Most meals are built around these staples. That means that finding a restaurant or going over to dinner at someone�s home and eating keto requires being very selective in what you choose. The best way to maintain your diet is to plan your meals and eat mostly what you make yourself.

The number of keto-specific options available at grocery stores and in restaurants has grown in recent years, but not enough to allow you to eat out at every meal and maintain your diet.

The biggest challenge of the keto diet is maintaining it over the long-term. Few people have the willpower to totally avoid pasta, bread, potatoes, fruit, sugar, and beans for years at a time. That does not mean you cannot try the diet out, switch to a regular or different diet, then switch back again if you choose.

Here for Your Health

As your chiropractic team, we are here to help you achieve and maintain optimal health. If you have questions about the ketogenic diet or other diets�or you just want to eat healthier�we would like to help. Contact us today to get started.


Benefits of Using Functional *FOOT ORTHOTICS* | El Paso, TX (2019)

 

Functional custom foot orthotics understand the anatomy of the foot. By supporting the 3 arches of the foot, functional custom foot orthotics can help promote proper posture to prevent a variety of health issues, including neck pain and back pain. Over the counter, inserts may create more harm than good. Functional custom foot orthotics can also help maintain overall health and wellness. Because every person is unique, functional custom foot orthotics can help balance a person’s unique body structure and function. Dr. Alex Jimenez can help provide functional custom foot orthotics to patients who need to improve their overall health and wellness.


 

Foot Orthotic Catalog

A properly aligned body will have symmetrical feet, level knees, pelvis, and shoulders. With custom orthotics, imbalances and�conditions caused by those imbalances are gone.

 

2019-01-Patient-Catalog

 

Metatarsalgia

99% of feet are normal at birth. But after the first year, 8% develop foot problems, 41% by age 5 and 80% by age 20.�By age 40, almost everyone has a foot condition of some sort. Many foot conditions eventually contribute to health concerns, especially the generalized condition of �back pain� or runner�s knee. Spotting a potential problem originating in the feet can prevent other injuries from affecting your health and lifestyle.

 

VasyliMedical Metatarsalgia

 

Foot Exercises

When there are problems with the feet, it can cause problems through the legs and all the way to the spine. This can cause the ankle to pronate, meaning it rolls inward. This alters the way the�bones of the foot�line up which extends through the tibia, or shin bone.

 

kids-foot-exercises

 

NCBI Resources

There are several significant�health benefits of a ketogenic diet. It was developed to be a way of life (WOL), not just a temporary diet and this was primarily due to the health benefits it provides. In fact, ketone diets were created to help allay or improve the symptoms of certain chronic health conditions, including epilepsy.

 

 

What The People Want To Know About The Ketogenic Diet El Paso, TX.

What The People Want To Know About The Ketogenic Diet El Paso, TX.

The ketogenic diet, also known as a low carb diet is being talked about in various circles. And while science has proven over and over about the numerous health benefits, there are still those that want to disclaim it. This guide will explain the ketogenic diet, ketones, and the many health benefits that this way of eating provides.

What are Exogenous Ketones?

In order to understand exogenous ketones, it is important to first know what ketones are. Simply put, ketones are carbon-based, organic compounds that are produced in the liver. They are used by the mitochondria within the body to generate energy and can replace glucose as a fuel source, putting the body in a state of ketosis.

Exogenous ketones are ketones that are taken into the body as nutritional supplements. Endogenous ketones are produced in the body, specifically, the liver. Exogenous ketones are not produced in the body, rather are introduced into the body through supplements.

ketogenic diet chiropractic clinic el paso tx

What is a Ketogenic Diet?

A ketogenic diet is characterized by three primary markers:

  • Low carbohydrate
  • Adequate protein
  • High fat

It is designed to put the body into a state of ketosis which means that instead of burning carbohydrates for energy, it is forced to burn fat.

ketogenic diet chiropractic clinic el paso tx

When the body consumes foods that are high in carbs, it begins to produce insulin and glucose. Glucose happens to be the path of least resistance when it comes to energy conversion and usage, so the body will opt for that route before any utilizing another energy source.

What are the Benefits of a Ketogenic Diet?

There are several significant health benefits of a ketogenic diet. It was developed to be a way of life (WOL), not just a temporary diet and this was primarily due to the health benefits it provides. In fact, ketone diets were created to help allay or improve the symptoms of certain chronic health conditions, including epilepsy. Other benefits of the ketogenic diet include:

  • Weight loss
  • Lower insulin levels and reduced blood sugar
  • Lower triglycerides
  • Effectively treats metabolic syndrome
  • Forces the body to burn fat
  • Increased HDL (�good� cholesterol) levels
  • Improve LDL
  • Prevention of certain cancers
  • Potential to kill certain cancer cells
  • Lowered blood pressure
  • Improve epilepsy symptoms
  • Help treat Parkinson�s Disease
  • Reverse and treat symptoms of Alzheimer�s

The weight loss occurs from a ketogenic diet is largely fat loss – particularly abdominal fat (visceral fat). It is visceral fat that increases the risk of heart disease, type 2 diabetes, and other health conditions.

A ketogenic diet helps to reduce many of the risks of some of the most debilitating and even deadly chronic health conditions that are so prevalent today. Exogenous ketones provide a powerful supplementation to the diet, improving its effectiveness.

A ketogenic diet is not a quick fix or fad diet; it is indeed a way of life. While many people do see very noticeable results quite quickly, the substantial health benefits that it provides make it worthy of a lifelong commitment. By adhering to this low carb lifestyle, you can reverse many health conditions and avoid others. In short, you will enjoy increased energy and better health for years to come.

6 Day *DETOX DIET* Treatment | El Paso, TX (2019)

ProLon� Fasting Mimicking Diet – Losing Weight & Feeling Great!

  • The 5 Day Fasting Mimicking Diet�, or FMD, is the first fasting meal program.
  • Made from natural ingredients.
  • Meals are consumed for five days.
  • The body�s ( cellular pathways) do not recognize the meals as food.
  • This keeps the body in a fasting mode.
  • This diet is proven to promote overall health.
  • Reduce excess fat.
  • Gives you freedom.

The Prolon� Fasting Mimicking Diet!

Basics Of The ProLon� Fasting Mimicking Diet

Basics Of The ProLon� Fasting Mimicking Diet

The fasting mimicking diet is an alternative to fasting. However, it can have several benefits for your overall health and wellness. We will discuss everything you need to know about the regimen. The article below describes how to do it, its benefits, and how it’s different from normal fasting. The benefits of the fast mimicking diet will have you wanting to try it for yourself.

What is the Fasting Mimicking Diet?

The fasting mimicking diet is a type of modified fasting. The regimen produces the same benefits of fasting by eating small amounts of food. The fast mimicking diet generally lasts about five days and it includes a healthy protocol of carbohydrates, proteins, and fats.

Calories are also maintained at approximately 40 percent of the average calorie intake. This permits the human body to remain nourished without the stress of normal fasting. Calorie restriction can cause health issues, however, the fast mimicking diet is safe and effective. Below, we will discuss just how much the fast mimicking diet differs from traditional fasting.

Traditional Fasting Vs Fast Mimicking Diet

The fasting mimicking diet is always compared to intermittent fasting. There are many myths about these types of modified fasts. Some claim that our muscles waste away while others claim that they change our metabolism, and that it’s downright unhealthy.

The health issues discussed above may be true for a person who’s actually restricting their calorie intake. Some types of fasting may cause metabolic damage which may not be recommended for people with underlying health conditions. However, the fast mimicking diet gives you all the advantages of fasting without the side effects. Below are the benefits of the fast mimicking diet.

Benefits of the Fast Mimicking Diet

The benefits of the fast mimicking diet are essentially the same as those of regular fasting. The benefits are listed below.

Benefits of the Fasting Mimicking Diet | El Paso, TX Chiropractor

The fast mimicking diet “tricks” the human body into feeling as though it’s fasting. Now that we have discussed what this alternate form of fasting is and why it is worth doing, the following advice will demonstrate how to do the diet itself.

How to do the Fast Mimicking Diet

Research studies have found that the best results for the fasting mimicking diet occur in about five days or when your glucose ketone index drops below 1.0. Doing this regimen anywhere between 3 to 7 days is also beneficial. The regimen should also be repeated every month to fully experience its benefits, unless otherwise instructed by a healthcare professional.

If you’re interested in monitoring your fasting outcomes, you should consider quantifying specific biomarkers. This could be measured through lab tests before and after following the fasting mimicking diet. Measuring blood glucose, ketones, and weight changes every day can also be helpful to determine your biomarkers. You might also want to set up your environment by:

  • Telling friends and family about what you are doing and asking them for their support.
  • Eliminating any snack foods at home or work that might interrupt your regimen.
  • Giving yourself more time to sleep, as you will probably be more exhausted than usual.
  • Planning for exercise and physical activity every day. But keep away from intense workouts during this time.

Now that we discussed how you can do the diet, let’s discuss the basics of the fast mimicking diet.

Dr Jimenez White Coat
The fasting mimicking diet provides the same great benefits of fasting while still providing your body with some nourishment. If you are following this regimen, make sure that you maintain a low-calorie intake and utilize appropriate supplements to achieve ketosis without experiencing health issues. Set up your environment for the diet. And if you decide to blend the ketogenic diet with this alternate form of fasting to get into ketosis faster, you can achieve the maximum advantages out of the two regimens. Be sure to consult a healthcare professional before following the fasting mimicking diet. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Fasting Mimicking Diet Basics

Some people today might eat a slightly higher amount of calories the first day as they ease into the fasting mimicking diet. They might then decrease their total caloric intake. You also want to make sure you eat smaller amounts of foods which are easy to digest.

ProLon� offers a pre-packaged box which contains all five days’ worth of meals for you to do the diet. The meals are all plant-based. One day, by way of instance, offers tea and a nut bar for breakfast, a small portion of vegetable soup and a few kale crackers for lunch, several olives in the afternoon, and finally another small portion of vegetable soup for dinner.

You can also do the fasting mimicking diet without the need for a pre-packaged box like ProLon�. Simply follow the right proportions and plan out how you will space them out every day. Macros for the fast mimicking diet are 34 percent carbohydrates, 10 percent protein, and 56 percent fat for the very first day and 47 percent carbohydrates, 9 percent protein, and 44 percent fat to the rest days.

A cup of black tea and coffee every day are generally allowed. Just make sure they don’t contain any added sugars or oils. Remember that people with health issues should consult a healthcare professional prior to doing the fast mimicking diet in your own home.

Foods

Dr. Anthony Gusting followed a four-day ketogenic fasting mimicking diet. Every day, he consumed different amounts of bone broth, coconut milk, coconut oil, BCAAs, and exogenous ketones. Avocados and grass-fed butter can also be included in the fast mimicking diet. This is a great way to combine the ketogenic diet with the fasting mimicking�diet to benefit from the two regimens.

Supplements

Taking nutritional supplements can also make the fasting mimicking diet easier by providing enough nutrition. These may include:

  • Electrolytes like magnesium and salt to replenish any lost during water loss
  • Grass-fed liver tablets to provide micronutrient support
  • Branch chain amino acids, or BCAAs, to help prevent loss of lean tissue
  • Greens powder to provide micronutrients
  • Algal oil or cod liver oil for omega-3s

You may also take exogenous ketones to achieve ketosis through the keto diet. The fast mimicking diet can also help you achieve ketosis before following a ketogenic diet. Below, we will discuss how the fast mimicking diet promotes ketosis.

Ketosis and the Fast Mimicking Diet

The fast mimicking diet is an excellent way to prepare you for the ketogenic diet. This is because it allows you to get into ketosis. Additionally, eating keto foods makes it possible to remain in ketosis throughout the regimen. To follow a ketogenic fasting mimicking diet you must maintain your macros over the suitable range of 5 to 10 percent of carbohydrates, 20 to 25percent of proteins, and 70 to 80 percent of fats. If you’re unsure about whether you’re properly maintaining your macros, always choose something with more fat.

The scope of our information is limited to chiropractic and spinal health issues as well as functional medicine topics and discussions. To further discuss the subject matter, please feel free to ask Dr. Alex Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

Xymogen Formulas - El Paso, TX

XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.

Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.

Please call our office in order for us to assign a doctor consultation for immediate access.

If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.

xymogen el paso, tx

For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download

* All the above XYMOGEN policies remain strictly in force.

***

Ketogenic Diet and Intermittent Fasting

Ketogenic Diet and Intermittent Fasting

Why is it that the ketogenic diet and intermittent fasting always seem to fall within the same topic of conversation? This is simply because intermittent fasting may be utilized as an instrument to achieve ketosis, the metabolic state associated with the keto diet. During intermittent fasting, the human body is depleted of glycogen stores. Once these glycogen stores are eliminated, fat stores are then released into the bloodstream in order to be converted into energy molecules, known as ketones, from the liver.

What is Ketosis?

Ketosis is a metabolic state which uses ketone bodies, or ketones, as fuel for energy. On a normal carbohydrate-based diet, the human body burns glucose as its main fuel source, where excess glucose is subsequently stored as glycogen. If the human body cannot utilize sugar as fuel for energy, it will utilize glycogen as fuel for energy. Once glycogen is depleted, you begin to burn fat. The ketogenic diet generates a metabolic state which enables you to break down fat into ketones, or ketone bodies, in the liver for energy.

There are 3 major types ketone bodies found in the blood, urine, and breath, including:

  • Acetoacetate: The type of ketone which is created first. It may be converted to beta-hydroxybutyrate or flipped into acetone.
  • Acetone: Made spontaneously in the breakdown of acetoacetate. It is a very volatile ketone and it is frequently detectable on the breath once an individual first enters ketosis.
  • Beta-hydroxybutyrate (BHB): The type of ketone which is utilized for energy and is most abundant on the bloodstream as soon as you’re completely into ketosis. It is the kind that is located in exogenous ketones and what blood tests quantify.

Intermittent Fasting in the Keto Diet

Intermittent fasting is composed of eating within a specific feeding window rather than eating throughout the day. Each individual, whether they are conscious of it or not, fasts intermittently from dinner to breakfast. There are lots of methods to intermittent fasting. A few individuals fast for 16-20 hours intervals on alternate days while others follow a 24-hour day fast. The most common intermittent fasting variety is the 16/8 method, in which you eat in an 8-hour window followed by a 16-hour fasting window.

Other fasting programs incorporate the 20/4 or even 14/10 methods. Other people follow 24-hour fasts one or two times each week. Intermittent fasting can get you in ketosis quicker because your cells will immediately absorb your glycogen stores and begin burning fat. However, what about once you get into ketosis? Is intermittent fasting worth following consistently? Following the ketogenic diet and intermittent fasting can be a great addition towards an individual’s overall health and wellness, providing various health benefits.

The keto diet and intermittent fasting can provide the following health benefits, including:

  • Healthy weight-loss
  • Fat reduction, not muscle reduction
  • Balancing cholesterol levels
  • Enhancing insulin sensitivity
  • Maintaining blood glucose levels steady

Health Benefits of the Ketogenic Diet

The ketogenic diet dramatically reduces your caloric intake, forcing your body to burn fat instead of sugar, which makes it a powerful tool for weight reduction. While individual results vary, the keto diet has always resulted in a decrease in body fat in a selection of situations. Within a 2017 study, subjects who followed a very low carbohydrate keto meal program significantly decreased body fat percentage and body fat mass, losing an average of 7.6 lbs and 2.6 percent body fat while preserving lean muscle mass.

Likewise, a 2004 research detecting the long-term consequences of a ketogenic diet in overweight patients discovered that the weight and body mass of those patients diminished dramatically over the span of two decades. Individuals who radically reduced their carb intake saw a substantial decline in LDL (bad) cholesterol, triglycerides, and enhanced insulin sensitivity. In 2012, researchers compared a ketogenic diet to eating fewer calories for overweight kids and adults. The results showed kids after the keto diet lost significantly more body fat. They also revealed a dramatic decline in insulin levels, a biomarker of Type 2 diabetes.

Health Benefits of Intermittent Fasting

Studies have shown that intermittent fasting may be an effective weight loss tool, more powerful than just cutting calories. In one analysis, intermittent fasting has been proven to be as successful as constant calorie restriction in combating obesity. In studies done by the NIH, there was reported weight reduction with over 84 percent of participants, regardless of which fasting program they picked.

Much like ketosis, intermittent fasting increases fat loss while preserving lean muscle mass. In one study, researchers reasoned that fasting led to greater weight loss compared to a low-carb diet, though the overall caloric consumption was exactly the same. If you are attempting to lose weight, then a keto diet or intermittent fasting can be a massive help. But that is not where the rewards stop.

Intermittent Fasting and the Keto Diet for Mental Health

Both intermittent fasting and the ketogenic diet can provide various mental health advantages. Both have been clinically shown to boost memory, improve mental clarity and focus, as well as prevent the development of neurological disorders like Alzheimer’s and epilepsy. On a carb-based diet, changes in glucose can cause changes in energy levels. During ketosis, your brain employs a more consistent supply of fuel: ketones from the fat stores, leading to better productivity and psychological performance.

Whenever you’ve got a consistent and clean energy source from ketones, the brain works better. In addition to this, ketones are better at protecting your brain. Studies reveal that ketone bodies might have antioxidant properties which protect your brain cells from free radicals and oxidative stress. In one study conducted on adults with diminished memory, the growth of BHB ketones in their own blood helped enhance cognition. Also, when you’ve got difficulty staying focused, your hormones can be to blame.

Your brain has two chief neurotransmitters: glutamate and GABA. Glutamate will help you form new memories, and get your brain cells to communicate with one another. GABA is what helps restrain glutamate. If there is too much glutamate, it can cause brain cells to quit working and finally perish. GABA is there to control and slow down glutamate. If GABA levels are reduced, glutamate reigns free and you experience mental fog. Ketones stop damage to cells by processing surplus glutamate into GABA. Considering that ketones raise GABA and lessen glutamate, they assist in preventing cell damage, preventing cell death and enhancing mental focus.

Researchers believe that intermittent fasting enhances memory, decreases oxidative stress, and conserves learning abilities. Since your cells are under moderate strain whilst fasting, the top cells adapt to the stress by improving their particular ability to deal with these circumstances while the weakest tissues die. This is much like the strain that your body gets when you reach the gym.

Exercise is a kind of stress that your body adjusts to improve and get more powerful. This also applies for intermittent fasting: so long as you are still alternate between routine eating habits and fasting, it is going to continue to benefit you. Implying equally that ketosis and intermittent fasting will help improve your cognitive functioning because of the synergistic and protective effects of ketones.

Dr Jimenez White Coat
The ketogenic diet and intermittent fasting are two different nutritional strategies which provide many common health benefits. According to various research studies, both the keto diet and intermittent fasting can help boost ketones, helping the body burn fat more efficiently than any other nutritional strategy. And when these are utilized together, they definitely form a powerful dietary program. The article above discusses the differences between the ketogenic diet and intermittent fasting as well as demonstrates the health benefits of both of these dietary programs and how they can help improve overall health and wellness. Dr. Alex Jimenez D.C., C.C.S.T. Insight

The Perks of Intermittent Fasting and the Keto Diet

The ketogenic diet and intermittent fasting possess similar health benefits because both approaches involve ketosis. Ketosis has lots of physical and mental advantages, from weight loss to enhanced brain function. People following a ketogenic diet may use intermittent fasting as a tool to achieve ketosis and enhance their general well-being. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

Keto Diet Health Benefits

Keto Diet Health Benefits

If you are currently thinking about the ketogenic diet, then you might be asking yourself, is the keto diet right for you? While you may have already heard about the benefits of the ketogenic diet, you might still be wondering about whether if it is worth it to completely change your diet to take advantage of these benefits.

The keto diet has many benefits, from weight loss and improved physical health to mental clarity and enhanced physical performance. In the following article, we will dive into the details of some of the ketogenic diet health benefits. These benefits can help with the particular health goal you may be attempting to attain.

Ketogenic Diet and Weight Loss

In comparison to low-fat dieting, a low-carb diet can deliver superior results within a shorter time period in terms of weight loss, and the management of cholesterol, and blood pressure. If you want to shed weight, the ketogenic diet plan provides the following benefits and will get you closer to attaining your objective. There can be many reasons for this, including:

  • Low-carb and ketogenic diets are more satisfying with their low carb content and higher quantities of fats and protein.
  • Going onto a low-carb diet usually makes you lose extra water weight.
  • Most individuals can undergo weight loss fairly quickly, especially within the first week�of beginning a ketogenic diet.

Increased HDL Cholesterol

Together with the high consumption of saturated fats and other healthy fats, the ketogenic diet may help raise HDL cholesterol and enhance triglycerides levels. Both of these are�considerably significant towards promoting heart health.

Ketogenic Diet and Physical Health

Acne

Following the ketogenic diet has been demonstrated to also be able to help reduce inflammation and lesions of the skin like those found in acne. This is believed to occur due to the effects of ketosis, or the state in which the cells use ketones instead of glucose for energy.

IBS Support

Moreover, several research studies have also associated a link between the reduced consumption of glucose, or sugar, and an improvement in symptoms of irritable bowel syndrome, or IBS. As a matter of fact, one research study demonstrated that following a ketogenic diet may improve bowel movement habits and help reduce abdominal pain, improving quality of life in people with IBS.

Ketogenic Diet and Physical Performance

Balanced Energy Levels

Do not be surprised if you’re ready to stop drinking coffee every day after adapting to the keto diet. Achieving and maintaining ketosis involves benefits like no day slumps, no mood swings, and reducing changes in energy levels that you might experience otherwise.

In addition, you’ll likely find it much easier to remain longer periods of time without feeling hungry. This is what ultimately helps with weight loss, steady blood sugar levels, and extended periods of fasting, which is one of the best ways to get into ketosis.

Enhanced Workouts

Adjusting to the ketogenic diet may take time, however, once your body gets used to burning fat for fuel rather than sugar, or glucose, from carbohydrates, you will likely notice a difference in your physical performance and endurance, such as more energy and focus for workouts. This makes sense because being in ketosis “instructs” the entire human body to burn fat for fuel more efficiently.

The most important first step in case you start the ketogenic diet and notice limitations in your physical performance is to give your body some time to adapt from utilizing carbohydrates as its primary fuel to utilizing ketones as a source of energy. For individuals who participate in a lot of physical activities and exercise as well as athletes may benefit from a cyclical or targeted ketogenic diet.

Fat Loss / Muscle Gain

The amount of protein intake on a ketogenic diet makes it excellent for building muscle mass. Results might seem to come more gradually than for someone fueling their workouts but that is usually because you’re building lean mass together with fat reduction. By way of instance, when documenting a keto fast for four days, the individual gained 2.4 lbs of muscle with 1.1 lbs of fat reduction.

Ketogenic Diet and Mental Clarity

Several research�studies have demonstrated that a ketogenic diet may have the ability to support mental clariy as well as help boost productivity, support better memory, and also, have positive effects in regard to moderate cognitive impairment.

Neurological Support

Early usage of the ketogenic diet has been used as a treatment for reducing seizures in people with epilepsy, especially children. Additionally, it has been shown to benefit people with Parkinson’s disease, Alzheimer’s disease, and other neurodegenerative disorders. This is likely because ketone bodies created through the keto diet can have neuroprotective effects.

Dr Jimenez White Coat
Weight loss is one of the most well-known advantages of the ketogenic diet, however, this nutritional plan can have many other health benefits. By reducing the consumption of carbohydrates, the cells will go into a state of ketosis and instead utilize ketones created from fats, providing a steadier supply of energy than that of glucose, or sugar. Furthermore, research studies have also demonstrated the ketogenic diet’s possible role in disease prevention, such as for people with epilepsy. Dr. Alex Jimenez D.C., C.C.S.T. Insight

The benefits of the ketogenic diet are essential, not just for weight loss, but for overall health and wellness. When you are eating more fats and proteins with fewer carbohydrates, you are more likely to end up eating fewer calories. With this, you also don’t experience a change of energy levels but instead maintain a level of energy that lets you remain focused on your everyday tasks.

Regardless of the health goal you have in mind, the ketogenic, or keto, offers many benefits to improve your quality of life. Being aware of the proper foods you should eat on the keto diet is also important. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

Essential Fats on the Ketogenic Diet

Essential Fats on the Ketogenic Diet

Have you started following the ketogenic diet? Are you confused with what type of fats you should eat to achieve and maintain ketosis? In the following article, we will list the different types of essential fats which are vital in the ketogenic diet.

Fats are crucial in the ketogenic diet. To promote the breaking down of fat rather than protein or carbohydrates, you need to consume fat, a process known as ketosis. However, the value of the healthy fats you eat is fundamental.�Fat is satiating and it tastes good. Simply, be sure to eat the ideal kind of fat. There are four categories of fat permitted on the ketogenic, or keto, diet:

  • Polyunsaturated fats
  • Monounsaturated fats (MUFAs)
  • Polyunsaturated fats (PUFAs), which comprises omega 3
  • Only naturally-occurring trans fats

Remember that a balance of omega-3s and omega-6s can help maintain overall health and wellness, improving brain and nerve function and decreasing the risk of cardiovascular disease, Alzheimer’s disease,�and type-2 diabetes. While omega-6 is vital, however, too much of it can cause inflammation in the human body, therefore, avoid eating high amounts of omega-6 from sources like peanuts and vegetable oils, such as corn oil or sunflower oil.

Instead, focus largely on the intake of omega-3s from fish sources like trout, salmon, tuna, and mackerel or take a high-quality fish oil supplement. Additionally, be cautious of seeds and nuts since they do include some carbohydrates, particularly pistachios and almonds. Make certain that the fat you eat�is currently coming out of nutrient-dense foods, such as fatty cuts of meat. Below is a food listing of the major types of fat in the ketogenic diet.

Dr Jimenez White Coat
Fats are the basis of the ketogenic diet. The high fat intake and the low fat intake helps achieve and maintain ketosis, or the creation of ketones. Utilizing ketones for fuel, the human body can burn fat instead of sugar or glucose from carbohydrates. Getting and keeping your body in the state of ketosis can provide many health benefits, including weight loss and overall health and wellness. The quality of fats you consume while on the keto diet is essential towards reaching ketosis. The following article discusses the different types of fats you can eat while on the ketogenic diet and which ones you should avoid. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Fats and Oils in the Ketogenic Diet

The value of your dietary fat on keto creates a massive difference in the results that you’ll see. If you are taking an unhealthy approach for your new low-carb diet program, then you will quickly discover reverse health consequences. That is why it’s vital to understand which sources of fat are actually considered safe and healthy to consume on while on the ketogenic diet.

The very first sort of healthy fat to begin including on your keto diet plan is saturated fat. Saturated fat was analyzed and proven to enhance HDL and LDL cholesterol levels, both good and bad cholesterol markers, and it may also strengthen bone density and improve the function of your immune system as well as promote the production of important hormones in the human body.

Saturated fats include:

  • Grass-fed and organic red meats
  • High fat dairy like ghee, grass-fed butter, and heavy cream
  • Lard, tallow, and eggs

These are animal-based saturated fats but there are also plant-based selections like olive oil and MCT oil that could provide you with the wholesome dose of saturated fats that you need to maintain your�well-being. Branching out of healthy unsaturated fats, both monounsaturated fatty acids and polyunsaturated fatty acids can help you accomplish your ketosis objectives. Take a look at the graph below to get a visual of these wholesome oils and fats to focus on if following a ketogenic diet.

Monounsaturated fats include:

  • Virgin olive oil, avocado oil, and macadamia nut oil (eating avocados and olives also helps you reap these healthy fats)
  • Certain nuts and seeds

Polyunsaturated fats include:

  • Nuts and seeds such as walnuts, flaxseeds, chia seeds, sunflower, and pumpkin seeds
  • Flaxseed oil, sesame oil, fish oil, avocado oil, and krill oil
  • Fatty fish like trout, mackerel, salmon, and tuna

Fats and Oils to Avoid in the Keto Diet

You will also have to learn that some dietary fats should be avoided altogether. Simply because you are after a high-fat ketogenic diet does not mean that you ought to indulge in each fat you encounter. All fats aren’t created equal. Stay away from unhealthy fats like:

Hydrogenated and partially hydrogenated oils. These fats can be present in packaged foods. They may also increase your risk of developing higher cholesterol, cancer, obesity, and heart disease along with inflammation. If you are relying on packaged foods to get you through the ketogenic diet, check the tag and ditch any foods with them.

Highly processed vegetable oils. Peanut oil, corn oil, canola oil, soybean oil, sunflower oil, and grapeseed oil are fats which seem healthier than they are. These fats are generally created with genetically modified seeds which are possible allergens. Extreme heat can also make these oils go rancid. Additionally, they may leave fatty deposits on your body that may result in heart attacks and premature death. Finally, these oils contain higher levels of omega 6 fatty acids which can lead to chronic inflammation.

Nuts and Seeds in the Ketogenic Diet

Another simple and gratifying way to sneak healthy fats into the ketogenic diet would be to reach for uncooked seeds and nuts. These nutrient powerhouses are packed with essential nutrients, such as magnesium, selenium, and manganese. Seeds and nuts may enhance brain health, fortify your immune system, and assist with digestion and blood sugar control.

They are also high in healthy fats, have a moderate quantity of protein, and are usually low carb, based on the kind you select. Nuts and seeds are also simple to�carry, which makes them among the best snacks when on a keto diet. Some nuts and seeds, however, are better than others. In keto, this implies that they have more fat and less carbohydrates.

The five best nuts in the ketogenic diet include:

  • Macadamia nuts
  • Pecans
  • Brazil nuts
  • Walnuts
  • Hazelnuts

Pine nuts, almonds, cashews, and pistachios are also great nuts to include into the ketogenic diet. However, because they have more carbohydrates compared to the top five, they need to be consumed in moderation so that you don’t accidentally tip on your carbohydrate count daily. Consuming one or more one of these nuts as nut butter is a handy way to receive a spoonful of nourishment during snack time. However, you are going to want to practice portion control too since the serving size is really small.

The following best seeds in the ketogenic diet include:�

  • Pumpkin seeds
  • Sesame seeds
  • Sunflower seeds and sunflower seed butter
  • Tahini (sesame seed paste)
  • Chia seeds
  • Flaxseeds

Nuts and Seeds to Avoid in the Keto Diet

Are you wondering why peanuts and peanut butter is not part of the list of ketogenic diet foods? The majority of us have grown up eating and snacking on peanut butter. But a lot of us don’t recognize that peanut butter isn’t really made out of nuts; peanuts are a legume, which is part of the exact same family as peas, soybeans, and lentils. While the macro dysfunction and low-fat level of a serving of peanuts might be like other nuts, that is where their healthy comparison stops.

Peanuts and peanut butter are:

  • Packed with unnecessary added sugars
  • Loaded with hydrogenated oils (essentially harmful trans fats)
  • Low in fat and filled with junk as a replacement
  • Hard to digest
  • Covered in pesticides
  • High in oxalates (which prevent proper nutrient absorption and can lead to kidney stones)
  • High in inflammatory omega-6 fatty acids

Dairy in the Ketogenic Diet

Most dairy products fit into the “fat” and “protein” category but they are accepted as part of the ketogenic diet as long as you’re not lactose intolerant. Simply make sure you eat the full-fat version and preferably choose organic and raw options, if possible. Dairy is not an extremely important element of a keto�diet. If you are lactose intolerant, you may safely omit it.

For people with dairy sensitivities:

  • Find hard and long-aged dairy
  • Use ghee, a butter alternative without the irritating milk solids
  • Get checked for a casein sensitivity to rule out the other common irritant found in dairy

Other dairy choices can include:

  • Unflavored greek yogurt, fermented yogurt, and kefir
  • Hard cheeses like blue cheese, gouda, and parmesan
  • Semi-hard cheese such as Colby, provolone, and swiss cheese
  • Softer cheeses like mozzarella, brie, muenster, and Monterey Jack
  • Cream cheese, mascarpone, creme fraiche, and cottage cheese, which are also okay on a high-fat diet

Dairy to Avoid in the Keto Diet

Very similar to healthy versus unhealthy fats, these dairy things are packed using the wrong ingredients and aren’t good if you are trying to achieve and maintain ketosis. To reach ketosis, avoid these 3 dairy products on the ketogenic diet.

Low fat, reduced fat, and fat-free milk. When fat is removed from dairy, sugar is added to fill in the gaps and make these taste much better. The sugar in these products will prevent you from going into ketosis. Whole milk is not much better, however, with 12.8 grams of carbohydrates per glass, you’re much better off enjoying low carb cheese over a glass of milk.

Half and half. Do not go with this particular half milk/half cream mix either. You are still getting a dose of sugar and less fat, two of which is not ideal for a keto diet. Reach for heavy whipping cream and you won’t hav carbohydrates or sugar to contend with.

Evaporated and condensed milk. Before incorporating these canned milk choices for your next recipe, you need to know these are essentially a cooked down variation of milk syrup and sugar in disguise. Luckily, it is simple to substitute this cooking staple with unsweetened, full-fat, canned coconut milk. Plus, as it is made from coconuts, you also receive healthy saturated fats.

Fats are ultimately essential in the ketogenic diet. Recognizing the different types of fats you can eat while on the keto diet is important in order to help you achieve and maintain ketosis. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

What Fats To Eat On The Ketogenic Diet

What Fats To Eat On The Ketogenic Diet

Fats are an essential�part of the ketogenic diet since they constitute approximately 70 percent of your dietary calories. However, the type of fat you eat on the ketogenic diet is also important and there may be some confusion regarding good fats and bad fats. The following article discusses exactly what fats you need to include and what fats you must avoid while on the keto diet.

Good Fats on the Ketogenic Diet

The type of “good” fats included while on the ketogenic diet are divided into four groups: saturated fats, monounsaturated fats (MUFAs), polyunsaturated fats (PUFAs), and naturally-occurring trans fats. All fats can be classified into more than one group, however, we classify them according to the most dominant of these mixtures. It’s essential to be able to recognize what type of fat you are eating on the ketogenic diet. Below, we will describe each group of good fat so you can properly implement them into your own food choices.

Saturated Fats

For many years, saturated fats were considered to be detrimental for heart health and we were advised to�limit their�consumption as much as possible. However, recent research studies have demonstrated no substantial connection between saturated fats and the increased risk of cardiovascular disease. As a matter of fact, including healthy saturated fats into your diet can have many benefits.

One type of saturated fat contains medium-chain triglycerides (MCTs), which can be largely found in coconut oil, or in small quantities in butter and palm oil, and it may be digested quite easily by the human body. Medium-chain triglycerides pass through the liver for immediate use as energy when consumed. MCTs are beneficial towards promoting weight loss and improving athletic performance.

Health benefits of saturated fats on the keto diet can include:

  • Improved HDL and LDL cholesterol levels
  • Maintenance of bone density
  • Boosting of immune system health
  • Support in creation of important hormones like cortisol and testosterone
  • Raising of HDL (good) cholesterol in the blood to prevent buildup of LDL in the arteries
  • Improved HDL to LDL ratio

Recommended types of saturated fats while on the ketogenic diet include:

  • Butter
  • Red meat
  • Cream
  • Lard
  • Coconut oil
  • Eggs
  • Palm oil
  • Cocoa butter

Monounsaturated Fats

Unlike saturated fats, monounsaturated fats, also referred to as monounsaturated fatty acids or MUFAs,�have been approved as a healthy source of fat for several years. A variety of research studies have connected them to numerous health benefits associated with improved levels of “good” cholesterol and better insulin resistance, among other health benefits, as described below.

Health benefits of MUFAs on the keto diet can include:

  • Increased HDL cholesterol
  • Lowered blood pressure
  • Lowered risk for heart disease
  • Reduced belly fat
  • Reduced insulin resistance

Recommended types of MUFAs while on the ketogenic diet include:

  • Extra virgin olive oil
  • Avocados and avocado oil
  • Macadamia nut oil
  • Goose fat
  • Lard and bacon fat

Healthy Polyunsaturated Fats

The most important point to keep in mind about eating polyunsaturated fats, also referred to as polyunsaturated fatty acids or PUFAs, on the ketogenic diet is that the specific type you consume actually matters. When heated, some polyunsaturated fats may produce substances that can cause inflammation in the human body, increasing the risk of cardiovascular disease and even cancer.

Many PUFAs must be consumed cold and they should never be utilized for cooking. PUFAs can be found both in very processed oils and in very healthy sources. The right types can additionally provide many health benefits on the ketogenic diet, particularly because several of these include omega 3s and omega 6s, both of which are essential nutrients in a healthy and balanced diet.

Health benefits of PUFAs on the keto diet can include:

  • Reduced risk of heart disease
  • Reduced risk of stroke
  • Lowered risk of autoimmune disorders and other inflammatory diseases
  • Improved symptoms of depression
  • Improved symptoms of ADHD

Recommended types of PUFAs while on the ketogenic diet include:

  • Extra virgin olive oil
  • Flaxseeds and flaxseed oil
  • Walnuts
  • Fatty fish and fish oil
  • Sesame oil
  • Chia seeds
  • Nut oils
  • Avocado oil

Naturally-Occurring Trans Fats

Many people might be confused to see trans fats classified as “good” fats. While most trans fats are considered to be extremely unhealthy and even harmful, one type of trans fat, known as vaccenic acid, can be found naturally in various kinds of food, such as in grass-fed animal products and dairy fats. These naturally-occurring trans fats also provide several health benefits on the keto diet.

Health benefits of naturally-occurring trans fats on the keto diet include:

  • Reduced risk of heart disease
  • Reduced risk of diabetes and obesity
  • Possible protection against cancer risk

Recommended types of naturally-occurring trans fats while on the ketogenic diet include:

  • Grass-fed animal products
  • Dairy fats like butter and yogurt
Dr Jimenez White Coat
When following a ketogenic diet, or any other low carb diet, eating the right type of fat is essential, especially since these make up about 70 percent of your daily caloric intake. The type of fat you eat is classified into various groups depending on the dominant amount found in the mixture. Extra Virgin Olive Oil, for example, is approximately 73 percent monounsaturated fat, therefore, it is considered a monounsaturated fat. Butter is about 65 percent saturated fat and thus, is a saturated fat.�It’s essential to be able to recognize what type of fat you are eating on the ketogenic diet in order to enjoy its health benefits. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Bad Fats on the Ketogenic Diet

One of the greatest advantages of the ketogenic diet is the capacity to eat lots of satisfying dietary fats such as those mentioned previously. However, we have to also cover the kinds of fats that you should reduce or eliminate from your diet in order to prevent damaging your�well-being. On the keto diet, the quality of food you eat is especially important to achieve ketosis.

Unhealthy Polyunsaturated Fats and Processed Trans Fats

Processed trans fats are the group of fat which most people as the “bad” fats and the truth is, they can actually be quite damaging to your overall health and wellness.� Artificial trans fats are made during food production via the processing of polyunsaturated fats. That is the reason why it’s very important to choose PUFAs which are unprocessed and not overheated or modified. The consumption of unhealthy PUFAs can create harmful free radicals where processed trans fats often contain genetically modified seeds.

Health risks of unhealthy polyunsaturated fats and processed trans fats include:

  • Increased risk of heart disease
  • Increased risk of cancer
  • Reduced HDL cholesterol and increased LDL cholesterol
  • Pro-inflammatory
  • Bad for the health of your gut

Examples of unhealthy polyunsaturated fats and processed trans fats to avoid include:

  • Hydrogenated and partially hydrogenated oils found in processed products like cookies, crackers, margarine, and fast food
  • Processed vegetable oils like cottonseed, sunflower, safflower, soybean, and canola oils

In conclusion, it’s essential to recognize what type of fat you are eating while on the ketogenic diet. In the end, the function of the ketogenic diet will always be to enhance your health, which includes eating the appropriate amount of fat, protein, and carbohydrate ratio as well as picking food resources which promote health and wellness. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

What Are Exogenous Ketones?

What Are Exogenous Ketones?

Ketones serve as a source of energy for the mitochondria found inside the cells of the human body. These are an alternative fuel to sugar. Ketones are basic substances with a simple molecular structure. Ketones are natural,�or carbon-based, chemicals made up of a central carbon atom double-bonded into an oxygen atom and two carbon-containing substituents, denoted by”R”.

Genetic Ketone Structure

In humans, there are 3 distinct ketones created by the mitochondria. These are referred to as ketone bodies. The 3 ketones are:

  1. Acetone
  2. Acetoacetate, also known as Acetoacetic Acid
  3. Beta-Hydroxybutyric Acid, also known as Beta Hydroxybutyrate or BHB. Additional compound names include 3-hydroxybutyric acid or 3-hydroxybutyrate.

BHB isn’t particularly considered a ketone because it comprises a reactive OH-group rather than a double-bonded oxygen which would generally function as demonstrated in the diagram below. However, BHB continues to function much like a ketone because it transforms into energy, such as acetone and acetoacetate. The following is demonstrated in the diagram below.

Structures of Ketone Bodies

Ketogenesis is the metabolism of fatty acids through ?-oxidation. This procedure provides acetyl CoA which converts to ?-hydroxy-?-methyglutaryl-CoA, or HMG-CoA, as shown below. HMG-CoA turns into Acetoacetone which may change back-and-forth to BHB. The conversion of Acetoacetate into Acetone is irreversible (as seen on the bottom left). Acetoacetate and BHB, through acetoacetate, are utilized to make energy when converted into acetyl-CoA in the cell’s mitochondria whilst Acetone is excreted in the breath and urine.

Formation of Ketone Bodies from Acetyl-CoA2

Understanding Exogenous Ketone Bodies

Exogenous ketone bodies are simply ketone bodies which are consumed via a nutritional supplement. Ketone bodies created in the liver are more correctly referred to as endogenous ketone bodies. The following is described below.

Most nutritional supplements depend�on BHB as the origin of the exogenous ketone bodies. BHB transforms into acetoacetic acid where a small amount is turned into acetone via an acetoacetate decarboxylase waste pathway. A percentage of that acetoacetic acid may enter the energy pathway utilizing beta-ketothialase, which transforms acetoacetic acid into 2 Acetyl-CoA molecules.

Ketosis Pathway Before Entering the Krebs (Energy) Pathway

The Acetyl-CoA will then enter the Krebs cycle and creates ATP. Exogenous ketone body nutritional supplements provide an instantaneous supply of ketones to consumers. Even when you’re not in the state of ketosis before eating, such as when ingesting a higher-carb diet. These also increase blood ketones even in the presence of insulin, which inhibits ketogenesis.

Researchers do not completely comprehend what the long-term ramifications of combining a non-ketogenic diet with exogenous ketone bodies nutritional supplements really are. Research studies are at their first phases and much more information is required. A standard issue involves why BHB is the ketone body to receive exogenous ketone nutritional supplements. The explanation is a mixture in the simplicity of its formula and its conversion to energy. it is simpler to devise BHB into a nutritional supplement.

Are “Raspberry Ketones” Similar to “Ketone Bodies”?

Raspberry ketones are a�common ingredient used in weight-loss nutritional supplements. However, despite their title, they don’t have any connection. This has generated some confusion for individuals considering ketone nutritional supplements that are exogenous.

Raspberry ketones are in reality phenolic compounds that provide raspberries their pleasant odor. They are similar to the stimulant synephrine. Regardless of the research studies, raspberry ketones don’t seem to have much impact on weight loss.

Ketone Salts vs. Ketone Esters

Exogenous ketones of all beta-hydroxybutyrate can be found in two kinds:

  1. Ketone Salts are naturally-derived chemicals which blend sodium as well as potassium and/or calcium with BHB to boost absorption. Commercially available nutritional supplements are all created from ketone salts now (contains KetoForce, KetoCaNa and Keto OS). These are also occasionally called “Ketone Mineral Salts” or “BHB Mineral Salts”.
  2. Ketone Esters are Synthetically-made chemicals that connect an alcohol to a ketone body, where this can be metabolized in the liver as a ketone. Ketone esters are used primarily in search for testing their effectiveness on improving ketone body levels. Below is a standard arrangement of a BHB ester. The very first Ketone Ester beverage is currently accessible by HVMN. Research esters are very unpleasant tasting, something which HVMN expects to modify soon.
Structure of a Beta-Hydroxybutyrate Ester

Ketone Esters increase blood levels of beta-hydroxybutyrate to greater levels compared to Ketone Salts. There’s strong evidence supporting that esters are more powerful than Ketone Salts, so much as their advantages proceed. It’s not apparent why this occurs, but it might be from the gastrointestinal, or GI, tract due to a gap in the absorption rate.

However, esters are normally somewhat tougher to endure because of gut distress after intake and they do not have the most agreeable taste, as stated previously in the article. Figure 1 below demonstrates the difference between eating equivalent quantities of BHB in the kind of a Ketone ester and Ketone salts on bloo BHB. The supplements contained are:

  • BMS (Beta-hydroxybutyrate Mineral Salt) — sodium/ potassium established (KetoForce)
  • KE (Ketone Ester) — (R- 3-hydroxybutyl-R-1,3-hydroxybutyrate) (HVMN)
Figure 1: Blood BHB level after consuming a ketone ester vs a ketone salt drink.

What are the Benefits of Exogenous Ketones?

Exogenous ketone nutritional supplements can offer a great number of benefits. These include more effective weight reduction, athletic performance improvement, cancer prevention, cognitive advancement,�and anti-inflammatory properties.

Weight Loss Goals

  • Appetite suppression: Appetite was quantified in 10 males and 5 females after taking a ketone ester, abbreviated as KE, or a dextrose, abbreviated as DEXT, beverage. The wish to consume and perception of appetite dropped after both supplements, however, the KE was 50 percent more successful for 1.5 to 4 hours. Insulin levels rose with both supplements but were 3 times lower with the KE beverage after 30 minutes, according to Figure 2. The desire hormone, ghrelin, was considerably lower between 2 to 4 hours after ingesting the KE, as seen on Figure 2. Ketone esters lower the urge and delays appetite.
Figure 2: Perceived hunger, fullness, and satiety after consuming a dextrose or ketone ester drink over time. Effects of ketone ester or dextrose drink on plasma insulin and ghrelin levels over time.
  • Extra ketones: In case someone has an inordinate number of ketones in the bloodstream, the human body, especially the kidneys, will function as swiftly as possible to filter out ketones via urine instead of converting them into adipose tissue. This isn’t to say you can not gain fat with�exogenous ketones, however, they are not as inclined to be converted into fat than other nourishment.
  • More tolerable compared to MCT oil: MCT oil was known to cause gastrointestinal distress in consumers, particularly when taken in high quantities. Exogenous ketones as ketone salts are well-tolerated. They prevent adverse GI events while supplying similar kinds of benefits. Figure 2 demonstrates how Ketone esters may be capable of reducing hunger. A combo of exogenous ketones and MCT oil can help with weight loss and permit a loading of nutritional supplements, with no GI distress.

Athletic Performance Goals

  • Athletic enhancem: The development of energy and�fuel pairing mechanisms. Exogenous ketone supplementation may boost these components of athletic performance. There’s a promising prognosis in this area for many different motives:
  1. Exogenous ketones induce severe ketosis, lasting for many hours. This is without having to possess depleted muscle glycogen stores. Low muscle nourishment is well-known to inhibit sustained physical functionality.
  2. The “carb-sparing” impact from BHB inhibits the breakdown of muscle glycogen. This contributes to reduced lactate levels. When raising exercise intensity, fat oxidation, or burning, reaches a limit. Carbohydrates are then burned�for energy.�But when swallowing Ketone esters, the body doesn’t make this change. This implies ketones are used instead.
  3. Exogenous ketones induce your system to rely on fat as fuel, as seen in Figure 3. Fat takes longer to metabolize compared to muscle glycogen for vitality. That is because fatty acids aren’t the fuel that is favored by the human body under exercise. This might be useful for athletes performing resistance training or cardiovascular exercises. This is especially helpful for�athletes that would like to experience cardiovascular or resistance training.
  4. Ketone esters boost free carnitine whilst exercising which appears to enhance physical performance.
  5. Exogenous ketones decrease the usage of Branched-chain amino acids, or BCAAs, as�energy, a process known as deamination. The growth was decreased by consumption of a ester beverage by 50 percent during exercise in muscle BCAAs.
Figure 3: Plasma free fatty acid (FFA) and glycerol concentrations after consuming high fat, carbohydrate, or ketone ester drink.
  • Increased cognition: Elevated plasma ketone concentrations divert the brain to use ketone bodies for the synthesis of phospholipids, which drives growth and myelination. Sugar is often the preferred�fuel for this process, which is not as efficient. BHB appears to work as a signal for pathways. These improve cognition, plasticity and stress immunity. In rat research studies, ingestion of a ketone ester for 5 days enhanced memory and their learning.

Health & Longevity

  • Anti-carcinogenic properties: Statistics appears to imply that exogenous ketones are a powerful anti-carcinogen. The motive for this is that cancer cells cannot utilize ketone bodies efficiently. In fact ketone supplementation was demonstrated to improve survival rates of mice with cancer.
  • Neuroprotection: As people age, the brain becomes more prone to neurodegeneration and following conditions like Alzheimer’s and Parkinson’s disease. Ketone supplementation seems to ameliorate the decline. The mechanism is that ketone bodies decrease hyperexcitability and the redness that’s ordinarily shown as sugar metabolism declines from the brain.
  • Anti-Inflammatory attributes: There’s proof that ketone bodies play an essential part in reducing inflammation by inhibiting a particular class of proteins known as inflammasones.
  • Gene regulation profile alterations: There’s proof that gene sets could be regulated with an alteration in mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase, or mHS, as see in rats on a ketogenic diet.
Dr Jimenez White Coat
Ketones are a source of energy which is produced when there is not enough sugar or glucose for the human body to burn as fuel. They serve as an alternative fuel source to glucose. Ketogenesis, the metabolism of fatty acids through ketosis, can have a variety of health benefits. Many people achieve these benefits by following the ketogenic diet, however, these advantages can be achieved without the keto diet as well. Exogenous ketone bodies are simply ketones which are consumed through a nutritional supplement. Although the over-consumption of any supplement can have risks, exogenous ketone bodies can provide similar benefits to ketosis. Dr. Alex Jimenez D.C., C.C.S.T. Insight

How Exogenous Ketones Function

Exogenous ketones possess many different physiological effects soon after ingestion:

  • For starters, ingesting ketones, particularly ketone esters, is an effective approach to Boost BHB from the bloodstream above 2 mMol for almost 8 hours. Ketone salts do not seem to elevate BHB from the bloodstream as efficiently or significantly where ketone esters do, however.
  • Exogenous ketone supplementation induces blood sugar to reduce significantly, likely as a result of an intense increase in insulin sensitivity. Exogenous ketones may pose a possible treatment.
  • Exogenous ketones additionally improve oxygen use, particularly in the central nervous system, or CNS. This effect reduces the odds of oxygen reaching potentially hazardous levels in the CNS, which then has a variety of additional favorable health effects like the ones discussed in the prior section.

Potential Downsides to Ketone Supplementation

Like any other nutritional supplement, side effects and drawbacks are possible after consuming exogenous ketones. As ketone supplementation becomes more notable, they are generally quite benign and will improve. The most frequent side effects to know about when using exogenous ketones consist of:

  • Electrolyte Imbalance: The physiological rationale supporting electrolytes during a state of ketosis is a result of the absence of water retention and frequent urination. The frequency of urination will�increase when supplementing exogenous ketones, but it will not deplete glycogen stores. It could be handy after taking ketones if you’re urinating a lot to drink an electrolyte solution, but it is dependent upon the way you are feeling.
  • Halitosis or bad breath: If you are on a ketogenic diet, you’re most likely aware that since the body begins to metabolize fat, ketones may cause bad breath. There is little one can do about this. This may arise when utilizing exogenous ketones, but it is not quite as durable as when on the ketogenic diet. If it turns into a problem, chewing gum or mints is the best choice. This issue may occur due to the over-consumption of this nutritional supplement, tailoring extra BHB.
  • Potential GI distress (flatulence) at exceptionally substantial doses: Exogenous ketones taken in massive doses sometimes lead to GI distress, particularly flatulence. On the other hand, this cause can be hypothesized to be a result of how ketones were blended in a fluid which was palatable. If you are taking a balanced dose of ketones GI distress can be avoided. If some GI distress is widespread, it must improve as you become accustomed to carrying ketones.
  • Hypoglycemia: Accepting exogenous ketones can induce blood sugar levels to become very low, but you’re unlikely to feel the normal signs of hypoglycemia. That is because if levels are large enough, they control energy in the brain; despite having low blood sugar, therefore, you may feel just fine. A research by George Cahill, discovered that if they had been administered insulin to induce hypoglycemia, ketone levels can protect fasted participants.

Future Research Studies

Research studies on exogenous ketones concentrates on the advantages of their use. Research studies will also concentrate more on their therapeutic use. The information on all those applications is currently limited. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

Ketogenic Diet in Cancer Treatment

Ketogenic Diet in Cancer Treatment

Cancer is the second leading cause of death in the United States. Research studies have estimated that approximately 595,690 Americans die from cancer every year, that’s about 1,600 deaths every day, on average. Cancer is frequently treated utilizing a combination of surgery, chemotherapy, and radiation. Recent research studies have analyzed a variety of nutritional strategies for cancer treatment. Early research studies suggest�that the ketogenic diet may help treat cancer.

What is the Ketogenic Diet?

The ketogenic diet is a very low-carb, high-fat diet which is often compared with the Atkins diet and other low carb diets. Also commonly known as the keto diet, this nutritional strategy entails drastically reducing your consumption of carbohydrates and instead substituting them with fat. This dietary shift is what causes the human body to enter a state of ketosis, the well-known metabolic state associated with the keto�diet. Ketosis utilizes fat as the cell’s main source of energy, rather than sugar or glucose.

Ketosis causes a considerable increase in the levels of ketones. In general, a ketogenic diet used for weight loss consists of about 60 to 75 percent of calories from fat, with 15 to 30 percent of calories from protein and 5 to 10 percent of calories from carbohydrates. However, when a ketogenic diet is used therapeutically to treat cancer, the fat content might be significantly higher, up to 90 percent of calories from fat, and the protein content will also be considerably lower, up to 5 percent of calories from protein.

 

The Role of Blood Sugar in Cancer

Many cancer treatments are designed to target the biological differences between cancer cells and normal cells. Nearly all cancer cells share one common characteristic: they feed off of blood sugar or glucose in order to grow and multiply. During the ketogenic diet, several conventional metabolic processes are modified and blood sugar levels decrease, “starving” cancer cells. As a result, cancer cells have been demonstrated to grow much slower, often decreasing in size or even dying.

This nutritional strategy as a form of cancer treatment was first proposed by Otto Heinrich Warburg,�a leading cell biologist. Otto Warburg led to the discovery that cancer cells are unable to flourish using energy produced from cellular respiration but instead from glucose fermentation. The Warburg effect developed from the role of glycolysis and lactic acid fermentation to transfer energy, compensating for lower dependence on oxidative phosphorylation and limited mitochondrial respiration.

Benefits of the Keto�Diet for Cancer

The ketogenic diet provides other benefits in cancer treatment. Primarily, reducing carbohydrates from your diet can quickly lower calorie intake, reducing the energy available to the cells. In turn, this may slow down tumor development and the progression of cancer. Additionally, the ketogenic diet may help lower insulin levels. Insulin is an anabolic hormone which promotes cell growth, including cancerous cells. Therefore, lower insulin may help slow down tumor development.

The Ketogenic Diet and Cancer in Animals

Researchers have analyzed the ketogenic diet as an alternative cancer treatment for many decades. Until recently, most research studies�were performed in animals. A big number of these animal research studies have demonstrated that the ketogenic diet can reduce tumor growth and improve survival levels in mice.

One research study in mice reviewed the cancer-fighting effects of the ketogenic diet along with other diets. Strikingly, the researchers found that 60 percent of mice following the ketogenic diet survived. This increased to 100 percent in mice that received a ketone supplement while on the keto�diet. None lived on a standard diet.

The Ketogenic Diet and Cancer in Humans

Despite the promising evidence of the benefits of the ketogenic diet as a form of cancer treatment in animals, research studies in humans have only just started. At present, the limited research studies does seem to demonstrate that a ketogenic diet may decrease tumor size and decrease the progression�of certain cancers. One of the few documented cases was conducted on a 65-year-old woman with brain cancer. Following surgery, she followed a ketogenic diet and the tumor’s progression decreased.

However, 10 weeks after returning to a normal diet, she experienced a substantial increase in tumor growth. Similar case reports analyzed the reactions to a ketogenic diet in two women who were undergoing therapy for advanced brain cancer. Researchers discovered that glucose uptake was decreased from the tumors of both patients. One of the women reported improved quality of life and stayed on the diet for 12 weeks. During that time her disease showed no further progression.

One research study tracked tumor growth in response to a high-carbohydrate diet versus a ketogenic diet in 27 patients with gastrointestinal cancer. Tumor growth increased by 32.2 percent in patients who received the high-carb diet while tumor growth decreased by 24.3 percent in patients on the ketogenic diet. In a different research study, three out of five patients on a ketogenic diet combined with radiation or chemotherapy experienced complete remission.

Can the Ketogenic Diet Help Prevent Cancer?

A variety of research studies have also demonstrated that the ketogenic diet can help prevent cancer in the first place. Primarily, it can help reduce several risk factors for cancer. The keto diet may help decrease IGF-1 levels. Insulin-like growth factor 1, or IGF-1, is a hormone that’s essential for cell growth while reducing programmed cell death. This hormone can play a part in the evolution and progression of cancer. The ketogenic diet is thought to decrease IGF-1 levels, thereby decreasing the effects insulin has on cell growth, reducing the risk of cancer.

The ketogenic diet can also help lower blood sugar levels and decrease the risk of diabetes. Other evidence indicates that people with elevated glucose and diabetes have an increased risk of developing cancer. Research studies show that a ketogenic diet can be extremely effective at lowering blood sugar levels and handling diabetes. The keto diet can reduce obesity. Obesity can be a risk factor for cancer. Since the ketogenic diet is a powerful weight loss tool, it may also help reduce the chance of cancer by fighting obesity.

Dr Jimenez White Coat
Emerging research studies continue to demonstrate that sugar or glucose is the main source of fuel for cancer. Researchers have attempted to demonstrate that regulating the metabolic functions within the human body is the real solution towards treating cancer. The ketogenic diet can help treat cancer because it limits the amount of sugar in the body and instead replaces it with ketones, “starving” cancer cells and decreasing cell growth and cancer progression. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Conclusion

A ketogenic diet offers many health advantages. Based on animal and early research studies in humans, it may also serve as a cancer treatment. However, it’s important to keep in mind that further research studies are still required to conclude the effects of the ketogenic diet on cancer. You shouldn’t avoid conventional cancer therapy in favor of an alternative treatment option like the keto�diet.�The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***

Multi-Dimensional Roles of Ketone Bodies

Multi-Dimensional Roles of Ketone Bodies

Ketone bodies are created by the liver and utilized as an energy source when glucose is not readily available in the human body. The two main ketone bodies are acetoacetate (AcAc) and 3-beta-hydroxybutyrate (3HB), while acetone is the third and least abundant, ketone body. Ketones are always present in the blood and their levels increase during fasting and prolonged exercise.�Ketogenesis is the biochemical process by which organisms produce ketone bodies through the breakdown of fatty acids and ketogenic amino acids.

Ketone bodies are mainly generated in the mitochondria of liver cells. Ketogenesis occurs when there are low glucose levels in the blood, particularly after other cellular carbohydrate stores, such as glycogen, have been exhausted. This mechanism can also occur when there is insufficient amounts of insulin. The production of ketone bodies is ultimately initiated to make available energy which is stored in the human body as fatty acids. Ketogenesis occurs in the mitochondria where it is independently regulated.

Abstract

Ketone body metabolism is a central node in physiological homeostasis. In this review, we discuss how ketones serve discrete fine-tuning metabolic roles that optimize organ and organism performance in varying nutrient remains and protect from inflammation and injury in multiple organ systems. Traditionally viewed as metabolic substrates enlisted only in carbohydrate restriction, recent observations underscore the importance of ketone bodies as vital metabolic and signaling mediators when carbohydrates are abundant. Complementing a repertoire of known therapeutic options for diseases of the nervous system, prospective roles for ketone bodies in cancer have arisen, as have intriguing protective roles in heart and liver, opening therapeutic options in obesity-related and cardiovascular disease. Controversies in ketone metabolism and signaling are discussed to reconcile classical dogma with contemporary observations.

Introduction

Ketone bodies are a vital alternative metabolic fuel source for all the domains of life, eukarya, bacteria, and archaea (Aneja et al., 2002; Cahill GF Jr, 2006; Krishnakumar et al., 2008). Ketone body metabolism in humans has been leveraged to fuel the brain during episodic periods of nutrient deprivation. Ketone bodies are interwoven with crucial mammalian metabolic pathways such as ?-oxidation (FAO), the tricarboxylic acid cycle (TCA), gluconeogenesis, de novo lipogenesis (DNL), and biosynthesis of sterols. In mammals, ketone bodies are produced predominantly in the liver from FAO-derived acetyl-CoA, and they are transported to extrahepatic tissues for terminal oxidation. This physiology provides an alternative fuel that is augmented by relatively brief periods of fasting, which increases fatty acid availability and diminishes carbohydrate availability (Cahill GF Jr, 2006; McGarry and Foster, 1980; Robinson and Williamson, 1980). Ketone body oxidation becomes a significant contributor to overall energy mammalian metabolism within extrahepatic tissues in a myriad of physiological states, including fasting, starvation, the neonatal period, post-exercise, pregnancy, and adherence to low carbohydrate diets. Circulating total ketone body concentrations in healthy adult humans normally exhibit circadian oscillations between approximately 100�250 �M, rise to ~1 mM after prolonged exercise or 24h of fasting, and can accumulate to as high as 20 mM in pathological states like diabetic ketoacidosis (Cahill GF Jr, 2006; Johnson et al., 1969b; Koeslag et al., 1980; Robinson and Williamson, 1980; Wildenhoff et al., 1974). The human liver produces up to 300 g of ketone bodies per day (Balasse and Fery, 1989), which contribute between 5�20% of total energy expenditure in fed, fasted, and starved states (Balasse et al., 1978; Cox et al., 2016).

Recent studies now highlight imperative roles for ketone bodies in mammalian cell metabolism, homeostasis, and signaling under a wide variety of physiological and pathological states. Apart from serving as energy fuels for extrahepatic tissues like brain, heart, or skeletal muscle, ketone bodies play pivotal roles as signaling mediators, drivers of protein post-translational modification (PTM), and modulators of inflammation and oxidative stress. In this review, we provide both classical and modern views of the pleiotropic roles of ketone bodies and their metabolism.

Overview of Ketone Body Metabolism

The rate of hepatic ketogenesis is governed by an orchestrated series of physiological and biochemical transformations of fat. Primary regulators include lipolysis of fatty acids from triacylglycerols, transport to and across the hepatocyte plasma membrane, transport into mitochondria via carnitine palmitoyltransferase 1 (CPT1), the ?-oxidation spiral, TCA cycle activity and intermediate concentrations, redox potential, and the hormonal regulators of these processes, predominantly glucagon and insulin [reviewed in (Arias et al., 1995; Ayte et al., 1993; Ehara et al., 2015; Ferre et al., 1983; Kahn et al., 2005; McGarry and Foster, 1980; Williamson et al., 1969)]. Classically ketogenesis is viewed as a spillover pathway, in which ?-oxidation-derived acetyl-CoA exceeds citrate synthase activity and/or oxaloacetate availability for condensation to form citrate. Three-carbon intermediates exhibit anti-ketogenic activity, presumably due to their ability to expand the oxaloacetate pool for acetyl-CoA consumption, but hepatic acetyl-CoA concentration alone does not determine ketogenic rate (Foster, 1967; Rawat and Menahan, 1975; Williamson et al., 1969). The regulation of ketogenesis by hormonal, transcriptional, and post-translational events together support the notion that the molecular mechanisms that fine-tune ketogenic rate remain incompletely understood (see Regulation of HMGCS2 and SCOT/OXCT1).

Ketogenesis occurs primarily in hepatic mitochondrial matrix at rates proportional to total fat oxidation. After transport of acyl chains across the mitochondrial membranes and ?-oxidation, the mitochondrial isoform of 3-hydroxymethylglutaryl-CoA synthase (HMGCS2) catalyzes the fate committing condensation of acetoacetyl-CoA (AcAc-CoA) and acetyl-CoA to generate HMG-CoA (Fig. 1A). HMG-CoA lyase (HMGCL) cleaves HMG-CoA to liberate acetyl-CoA and acetoacetate (AcAc), and the latter is reduced to d-?-hydroxybutyrate (d-?OHB) by phosphatidylcholine-dependent mitochondrial d-?OHB dehydrogenase (BDH1) in a NAD+/NADH-coupled near-equilibrium reaction (Bock and Fleischer, 1975; LEHNINGER et al., 1960). The BDH1 equilibrium constant favors d-?OHB production, but the ratio of AcAc/d-?OHB ketone bodies is directly proportional to mitochondrial NAD+/NADH ratio, and thus BDH1 oxidoreductase activity modulates mitochondrial redox potential (Krebs et al., 1969; Williamson et al., 1967). AcAc can also spontaneously decarboxylate to acetone (Pedersen, 1929), the source of sweet odor in humans suffering ketoacidosis (i.e., total serum ketone bodies > ~7 mM; AcAc pKa 3.6, ?OHB pKa 4.7). The mechanisms through which ketone bodies are transported across the mitochondrial inner membrane are not known, but AcAc/d-?OHB are released from cells via monocarboxylate transporters (in mammals, MCT 1 and 2, also known as solute carrier 16A family members 1 and 7) and transported in the circulation to extrahepatic tissues for terminal oxidation (Cotter et al., 2011; Halestrap and Wilson, 2012; Halestrap, 2012; Hugo et al., 2012). Concentrations of circulating ketone bodies are higher than those in the extrahepatic tissues (Harrison and Long, 1940) indicating ketone bodies are transported down a concentration gradient. Loss-of-function mutations in MCT1 are associated with spontaneous bouts of ketoacidosis, suggesting a critical role in ketone body import.

� With the exception of potential diversion of ketone bodies into non-oxidative fates (see Non-oxidative metabolic fates of ketone bodies), hepatocytes lack the ability to metabolize the ketone bodies they produce. Ketone bodies synthesized de novo by liver are (i) catabolized in mitochondria of extrahepatic tissues to acetyl-CoA, which is available to the TCA cycle for terminal oxidation (Fig. 1A), (ii) diverted to the lipogenesis or sterol synthesis pathways (Fig. 1B), or (iii) excreted in the urine. As an alternative energetic fuel, ketone bodies are avidly oxidized in heart, skeletal muscle, and brain (Balasse and Fery, 1989; Bentourkia et al., 2009; Owen et al., 1967; Reichard et al., 1974; Sultan, 1988). Extrahepatic mitochondrial BDH1 catalyzes the first reaction of ?OHB oxidation, converting it to back AcAc (LEHNINGER et al., 1960; Sandermann et al., 1986). A cytoplasmic d-?OHB-dehydrogenase (BDH2) with only 20% sequence identity to BDH1 has a high Km for ketone bodies, and also plays a role in iron homeostasis (Davuluri et al., 2016; Guo et al., 2006). In extrahepatic mitochondrial matrix, AcAc is activated to AcAc-CoA through exchange of a CoA-moiety from succinyl-CoA in a reaction catalyzed by a unique mammalian CoA transferase, succinyl-CoA:3-oxoacid-CoA transferase (SCOT, CoA transferase; encoded by OXCT1), through a near equilibrium reaction. The free energy released by hydrolysis of AcAc-CoA is greater than that of succinyl-CoA, favoring AcAc formation. Thus ketone body oxidative flux occurs due to mass action: an abundant supply of AcAc and rapid consumption of acetyl-CoA through citrate synthase favors AcAc-CoA (+ succinate) formation by SCOT. Notably, in contrast to glucose (hexokinase) and fatty acids (acyl-CoA synthetases), the activation of ketone bodies (SCOT) into an oxidizable form does not require the investment of ATP. A reversible AcAc-CoA thiolase reaction [catalyzed by any of the four mitochondrial thiolases encoded by either ACAA2 (encoding an enzyme known as T1 or CT), ACAT1 (encoding T2), HADHA, or HADHB] yields two molecules of acetyl-CoA, which enter the TCA cycle (Hersh and Jencks, 1967; Stern et al., 1956; Williamson et al., 1971). During ketotic states (i.e., total serum ketones > 500 �M), ketone bodies become significant contributors to energy expenditure�and are utilized in tissues rapidly until uptake or saturation of oxidation occurs (Balasse et al., 1978; Balasse and Fery, 1989; Edmond et al., 1987). A very small fraction of liver-derived ketone bodies can be readily measured in the urine, and utilization and reabsorption rates by the kidney are proportionate to circulating concentration (Goldstein, 1987; Robinson and Williamson, 1980). During highly ketotic states (> 1 mM in plasma), ketonuria serves as a semi-quantitative reporter of ketosis, although most clinical assays of urine ketone bodies detect AcAc but not ?OHB (Klocker et al., 2013).

Ketogenic Substrates and their Impact on Hepatocyte Metabolism

Ketogenic substrates include fatty acids and amino acids (Fig. 1B). The catabolism of amino acids, especially leucine, generates about 4% of ketone bodies in post-absorptive state (Thomas et al., 1982). Thus the acetyl-CoA substrate pool to generate ketone bodies mainly derives from fatty acids, because during states of diminished carbohydrate supply, pyruvate enters the hepatic TCA cycle primarily via anaplerosis, i.e., ATP-dependent carboxylation to oxaloacetate (OAA), or to malate (MAL), and not oxidative decarboxylation to acetyl-CoA (Jeoung et al., 2012; Magnusson et al., 1991; Merritt et al., 2011). In liver, glucose and pyruvate contribute negligibly to ketogenesis, even when pyruvate decarboxylation to acetyl-CoA is maximal (Jeoung et al., 2012).

Acetyl-CoA subsumes several roles integral to hepatic intermediary metabolism beyond ATP generation via terminal oxidation (also see The integration of ketone body metabolism, post-translational modification, and cell physiology). Acetyl-CoA allosterically activates (i) pyruvate carboxylase (PC), thereby activating a metabolic control mechanism that augments anaplerotic entry of metabolites into the TCA cycle (Owen et al., 2002; Scrutton and Utter, 1967) and (ii) pyruvate dehydrogenase kinase, which phosphorylates and inhibits pyruvate dehydrogenase (PDH) (Cooper et al., 1975), thereby further enhancing flow of pyruvate into the TCA cycle via anaplerosis. Furthermore, cytoplasmic acetyl-CoA, whose pool is augmented by mechanisms that convert mitochondrial acetyl-CoA to transportable metabolites, inhibits fatty acid oxidation: acetyl-CoA carboxylase (ACC) catalyzes the conversion of acetyl-CoA to malonyl-CoA, the lipogenic substrate and allosteric inhibitor of mitochondrial CPT1 [reviewed in (Kahn et al., 2005; McGarry and Foster, 1980)]. Thus, the mitochondrial acetyl-CoA pool both regulates and is regulated by the spillover pathway of ketogenesis, which orchestrates key aspects of hepatic intermediary metabolism.

Non-Oxidative Metabolic Fates of Ketone Bodies

The predominant fate of liver-derived ketones is SCOT-dependent extrahepatic oxidation. However, AcAc can be exported from mitochondria and utilized in anabolic pathways via conversion to AcAc-CoA by an ATP-dependent reaction catalyzed by cytoplasmic acetoacetyl-CoA synthetase (AACS, Fig. 1B). This pathway is active during brain development and in lactating mammary gland (Morris, 2005; Robinson and Williamson, 1978; Ohgami et al., 2003). AACS is also highly expressed in adipose tissue, and activated osteoclasts (Aguilo et al., 2010; Yamasaki et al., 2016). Cytoplasmic AcAc-CoA can be either directed by cytosolic HMGCS1 toward sterol biosynthesis, or cleaved by either of two cytoplasmic thiolases to acetyl-CoA (ACAA1 and ACAT2), carboxylated to malonyl-CoA, and contribute to the synthesis of fatty acids (Bergstrom et al., 1984; Edmond, 1974; Endemann et al., 1982; Geelen et al., 1983; Webber and Edmond, 1977).

While the physiological significance is yet to be established, ketones can serve as anabolic substrates even in the liver. In artificial experimental contexts, AcAc can contribute to as much as half of newly synthesized lipid, and up to 75% of new synthesized cholesterol (Endemann et al., 1982; Geelen et al., 1983; Freed et al., 1988). Because AcAc is derived from incomplete hepatic fat oxidation, the ability of AcAc to contribute to lipogenesis in vivo would imply hepatic futile cycling, where fat-derived ketones can be utilized for lipid production, a notion whose physiological significance requires experimental validation, but could serve adaptive or maladaptive roles (Solinas et al., 2015). AcAc avidly supplies cholesterogenesis, with a low AACS Km-AcAc (~50 �M) favoring AcAc activation even in the fed state (Bergstrom et al., 1984). The dynamic role of cytoplasmic ketone metabolism has been suggested in primary mouse embryonic neurons and in 3T3-L1 derived-adipocytes, as AACS knockdown impaired differentiation of each cell type (Hasegawa et al., 2012a; Hasegawa et al., 2012b). Knockdown of AACS in mice in vivo decreased serum cholesterol (Hasegawa et al., 2012c). SREBP-2, a master transcriptional regulator of cholesterol biosynthesis, and peroxisome proliferator activated receptor (PPAR)-? are AACS transcriptional activators, and regulate its transcription during neurite development and in the liver (Aguilo et al., 2010; Hasegawa et al., 2012c). Taken together, cytoplasmic ketone body metabolism may be important in select conditions or disease natural histories, but are inadequate to dispose of liver-derived ketone bodies, as massive hyperketonemia occurs in the setting of selective impairment of the primary oxidative fate via loss of function mutations to SCOT (Berry et al., 2001; Cotter et al., 2011).

Regulation of HMGCS2 and SCOT/OXCT1

The divergence of a mitochondrial from the gene encoding cytosolic HMGCS occurred early in vertebrate evolution due to the need to support hepatic ketogenesis in species with higher brain to body weight ratios (Boukaftane et al., 1994; Cunnane and Crawford, 2003). Naturally occurring loss-of-function HMGCS2 mutations in humans cause bouts of hypoketotic hypoglycemia (Pitt et al., 2015; Thompson et al., 1997). Robust HMGCS2 expression is restricted to hepatocytes and colonic epithelium, and its expression and enzymatic activity are coordinated through diverse mechanisms (Mascaro et al., 1995; McGarry and Foster, 1980; Robinson and Williamson, 1980). While the full scope of physiological states that influence HMGCS2 requires further elucidation, its expression and/or activity is regulated during the early postnatal period, aging, diabetes, starvation or ingestion of ketogenic diet (Balasse and Fery, 1989; Cahill GF Jr, 2006; Girard et al., 1992; Hegardt, 1999; Satapati et al., 2012; Sengupta et al., 2010). In the fetus, methylation of 5� flanking region of Hmgcs2 gene inversely correlates with its transcription, and is partially reversed after birth (Arias et al., 1995; Ayte et al., 1993; Ehara et al., 2015; Ferre et al., 1983). Similarly, hepatic Bdh1 exhibits a developmental expression pattern, increasing from birth to weaning, and is also induced by ketogenic diet in a fibroblast growth factor (FGF)-21-dependent manner (Badman et al., 2007; Zhang et al., 1989). Ketogenesis in mammals is highly responsive to both insulin and glucagon, being suppressed and stimulated, respectively (McGarry and Foster, 1977). Insulin suppresses adipose tissue lipolysis, thus depriving ketogenesis of its substrate, while glucagon increases ketogenic flux through a direct effect on the liver (Hegardt, 1999). Hmgcs2 transcription is stimulated by forkhead transcriptional factor FOXA2, which is inhibited via insulin-phosphatidylinositol-3-kinase/Akt, and is induced by glucagon-cAMP-p300 signaling (Arias et al., 1995; Hegardt, 1999; Quant et al., 1990; Thumelin et al., 1993; von Meyenn et al., 2013; Wolfrum et al., 2004; Wolfrum et al., 2003). PPAR? (Rodriguez et al., 1994) together with its target, FGF21 (Badman et al., 2007) also induce Hmgcs2 transcription in the liver during starvation or administration of ketogenic diet (Badman et al., 2007; Inagaki et al., 2007). Induction of PPAR? may occur before the transition from fetal to neonatal physiology, while FGF21 activation may be favored in the early neonatal period via ?OHB-mediated inhibition of histone deacetylase (HDAC)-3 (Rando et al., 2016). mTORC1 (mammalian target of rapamycin complex 1) dependent inhibition of PPAR? transcriptional activity is also a key regulator of Hmgcs2 gene expression (Sengupta et al., 2010), and liver PER2, a master circadian oscillator, indirectly regulates Hmgcs2 expression (Chavan et al., 2016). Recent observations indicate that extrahepatic tumor-induced interleukin-6 impairs ketogenesis via PPAR? suppression (Flint et al., 2016). Despite these observations, it is important to note that physiological shifts in Hmgcs2 gene expression have not been mechanistically linked to HMGCS2 protein abundance or to variations of ketogenic rate.

HMGCS2 enzyme activity is regulated through multiple PTMs. HMGCS2 serine phosphorylation enhanced its activity in vitro (Grimsrud et al., 2012). HMGCS2 activity is allosterically inhibited by succinyl-CoA and lysine residue succinylation (Arias et al., 1995; Hegardt, 1999; Lowe and Tubbs, 1985; Quant et al., 1990; Rardin et al., 2013; Reed et al., 1975; Thumelin et al., 1993). Succinylation of HMGCS2, HMGCL, and BDH1 lysine residues in hepatic mitochondria are targets of the NAD+ dependent deacylase sirtuin 5 (SIRT5) (Rardin et al., 2013). HMGCS2 activity is also enhanced by SIRT3 lysine deacetylation, and it is possible that crosstalk between acetylation and succinylation regulates HMGCS2 activity (Rardin et al., 2013; Shimazu et al., 2013). Despite the ability of these PTMs to regulate HMGCS2 Km and Vmax, fluctuations of these PTMs have not yet been carefully mapped and have not been confirmed as mechanistic drivers of ketogenesis in vivo.

SCOT is expressed in all mammalian cells that harbor mitochondria, except those of hepatocytes. The importance of SCOT activity and ketolysis was demonstrated in SCOT-KO mice, which exhibited uniform lethality due to hyperketonemic hypoglycemia within 48h after birth (Cotter et al., 2011). Tissue-specific loss of SCOT in neurons or skeletal myocytes induces metabolic abnormalities during starvation but is not lethal (Cotter et al., 2013b). In humans, SCOT deficiency presents early in life with severe ketoacidosis, causing lethargy, vomiting, and coma (Berry et al., 2001; Fukao et al., 2000; Kassovska-Bratinova et al., 1996; Niezen-Koning et al., 1997; Saudubray et al., 1987; Snyderman et al., 1998; Tildon and Cornblath, 1972). Relatively little is known at the cellular level about SCOT gene and protein expression regulators. Oxct1 mRNA expression and SCOT protein and activity are diminished in ketotic states, possibly through PPAR-dependent mechanisms (Fenselau and Wallis, 1974; Fenselau and Wallis, 1976; Grinblat et al., 1986; Okuda et al., 1991; Turko et al., 2001; Wentz et al., 2010). In diabetic ketoacidosis, the mismatch between hepatic ketogenesis and extrahepatic oxidation becomes exacerbated by impairment of SCOT activity. Overexpression of insulin-independent glucose transporter (GLUT1/SLC2A1) in cardiomyocytes also inhibits Oxct1 gene expression and downregulates ketones terminal oxidation in a non-ketotic state (Yan et al., 2009). In liver, Oxct1 mRNA abundance is suppressed by microRNA-122 and histone methylation H3K27me3 that are evident during the transition from fetal to the neonatal period (Thorrez et al., 2011). However, suppression of hepatic Oxct1 expression in the postnatal period is primarily attributable to the evacuation of Oxct1-expressing hematopoietic progenitors from the liver, rather than a loss of previously existing Oxct1 expression in terminally differentiated hepatocytes. In fact, expression of Oxct1 mRNA and SCOT protein in differentiated hepatocytes are extremely low (Orii et al., 2008).

SCOT is also regulated by PTMs. The enzyme is hyper-acetylated in brains of SIRT3 KO mice, which also exhibit diminished AcAc dependent acetyl-CoA production (Dittenhafer-Reed et al., 2015). Non-enzymatic nitration of tyrosine residues of SCOT also attenuates its activity, which has been reported in hearts of various diabetic mice models (Marcondes et al., 2001; Turko et al., 2001; Wang et al., 2010a). In contrast, tryptophan residue nitration augments SCOT activity (Br�g�re et al., 2010; Rebrin et al., 2007). Molecular mechanisms of residue-specific nitration or de-nitration designed to modulate SCOT activity may exist and require elucidation.

Controversies in Extrahepatic Ketogenesis

In mammals the primary ketogenic organ is liver, and only hepatocytes and gut epithelial cells abundantly express the mitochondrial isoform of HMGCS2 (Cotter et al., 2013a; Cotter et al., 2014; McGarry and Foster, 1980; Robinson and Williamson, 1980). Anaerobic bacterial fermentation of complex polysaccharides yields butyrate, which is absorbed by colonocytes in mammalians for terminal oxidation or ketogenesis (Cherbuy et al., 1995), which may play a role in colonocyte differentiation (Wang et al., 2016). Excluding gut epithelial cells and hepatocytes, HMGCS2 is nearly absent in almost all other mammalian cells, but the prospect of extrahepatic ketogenesis has been raised in tumor cells, astrocytes of the central nervous system, the kidney, pancreatic ? cells, retinal pigment epithelium (RPE), and even in skeletal muscle (Adijanto et al., 2014; Avogaro et al., 1992; El Azzouny et al., 2016; Grabacka et al., 2016; Kang et al., 2015; Le Foll et al., 2014; Nonaka et al., 2016; Takagi et al., 2016a; Thevenet et al., 2016; Zhang et al., 2011). Ectopic HMGCS2 has been observed in tissues that lack net ketogenic capacity (Cook et al., 2016; Wentz et al., 2010), and HMGCS2 exhibits prospective ketogenesis-independent �moonlighting� activities, including within the cell nucleus (Chen et al., 2016; Kostiuk et al., 2010; Meertens et al., 1998).

Any extrahepatic tissue that oxidizes ketone bodies also has the potential to accumulate ketone bodies via HMGCS2 independent mechanisms (Fig. 2A). However, there is no extrahepatic tissue in which a steady state ketone body concentration exceeds that in the circulation (Cotter et al., 2011; Cotter et al., 2013b; Harrison and Long, 1940), underscoring that ketone bodies are transported down a concentration gradient via MCT1/2-dependent mechanisms. One mechanism of apparent extrahepatic ketogenesis may actually reflect relative impairment of ketone oxidation. Additional potential explanations fall within the realm of ketone body formation. First, de novo ketogenesis may occur via reversible enzymatic activity of thiolase and SCOT (Weidemann and Krebs, 1969). When the concentration of acetyl-CoA is relatively high, reactions normally responsible for AcAc oxidation operate in the reverse direction (GOLDMAN, 1954). A second mechanism occurs when ?-oxidation-derived intermediates accumulate due to a TCA cycle bottleneck, AcAc-CoA is converted to l-?OHB-CoA through a reaction catalyzed by mitochondrial 3-hydroxyacyl-CoA dehydrogenase, and further by 3-hydroxybutyryl CoA deacylase to l-?OHB, which is indistinguishable by mass spectrometry or resonance spectroscopy from the physiological enantiomer d-?OHB (Reed and Ozand, 1980). l-?OHB can be chromatographically or enzymatically distinguished from d-?OHB, and is present in extrahepatic tissues, but not in liver or blood (Hsu et al., 2011). Hepatic ketogenesis produces only d-?OHB, the only enantiomer that is a BDH substrate (Ito et al., 1984; Lincoln et al., 1987; Reed and Ozand, 1980; Scofield et al., 1982; Scofield et al., 1982). A third HMGCS2-independent mechanism generates d-?OHB through amino acid catabolism, particularly that of leucine and lysine. A fourth mechanism is only apparent because it is due to a labeling artifact and is thus termed pseudoketogenesis. This phenomenon is attributable to the reversibility of the SCOT and thiolase reactions, and can cause overestimation of ketone body turnover due to the isotopic dilution of ketone body tracer in extrahepatic tissue (Des Rosiers et al., 1990; Fink et al., 1988). Nonetheless, pseudoketogenesis may be negligible in most contexts (Bailey et al., 1990; Keller et al., 1978). A schematic (Fig. 2A) indicates a useful approach to apply while considering elevated tissue steady state concentration of ketones.

� Kidney has recently received attention as a potentially ketogenic organ. In the vast majority of states, the kidney is a net consumer of liver-derived ketone bodies, excreting or reabsorbing ketone bodies from the bloodstream, and kidney is generally not a net ketone body generator or concentrator (Robinson and Williamson, 1980). The authors of a classical study concluded that minimal renal ketogenesis quantified in an artificial experimental system was not physiologically relevant (Weidemann and Krebs, 1969). Recently, renal ketogenesis has been inferred in diabetic and autophagy deficient mouse models, but it is more likely that multi-organ shifts in metabolic homeostasis alter integrative ketone metabolism through inputs on multiple organs (Takagi et al., 2016a; Takagi et al., 2016b; Zhang et al., 2011). One recent publication suggested renal ketogenesis as a protective mechanism against ischemia-reperfusion injury in the kidney (Tran et al., 2016). Absolute steady state concentrations of ?OHB from extracts of mice renal tissue were reported at ~4�12 mM. To test whether this was tenable, we quantified ?OHB concentrations in renal extracts from fed and 24h fasted mice. Serum ?OHB concentrations increased from ~100 �M to 2 mM with 24h fasting (Fig. 2B), while renal steady state ?OHB concentrations approximate 100 �M in the fed state, and only 1 mM in the 24h fasted state (Fig. 2C�E), observations that are consistent with concentrations quantified over 45 years ago (Hems and Brosnan, 1970). It remains possible that in ketotic states, liver-derived ketone bodies could be renoprotective, but evidence for renal ketogenesis requires further substantiation. Compelling evidence that supports true extrahepatic ketogenesis was presented in RPE (Adijanto et al., 2014). This intriguing metabolic transformation was suggested to potentially allow RPE-derived ketones to flow to photoreceptor or M�ller glia cells, which could aid in the regeneration of photoreceptor outer segment.

?OHB as a Signaling Mediator

Although they are energetically rich, ketone bodies exert provocative �non-canonical� signaling roles in cellular homeostasis (Fig. 3) (Newman and Verdin, 2014; Rojas-Morales et al., 2016). For example, ?OHB inhibits Class I HDACs, which increases histone acetylation and thereby induces the expression of genes that curtail oxidative stress (Shimazu et al., 2013). ?OHB itself is a histone covalent modifier at lysine residues in livers of fasted or streptozotocin induced diabetic mice (Xie et al., 2016) (also see below, The integration of ketone body metabolism, post-translational modification, and cell physiology, and Ketone bodies, oxidative stress, and neuroprotection).

?OHB is also an effector via G-protein coupled receptors. Through unclear molecular mechanisms, it suppresses sympathetic nervous system activity and reduces total energy expenditure and heart rate by inhibiting short chain fatty acid signaling through G protein coupled receptor 41 (GPR41) (Kimura et al., 2011). One of the most studied signaling effects of ?OHB proceeds through GPR109A (also known as HCAR2), a member of the hydrocarboxylic acid GPCR sub-family expressed in adipose tissues (white and brown) (Tunaru et al., 2003), and in immune cells (Ahmed et al., 2009). ?OHB is the only known endogenous ligand of GPR109A receptor (EC50 ~770 �M) activated by d-?OHB, l-?OHB, and butyrate, but not AcAc (Taggart et al., 2005). The high concentration threshold for GPR109A activation is achieved through adherence to a ketogenic diet, starvation, or during ketoacidosis, leading to inhibition of adipose tissue lipolysis. The anti-lipolytic effect of GPR109A proceeds through inhibition of adenylyl cyclase and decreased cAMP, inhibiting hormone sensitive triglyceride lipase (Ahmed et al., 2009; Tunaru et al., 2003). This creates a negative feedback loop in which ketosis places a modulatory brake on ketogenesis by diminishing the release of non-esterified fatty acids from adipocytes (Ahmed et al., 2009; Taggart et al., 2005), an effect that can be counterbalanced by the sympathetic drive that stimulates lipolysis. Niacin (vitamin B3, nicotinic acid) is a potent (EC50 ~ 0.1 �M) ligand for GRP109A, effectively employed for decades for dyslipidemias (Benyo et al., 2005; Benyo et al., 2006; Fabbrini et al., 2010a; Lukasova et al., 2011; Tunaru et al., 2003). While niacin enhances reverse cholesterol transport in macrophages and reduces atherosclerotic lesions (Lukasova et al., 2011), the effects of ?OHB on atherosclerotic lesions remain unknown. Although GPR109A receptor exerts protective roles, and intriguing connections exist between ketogenic diet use in stroke and neurodegenerative diseases (Fu et al., 2015; Rahman et al., 2014), a protective role of ?OHB via GPR109A has not been demonstrated in vivo.

Finally, ?OHB may influence appetite and satiety. A meta-analysis of studies that measured the effects of ketogenic and very low energy diets concluded that participants consuming these diets exhibit higher satiety, compared to control diets (Gibson et al., 2015). However, a plausible explanation for this effect is the additional metabolic or hormonal elements that might modulate appetite. For example, mice maintained on a rodent ketogenic diet exhibited increased energy expenditure compared to chow control-fed mice, despite similar caloric intake, and circulating leptin or genes of peptides regulating feeding behavior were not changed (Kennedy et al., 2007). Among proposed mechanisms that suggest appetite suppression by ?OHB includes both signaling and oxidation (Laeger et al., 2010). Hepatocyte specific deletion of circadian rhythm gene (Per2)�and chromatin immunoprecipitation studies revealed that PER2 directly activates the Cpt1a gene, and indirectly regulates Hmgcs2, leading to impaired ketosis in Per2 knockout mice (Chavan et al., 2016). These mice exhibited impaired food anticipation, which was partially restored by systemic ?OHB administration. Future studies will be needed to confirm the central nervous system as a direct ?OHB target, and whether ketone oxidation is required for the observed effects, or whether another signaling mechanism is involved. Other investigators have invoked the possibility of local astrocyte-derived ketogenesis within the ventromedial hypothalamus as a regulator of food intake, but these preliminary observations also will benefit from genetic and flux-based assessments (Le Foll et al., 2014). The relationship between ketosis and nutrient deprivation remains of interest because hunger and satiety are important elements in failed weight loss attempts.

Integration of Ketone Body Metabolism, Post-Translational Modification, and Cell Physiology

Ketone bodies contribute to compartmentalized pools of acetyl-CoA, a key intermediate that exhibits prominent roles in cellular metabolism (Pietrocola et al., 2015). One role of acetyl-CoA is to serve as a substrate for acetylation, an enzymatically-catalyzed histone covalent modification (Choudhary et al., 2014; Dutta et al., 2016; Fan et al., 2015; Menzies et al., 2016). A large number of dynamically acetylated mitochondrial proteins, many of which may occur through non-enzymatic mechanisms, have also emerged from computational proteomics studies (Dittenhafer-Reed et al., 2015; Hebert et al., 2013; Rardin et al., 2013; Shimazu et al., 2010). Lysine deacetylases use a zinc cofactor (e.g., nucleocytosolic HDACs) or NAD+ as co-substrate (sirtuins, SIRTs) (Choudhary et al., 2014; Menzies et al., 2016). The acetylproteome serves as both sensor and effector of the total cellular acetyl-CoA pool, as physiological and genetic manipulations each result in non-enzymatic global variations of acetylation (Weinert et al., 2014). As intracellular metabolites serve as modulators of lysine residue acetylation, it is important to consider the role of ketone bodies, whose abundance is highly dynamic.

?OHB is an epigenetic modifier through at least two mechanisms. Increased ?OHB levels induced by fasting, caloric restriction, direct administration or prolonged exercise provoke HDAC inhibition or histone acetyltransferase activation (Marosi et al., 2016; Sleiman et al., 2016) or to oxidative stress (Shimazu et al., 2013). ?OHB inhibition of HDAC3 could regulate newborn metabolic physiology (Rando et al., 2016). Independently, ?OHB itself directly modifies histone lysine residues (Xie et al., 2016). Prolonged fasting, or steptozotocin-induced diabetic ketoacidosis increased histone ?-hydroxybutyrylation. Although the number of lysine ?-hydroxybutyrylation and acetylation sites was comparable, stoichiometrically greater histone ?-hydroxybutyrylation than acetylation was observed. Distinct genes were impacted by histone lysine ?-hydroxybutyrylation, versus acetylation or methylation, suggesting distinct cellular functions. Whether ?-hydroxybutyrylation is spontaneous or enzymatic is not known, but expands the range of mechanisms through ketone bodies dynamically influence transcription.

Essential cell reprogramming events during caloric restriction and nutrient deprivation may be mediated in SIRT3- and SIRT5-dependent mitochondrial deacetylation and desuccinylation, respectively, regulating ketogenic and ketolytic proteins at post-translational level in liver and extrahepatic tissues (Dittenhafer-Reed et al., 2015; Hebert et al., 2013; Rardin et al., 2013; Shimazu et al., 2010). Even though stoichiometric comparison of occupied sites does not necessarily link directly to shifts in metabolic flux, mitochondrial acetylation is dynamic and may be driven by acetyl-CoA concentration or mitochondrial pH, rather than enzymatic acetyltransferases (Wagner and Payne, 2013). That SIRT3 and SIRT5 modulate activities of ketone body metabolizing enzymes provokes the question of the reciprocal role of ketones in sculpting the acetylproteome, succinylproteome, and other dynamic cellular targets. Indeed, as variations of ketogenesis reflect NAD+ concentrations, ketone production and abundance could regulate sirtuin activity, thereby influencing total acetyl-CoA/succinyl-CoA pools, the acylproteome, and thus mitochondrial and cell physiology. ?-hydroxybutyrylation of enzyme lysine residues could add another layer to cellular reprogramming. In extrahepatic tissues, ketone body oxidation may stimulate analogous changes in cell homeostasis. While compartmentation of acetyl-CoA pools is highly regulated and coordinates a broad spectrum of cellular changes, the ability of ketone bodies to directly shape both mitochondrial and cytoplasmic acetyl-CoA concentrations requires elucidation (Chen et al., 2012; Corbet et al., 2016; Pougovkina et al., 2014; Schwer et al., 2009; Wellen and Thompson, 2012). Because acetyl-CoA concentrations are tightly regulated, and acetyl-CoA is membrane impermeant, it is crucial to consider the driver mechanisms coordinating acetyl-CoA homeostasis, including the rates of production and terminal oxidation in the TCA cycle, conversion into ketone bodies, mitochondrial efflux via carnitine acetyltransferase (CrAT), or acetyl-CoA export to cytosol after conversion to citrate and release by ATP citrate lyase (ACLY). The key roles of these latter mechanisms in cell acetylproteome and homeostasis require matched understanding of the roles of ketogenesis and ketone oxidation (Das et al., 2015; McDonnell et al., 2016; Moussaieff et al., 2015; Overmyer et al., 2015; Seiler et al., 2014; Seiler et al., 2015; Wellen et al., 2009; Wellen and Thompson, 2012). Convergent technologies in metabolomics and acylproteomics in the setting of genetically manipulated models will be required to specify targets and outcomes.

Anti- and Pro-Inflammatory Responses to Ketone Bodies

Ketosis and ketone bodies modulate inflammation and immune cell function, but varied and even discrepant mechanisms have been proposed. Prolonged nutrient deprivation reduces inflammation (Youm et al., 2015), but the chronic ketosis of type 1 diabetes is a pro-inflammatory state (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kurepa et al., 2012). Mechanism-based signaling roles for ?OHB in inflammation emerge because many immune system cells, including macrophages or monocytes, abundantly express GPR109A. While ?OHB exerts a predominantly anti-inflammatory response (Fu et al., 2014; Gambhir et al., 2012; Rahman et al., 2014; Youm et al., 2015), high concentrations of ketone bodies, particularly AcAc, may trigger a pro-inflammatory response (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kurepa et al., 2012).

Anti-inflammatory roles of GPR109A ligands in atherosclerosis, obesity, inflammatory bowel disease, neurological disease, and cancer have been reviewed (Graff et al., 2016). GPR109A expression is augmented in RPE cells of diabetic models, human diabetic patients (Gambhir et al., 2012), and in microglia during neurodegeneration (Fu et al., 2014). Anti-inflammatory effects of ?OHB are enhanced by GPR109A overexpression in RPE cells, and abrogated by pharmacological inhibition or genetic knockout of GPR109A (Gambhir et al., 2012). ?OHB and exogenous nicotinic acid (Taggart et al., 2005), both confer anti-inflammatory effects in TNF? or LPS-induced inflammation by decreasing the levels of pro-inflammatory proteins (iNOS, COX-2), or secreted cytokines (TNF?, IL-1?, IL-6, CCL2/MCP-1), in part through inhibiting NF-?B translocation (Fu et al., 2014; Gambhir et al., 2012). ?OHB decreases ER stress and the NLRP3 inflammasome, activating the antioxidative stress response (Bae et al., 2016; Youm et al., 2015). However, in neurodegenerative inflammation, GPR109A-dependent ?OHB-mediated protection does not involve inflammatory mediators like MAPK pathway signaling (e.g., ERK, JNK, p38) (Fu et al., 2014), but may require COX-1-dependent PGD2 production (Rahman et al., 2014). It is intriguing that macrophage GPR109A is required to exert a neuroprotective effect in an ischemic stroke model (Rahman et al., 2014), but the ability of ?OHB to inhibit the NLRP3 inflammasome in bone marrow derived macrophages is GPR109A independent (Youm et al., 2015). Although most studies link ?OHB to anti-inflammatory effects, ?OHB may be pro-inflammatory and increase markers of lipid peroxidation in calf hepatocytes (Shi et al., 2014). Anti- versus pro-inflammatory effects of ?OHB may thus depend on cell type, ?OHB concentration, exposure duration, and the presence or absence of co-modulators.

Unlike ?OHB, AcAc may activate pro-inflammatory signaling. Elevated AcAc, especially with a high glucose concentration, intensifies endothelial cell injury through an NADPH oxidase/oxidative stress dependent mechanism (Kanikarla-Marie and Jain, 2015). High AcAc concentrations in umbilical cord of diabetic mothers were correlated with higher protein oxidation rate and MCP-1 concentration (Kurepa et al., 2012). High AcAc in diabetic patients was correlated with TNF? expression (Jain et al., 2002), and AcAc, but not ?OHB, induced TNF?, MCP-1 expression, ROS accumulation, and diminished cAMP level in U937 human monocyte cells (Jain et al., 2002; Kurepa et al., 2012).

Ketone body dependent signaling phenomena are frequently triggered only with high ketone body concentrations (> 5 mM), and in the case of many studies linking ketones to pro- or anti-inflammatory effects, through unclear mechanisms. In addition, due to the contradictory effects of ?OHB versus AcAc on inflammation, and the ability of AcAc/?OHB ratio to influence mitochondrial redox potential, the best experiments assessing the roles of ketone bodies on cellular phenotypes compare the effects of AcAc and ?OHB in varying ratios, and at varying cumulative concentrations [e.g., (Saito et al., 2016)]. Finally, AcAc can be purchased commercially only as a lithium salt or as an ethyl ester that requires base hydrolysis before use. Lithium cation independently induces signal transduction cascades (Manji et al., 1995), and AcAc anion is labile. Finally, studies using racemic d/l-?OHB can be confounded, as only the d-?OHB stereoisomer can be oxidized to AcAc, but d-?OHB and l-?OHB can each signal through GPR109A, inhibit the NLRP3 inflammasome, and serve as lipogenic substrates.

Ketone Bodies, Oxidative Stress, and Neuroprotection

Oxidative stress is typically defined as a state in which ROS are presented in excess, due to excessive production and/or impaired elimination. Antioxidant and oxidative stress mitigating roles of ketone bodies have been widely described both in vitro and in vivo, particularly in the context of neuroprotection. As most neurons do not effectively generate high-energy phosphates from fatty acids�but do oxidize ketone bodies when carbohydrates are in short supply, neuroprotective effects of ketone bodies are especially important (Cahill GF Jr, 2006; Edmond et al., 1987; Yang et al., 1987). In oxidative stress models, BDH1 induction and SCOT suppression suggest that ketone body metabolism can be reprogrammed to sustain diverse cell signaling, redox potential, or metabolic requirements (Nagao et al., 2016; Tieu et al., 2003).

Ketone bodies decrease the grades of cellular damage, injury, death and lower apoptosis in neurons and cardiomyocytes (Haces et al., 2008; Maalouf et al., 2007; Nagao et al., 2016; Tieu et al., 2003). Invoked mechanisms are varied and not always linearly related to concentration. Low millimolar concentrations of (d or l)-?OHB scavenge ROS (hydroxyl anion), while AcAc scavenges numerous ROS species, but only at concentrations that exceed the physiological range (IC50 20�67 mM) (Haces et al., 2008). Conversely, a beneficial influence over the electron transport chain�s redox potential is a mechanism commonly linked to d-?OHB. While all three ketone bodies (d/l-?OHB and AcAc) reduced neuronal cell death and ROS accumulation triggered by chemical inhibition of glycolysis, only d-?OHB and AcAc prevented neuronal ATP decline. Conversely, in a hypoglycemic in vivo model, (d or l)-?OHB, but not AcAc prevented hippocampal lipid peroxidation (Haces et al., 2008; Maalouf et al., 2007; Marosi et al., 2016; Murphy, 2009; Tieu et al., 2003). In vivo studies of mice fed a ketogenic diet (87% kcal fat and 13% protein) exhibited neuroanatomical variation of antioxidant capacity (Ziegler et al., 2003), where the most profound changes were observed in hippocampus, with increase glutathione peroxidase and total antioxidant capacities.

Ketogenic diet, ketone esters (also see Therapeutic use of ketogenic diet and exogenous ketone bodies), or ?OHB administration exert neuroprotection in models of ischemic stroke (Rahman et al., 2014); Parkinson�s disease (Tieu et al., 2003); central nervous system oxygen toxicity seizure (D’Agostino et al., 2013); epileptic spasms (Yum et al., 2015); mitochondrial encephalomyopathy, lactic acidosis and stroke-like (MELAS) episodes syndrome (Frey et al., 2016) and Alzheimer�s disease (Cunnane and Crawford, 2003; Yin et al., 2016). Conversely, a recent report demonstrated histopathological evidence of neurodegenerative progression by a ketogenic diet in a transgenic mouse model of abnormal mitochondrial DNA repair, despite increases in mitochondrial biogenesis and antioxidant signatures (Lauritzen et al., 2016). Other conflicting reports suggest that exposure to high ketone body concentrations elicits oxidative stress. High ?OHB or AcAc doses induced nitric oxide secretion, lipid peroxidation, reduced expression of SOD, glutathione peroxidase and catalase in calf hepatocytes, while in rat hepatocytes the MAPK pathway induction was attributed to AcAc but not ?OHB (Abdelmegeed et al., 2004; Shi et al., 2014; Shi et al., 2016).

Taken together, most reports link ?OHB to attenuation of oxidative stress, as its administration inhibits ROS/superoxide production, prevents lipid peroxidation and protein oxidation, increases antioxidant protein levels, and improves mitochondrial respiration and ATP production (Abdelmegeed et al., 2004; Haces et al., 2008; Jain et al., 1998; Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Maalouf et al., 2007; Maalouf and Rho, 2008; Marosi et al., 2016; Tieu et al., 2003; Yin et al., 2016; Ziegler et al., 2003). While AcAc has been more directly correlated than ?OHB with the induction of oxidative stress, these effects are not always easily dissected from prospective pro-inflammatory responses (Jain et al., 2002; Kanikarla-Marie and Jain, 2015; Kanikarla-Marie and Jain, 2016). Moreover, it is critical to consider that the apparent antioxidative benefit conferred by pleiotropic ketogenic diets may not be transduced by ketone bodies themselves, and neuroprotection conferred by ketone bodies may not entirely be attributable to oxidative stress. For example during glucose deprivation, in a model of glucose deprivation in cortical neurons, ?OHB stimulated autophagic flux and prevented autophagosome accumulation, which was associated with decreased neuronal death (Camberos-Luna et al., 2016). d-?OHB induces also the canonical antioxidant proteins FOXO3a, SOD, MnSOD, and catalase, prospectively through HDAC inhibition (Nagao et al., 2016; Shimazu et al., 2013).

Non-Alcoholic Fatty Liver Disease (NAFLD) and Ketone Body Metabolism

Obesity-associated NAFLD and nonalcoholic steatohepatitis (NASH) are the most common causes of liver disease in Western countries (Rinella and Sanyal, 2016), and NASH-induced liver failure is one of the most common reasons for liver transplantation. While excess storage of triacylglycerols in hepatocytes >5% of liver weight (NAFL) alone does not cause degenerative liver function, the progression to NAFLD in humans correlates with systemic insulin resistance and increased risk of type 2 diabetes, and may contribute to the pathogenesis of cardiovascular disease and chronic kidney disease (Fabbrini et al., 2009; Targher et al., 2010; Targher and Byrne, 2013). The pathogenic mechanisms of NAFLD and NASH are incompletely understood but include abnormalities of hepatocyte metabolism, hepatocyte autophagy and endoplasmic reticulum stress, hepatic immune cell function, adipose tissue inflammation, and systemic inflammatory mediators (Fabbrini et al., 2009; Masuoka and Chalasani, 2013; Targher et al., 2010; Yang et al., 2010). Perturbations of carbohydrate, lipid, and amino acid metabolism occur in and contribute to obesity, diabetes, and NAFLD in humans and in model organisms [reviewed in (Farese et al., 2012; Lin and Accili, 2011; Newgard, 2012; Samuel and Shulman, 2012; Sun and Lazar, 2013)]. While hepatocyte abnormalities in cytoplasmic lipid metabolism are commonly observed in NAFLD (Fabbrini et al., 2010b), the role of mitochondrial metabolism, which governs oxidative disposal of fats is less clear in NAFLD pathogenesis. Abnormalities of mitochondrial metabolism occur in and contribute to NAFLD/NASH pathogenesis (Hyotylainen et al., 2016; Serviddio et al., 2011; Serviddio et al., 2008; Wei et al., 2008). There is general (Felig et al., 1974; Iozzo et al., 2010; Koliaki et al., 2015; Satapati et al., 2015; Satapati et al., 2012; Sunny et al., 2011) but not uniform (Koliaki and Roden, 2013; Perry et al., 2016; Rector et al., 2010) consensus that, prior to the development of bona fide NASH, hepatic mitochondrial oxidation, and in particular fat oxidation, is augmented in obesity, systemic insulin resistance, and NAFLD. It is likely that as NAFLD progresses, oxidative capacity heterogenity, even among individual mitochondria, emerges, and ultimately oxidative function becomes impaired (Koliaki et al., 2015; Rector et al., 2010; Satapati et al., 2008; Satapati et al., 2012).

Ketogenesis is often used as a proxy for hepatic fat oxidation. Impairments of ketogenesis emerge as NAFLD progresses in animal models, and likely in humans. Through incompletely defined mechanisms, hyperinsulinemia suppresses ketogenesis, possibly contributing to hypoketonemia compared to lean controls (Bergman et al., 2007; Bickerton et al., 2008; Satapati et al., 2012; Soeters et al., 2009; Sunny et al., 2011; Vice et al., 2005). Nonetheless, the ability of circulating ketone body concentrations to predict NAFLD is controversial (M�nnist� et al., 2015; Sanyal et al., 2001). Robust quantitative magnetic resonance spectroscopic methods in animal models revealed increased ketone turnover rate with moderate insulin resistance, but decreased rates were evident with more severe insulin resistance (Satapati et al., 2012; Sunny et al., 2010). In obese humans with fatty liver, ketogenic rate is normal (Bickerton et al., 2008; Sunny et al., 2011), and hence, the rates of ketogenesis are diminished relative to the increased fatty acid load within hepatocytes. Consequently, ?-oxidation-derived acetyl-CoA may be directed to terminal oxidation in the TCA cycle, increasing terminal oxidation, phosphoenolpyruvate-driven gluconeogenesis via anaplerosis/cataplerosis, and oxidative stress. Acetyl-CoA also possibly undergoes export from mitochondria as citrate, a precursor substrate for lipogenesis (Fig. 4) (Satapati et al., 2015; Satapati et al., 2012; Solinas et al., 2015). While ketogenesis becomes less responsive to insulin or fasting with prolonged obesity (Satapati et al., 2012), the underlying mechanisms and downstream consequences of this remain incompletely understood. Recent evidence indicates that mTORC1 suppresses ketogenesis in a manner that may be downstream of insulin signaling (Kucejova et al., 2016), which is concordant with the observations that mTORC1 inhibits PPAR?-mediated Hmgcs2 induction (Sengupta et al., 2010) (also see Regulation of HMGCS2 and SCOT/OXCT1).

Preliminary observations from our group suggest adverse hepatic consequences of ketogenic insufficiency (Cotter et al., 2014). To test the hypothesis that impaired ketogenesis, even in carbohydrate-replete and thus �non-ketogenic� states, contributes to abnormal glucose metabolism and provokes steatohepatitis, we generated a mouse model of marked ketogenic insufficiency by administration of antisense oligonucleotides (ASO) targeted to Hmgcs2. Loss of HMGCS2 in standard low-fat chow-fed adult mice caused mild hyperglycemia and markedly increased production of hundreds of hepatic metabolites, a suite of which strongly suggested lipogenesis activation. High-fat diet feeding of mice with insufficient ketogenesis resulted in extensive hepatocyte injury and inflammation. These findings support the central hypotheses that (i) ketogenesis is not a passive overflow pathway but rather a dynamic node in hepatic and integrated physiological homeostasis, and (ii) prudent ketogenic augmentation to mitigate NAFLD/NASH and disordered hepatic glucose metabolism is worthy of exploration.

How might impaired ketogenesis contribute to hepatic injury and altered glucose homeostasis? The first consideration is whether the culprit is deficiency of ketogenic flux, or ketones themselves. A recent report suggests that ketone bodies may mitigate oxidative stress-induced hepatic injury in response to n-3 polyunsaturated fatty acids (Pawlak et al., 2015). Recall that due to lack of SCOT expression in hepatocytes, ketone bodies are not oxidized, but they can contribute to lipogenesis, and serve a variety of signaling roles independent of their oxidation (also see Non-oxidative metabolic fates of ketone bodies and ?OHB as a signaling mediator). It is also possible that hepatocyte-derived ketone bodies may serve as a signal and/or metabolite for neighboring cell types within the hepatic acinus, including stellate cells and Kupffer cell macrophages. While the limited literature available suggests that macrophages are unable to oxidize ketone bodies, this has only been measured using classical methodologies, and only in peritoneal macrophages (Newsholme et al., 1986; Newsholme et al., 1987), indicating that a re-assessment is appropriate given abundant SCOT expression in bone marrow-derived macrophages (Youm et al., 2015).

Hepatocyte ketogenic flux may also be cytoprotective. While salutary mechanisms may not depend on ketogenesis per se, low carbohydrate ketogenic diets have been associated with amelioration of NAFLD (Browning et al., 2011; Foster et al., 2010; Kani et al., 2014; Schugar and Crawford, 2012). Our observations indicate that hepatocyte ketogenesis may feedback and regulate TCA cycle flux, anaplerotic flux, phosphoenolpyruvate-derived gluconeogenesis (Cotter et al., 2014), and even glycogen turnover. Ketogenic impairment directs acetyl-CoA to increase TCA flux, which in liver has been linked to increased ROS-mediated injury (Satapati et al., 2015; Satapati et al., 2012); forces diversion of carbon into de novo synthesized lipid species that could prove cytotoxic; and prevents NADH re-oxidation to NAD+ (Cotter et al., 2014) (Fig. 4). Taken together, future experiments are required to address mechanisms through which relative ketogenic insufficiency may become maladaptive, contribute to hyperglycemia, provoke steatohepatitis, and whether these mechanisms are operant in human NAFLD/NASH. As epidemiological evidence suggests impaired ketogenesis during the progression of steatohepatitis (Embade et al., 2016; Marinou et al., 2011; M�nnist� et al., 2015; Pramfalk et al., 2015; Safaei et al., 2016) therapies that increase hepatic ketogenesis could prove salutary (Degirolamo et al., 2016; Honda et al., 2016).

Ketone Bodies and Heart Failure (HF)

With a metabolic rate exceeding 400 kcal/kg/day, and a turnover of 6�35 kg ATP/day, the heart is the organ with the highest energy expenditure and oxidative demand (Ashrafian et al., 2007; Wang et al., 2010b). The vast majority of myocardial energy turnover resides within mitochondria, and 70% of this supply originates from FAO. The heart is omnivorous and flexible under normal conditions, but the pathologically remodeling heart (e.g., due to hypertension or myocardial infarction) and the diabetic heart each become metabolically inflexible (Balasse and Fery, 1989; BING, 1954; Fukao et al., 2004; Lopaschuk et al., 2010; Taegtmeyer et al., 1980; Taegtmeyer et al., 2002; Young et al., 2002). Indeed, genetically programmed abnormalities of cardiac fuel metabolism in mouse models provoke cardiomyopathy (Carley et al., 2014; Neubauer, 2007). Under physiological conditions normal hearts oxidize ketone bodies in proportion to their delivery, at the expense of fatty acid and glucose oxidation, and myocardium is the highest ketone body consumer per unit mass (BING, 1954; Crawford et al., 2009; GARLAND et al., 1962; Hasselbaink et al., 2003; Jeffrey et al., 1995; Pelletier et al., 2007; Tardif et al., 2001; Yan et al., 2009). Compared to fatty acid oxidation, ketone bodies are more energetically efficient, yielding more energy available for ATP synthesis per molecule of oxygen invested (P/O ratio) (Kashiwaya et al., 2010; Sato et al., 1995; Veech, 2004). Ketone body oxidation also yields potentially higher energy than FAO, keeping ubiquinone oxidized, which raises redox span in the electron transport chain and makes more energy available to synthetize ATP (Sato et al., 1995; Veech, 2004). Oxidation of ketone bodies may also curtail ROS production, and thus oxidative stress (Veech, 2004).

Preliminary interventional and observational studies indicate a potential salutary role of ketone bodies in the heart. In the experimental ischemia/reperfusion injury context, ketone bodies conferred potential cardioprotective effects (Al-Zaid et al., 2007; Wang et al., 2008), possibly due to the increase mitochondrial abundance in heart or up-regulation of crucial oxidative phosphorylation mediators (Snorek et al., 2012; Zou et al., 2002). Recent studies indicate that ketone body utilization is increased in failing hearts of mice (Aubert et al., 2016) and humans (Bedi et al., 2016), supporting prior observations in humans (BING, 1954; Fukao et al., 2000; Janardhan et al., 2011; Longo et al., 2004; Rudolph and Schinz, 1973; Tildon and Cornblath, 1972). Circulating ketone body concentrations are increased in heart failure patients, in direct proportion to filling pressures, observations whose mechanism and significance remains unknown (Kupari et al., 1995; Lommi et al., 1996; Lommi et al., 1997; Neely et al., 1972), but mice with selective SCOT deficiency in cardiomyocytes exhibit accelerated pathological ventricular remodeling and ROS signatures in response to surgically induced pressure overload injury (Schugar et al., 2014).

Recent intriguing observations in diabetes therapy have revealed a potential link between myocardial ketone metabolism and pathological ventricular remodeling (Fig. 5). Inhibition of the renal proximal tubular sodium/glucose co-transporter 2 (SGLT2i) increases circulating ketone body concentrations in humans (Ferrannini et al., 2016a; Inagaki et al., 2015) and mice (Suzuki et al., 2014) via increased hepatic ketogenesis (Ferrannini et al., 2014; Ferrannini et al., 2016a; Katz and Leiter, 2015; Mudaliar et al., 2015). Strikingly, at least one of these agents decreased HF hospitalization (e.g., as revealed by the EMPA-REG OUTCOME trial), and improved cardiovascular mortality (Fitchett et al., 2016; Sonesson et al., 2016; Wu et al., 2016a; Zinman et al., 2015). While the driver mechanisms behind beneficial HF outcomes to linked SGLT2i remain actively debated, the survival benefit is likely multifactorial, prospectively including ketosis but also salutary effects on weight, blood pressure, glucose and uric acid levels, arterial stiffness, the sympathetic nervous system, osmotic diuresis/reduced plasma volume, and increased hematocrit (Raz and Cahn, 2016; Vallon and Thomson, 2016). Taken together, the notion that therapeutically increasing ketonemia either in HF patients, or those at high risk to develop HF, remains controversial but is under active investigation in pre-clinical and clinical studies (Ferrannini et al., 2016b; Kolwicz et al., 2016; Lopaschuk and Verma, 2016; Mudaliar et al., 2016; Taegtmeyer, 2016).

Ketone Bodies in Cancer Biology

Connections between ketone bodies and cancer are rapidly emerging, but studies in both animal models and humans have yielded diverse conclusions. Because ketone metabolism is dynamic and nutrient state responsive, it is enticing to pursue biological connections to cancer because of the potential for precision-guided nutritional therapies. Cancer cells undergo metabolic reprogramming in order to maintain rapid cell proliferation and growth (DeNicola and Cantley, 2015; Pavlova and Thompson, 2016). The classical Warburg effect in cancer cell metabolism arises from the dominant role of glycolysis and lactic acid fermentation to transfer energy and compensate for lower dependence on oxidative phosphorylation and limited mitochondrial respiration (De Feyter et al., 2016; Grabacka et al., 2016; Kang et al., 2015; Poff et al., 2014; Shukla et al., 2014). Glucose carbon is primarily directed through glycolysis, the pentose phosphate pathway, and lipogenesis, which together provide intermediates necessary for tumor biomass expansion (Grabacka et al., 2016; Shukla et al., 2014; Yoshii et al., 2015). Adaptation of cancer cells to glucose deprivation occurs through the ability to exploit alternative fuel sources, including acetate, glutamine, and aspartate (Jaworski et al., 2016; Sullivan et al., 2015). For example, restricted access to pyruvate reveals the ability of cancer cells to convert glutamine into acetyl-CoA by carboxylation, maintaining both energetic and anabolic needs (Yang et al., 2014). An interesting adaptation of cancer cells is the utilization of acetate as a fuel (Comerford et al., 2014; Jaworski et al., 2016; Mashimo et al., 2014; Wright and Simone, 2016; Yoshii et al., 2015). Acetate is also a substrate for lipogenesis, which is critical for tumor cell proliferation, and gain of this lipogenic conduit is associated with shorter patient survival and greater tumor burden (Comerford et al., 2014; Mashimo et al., 2014; Yoshii et al., 2015).

Non-cancer cells easily shift their energy source from glucose to ketone bodies during glucose deprivation. This plasticity may be more variable among cancer cell types, but in vivo implanted brain tumors oxidized [2,4-13C2]-?OHB to a similar degree as surrounding brain tissue (De Feyter et al., 2016). �Reverse Warburg effect� or �two compartment tumor metabolism� models hypothesize that cancer cells induce ?OHB production in adjacent fibroblasts, furnishing the tumor cell�s energy needs (Bonuccelli et al., 2010; Martinez-Outschoorn et al., 2012). In liver, a shift in hepatocytes from ketogenesis to ketone oxidation in hepatocellular carcinoma (hepatoma) cells is consistent with activation of BDH1 and SCOT activities observed in two hepatoma cell lines (Zhang et al., 1989). Indeed, hepatoma cells express OXCT1 and BDH1 and oxidize ketones, but only when serum starved (Huang et al., 2016). Alternatively, tumor cell ketogenesis has also been proposed. Dynamic shifts in ketogenic gene expression are exhibited during cancerous transformation of colonic epithelium, a cell type that normally expresses HMGCS2, and a recent report suggested that HMGCS2 may be a prognostic marker of poor prognosis in colorectal and squamous cell carcinomas (Camarero et al., 2006; Chen et al., 2016). Whether this association requires or involves ketogenesis, or a moonlighting function of HMGCS2, remains to be determined. Conversely, apparent ?OHB production by melanoma and glioblastoma cells, stimulated by the PPAR? agonist fenofibrate, was associated with growth arrest (Grabacka et al., 2016). Further studies are required to characterize roles of HMGCS2/SCOT expression, ketogenesis, and ketone oxidation in cancer cells.

Beyond the realm of fuel metabolism, ketones have recently been implicated in cancer cell biology via a signaling mechanism. Analysis of BRAF-V600E+ melanoma indicated OCT1-dependent induction of HMGCL in an oncogenic BRAF-dependent manner (Kang et al., 2015). HMGCL augmentation was correlated with higher cellular AcAc concentration, which in turn enhanced BRAFV600E-MEK1 interaction, amplifying MEK-ERK signaling in a feed-forward loop that drives tumor cell proliferation and growth. These observations raise the intriguing question of prospective extrahepatic ketogenesis that then supports a signaling mechanism (also see ?OHB as a signaling mediator and Controversies in extrahepatic ketogenesis). It is also important to consider independent effects of AcAc, d-?OHB, and l-?OHB on cancer metabolism, and when considering HMGCL, leucine catabolism may also be deranged.

The effects of ketogenic diets (also see Therapeutic use of ketogenic diet and exogenous ketone bodies) in cancer animal models are varied (De Feyter et al., 2016; Klement et al., 2016; Meidenbauer et al., 2015; Poff et al., 2014; Seyfried et al., 2011; Shukla et al., 2014). While epidemiological associations among obesity, cancer, and ketogenic diets are debated (Liskiewicz et al., 2016; Wright and Simone, 2016), a meta-analysis using ketogenic diets in animal models and in human studies suggested a salutary impact on survival, with benefits prospectively linked to the magnitude of ketosis, time of diet initiation, and tumor location (Klement et al., 2016; Woolf et al., 2016). Treatment of pancreatic cancer cells with ketone bodies (d-?OHB or AcAc) inhibited growth, proliferation and glycolysis, and a ketogenic diet (81% kcal fat, 18% protein, 1% carbohydrate) reduced in vivo tumor weight, glycemia, and increased muscle and body weight in animals with implanted cancer (Shukla et al., 2014). Similar results were observed using a metastatic glioblastoma cell model in mice that received ketone supplementation in the diet (Poff et al., 2014). Conversely, a ketogenic diet (91% kcal fat, 9% protein) increased circulating ?OHB concentration and diminished glycemia�but had no impact on either tumor volume or survival duration in glioma-bearing rats (De Feyter et al., 2016). A glucose ketone index has been proposed as a clinical indicator that improves metabolic management of ketogenic diet-induced brain cancer therapy in humans and mice (Meidenbauer et al., 2015). Taken together, roles of ketone body metabolism and ketone bodies in cancer biology are tantalizing because they each pose tractable therapeutic options, but fundamental aspects remain to be elucidated, with clear influences emerging from a matrix of variables, including (i) differences between exogenous ketone bodies versus ketogenic diet, (ii) cancer cell type, genomic polymorphisms, grade, and stage; and (iii) timing and duration of exposure to the ketotic state.

Dr Jimenez White Coat
Ketogenesis is created by ketone bodies through the breakdown of fatty acids and ketogenic amino acids. This biochemical process provides energy to various organs, specifically the brain, under circumstances of fasting as a response to an unavailability of blood glucose. Ketone bodies are mainly produced in the mitochondria of liver cells. While other cells are capable of carrying out ketogenesis, they are not as effective at doing so as liver cells. Because ketogenesis occurs in the mitochondria, its processes are regulated independently. Dr. Alex Jimenez D.C., C.C.S.T. Insight

Therapeutic Application of Ketogenic Diet and Exogenous Ketone Bodies

The applications of ketogenic diets and ketone bodies as therapeutic tools have also arisen in non-cancerous contexts including obesity and NAFLD/NASH (Browning et al., 2011; Foster et al., 2010; Schugar and Crawford, 2012); heart failure (Huynh, 2016; Kolwicz et al., 2016; Taegtmeyer, 2016); neurological and neurodegenerative disease (Martin et al., 2016; McNally and Hartman, 2012; Rho, 2015; Rogawski et al., 2016; Yang and Cheng, 2010; Yao et al., 2011); inborn errors of metabolism (Scholl-B�rgi et al, 2015); and exercise performance (Cox et al., 2016). The efficacy of ketogenic diets has been especially appreciated in therapy of epileptic seizure, particularly in drug-resistant patients. Most studies have evaluated ketogenic diets in pediatric patients, and reveal up to a ~50% reduction in seizure frequency after 3 months, with improved effectiveness in select syndromes (Wu et al., 2016b). The experience is more limited in adult epilepsy, but a similar reduction is evident, with better response in symptomatic generalized epilepsy patients (Nei et al., 2014). Underlying anti-convulsant mechanisms remain unclear, although postulated hypotheses include reduced glucose utilization/glycolysis, reprogrammed glutamate transport, indirect impact on ATP-sensitive potassium channel or adenosine A1 receptor, alteration of sodium channel isoform expression, or effects on circulating hormones including leptin (Lambrechts et al., 2016; Lin et al., 2017; Lutas and Yellen, 2013). It remains unclear whether the anti-convulsant effect is primarily attributable to ketone bodies, or due to the cascade metabolic consequences of low carbohydrate diets. Nonetheless, ketone esters (see below) appear to elevate the seizure threshold in animal models of provoked seizures (Ciarlone et al., 2016; D’Agostino et al., 2013; Viggiano et al., 2015).

Atkins-style and ketogenic, low carbohydrate diets are often deemed unpleasant, and can cause constipation, hyperuricemia, hypocalcemia, hypomagnesemia, lead to nephrolithiasis, ketoacidosis, cause hyperglycemia, and raise circulating cholesterol and free fatty acid concentrations (Bisschop et al., 2001; Kossoff and Hartman, 2012; Kwiterovich et al., 2003; Suzuki et al., 2002). For these reasons, long-term adherence poses challenges. Rodent studies commonly use a distinctive macronutrient distribution (94% kcal fat, 1% kcal carbohydrate, 5% kcal protein, Bio-Serv F3666), which provokes a robust ketosis. However, increasing the protein content, even to 10% kcal substantially diminishes the ketosis, and 5% kcal protein restriction confers confounding metabolic and physiological effects. This diet formulation is also choline depleted, another variable that influences susceptibility to liver injury, and even ketogenesis (Garbow et al., 2011; Jornayvaz et al., 2010; Kennedy et al., 2007; Pissios et al., 2013; Schugar et al., 2013). Effects of long-term consumption of ketogenic diets in mice remain incompletely defined, but recent studies in mice revealed normal survival and the absence of liver injury markers in mice on ketogenic diets over their lifespan, although amino acid metabolism, energy expenditure, and insulin signaling were markedly reprogrammed (Douris et al., 2015).

Mechanisms increasing ketosis through mechanisms alternative to ketogenic diets include the use of ingestible ketone body precursors. Administration of exogenous ketone bodies could create a unique physiological state not encountered in normal physiology, because circulating glucose and insulin concentrations are relatively normal, while cells might spare glucose uptake and utilization. Ketone bodies themselves have short half-lives, and ingestion or infusion of sodium ?OHB salt to achieve therapeutic ketosis provokes an untoward sodium load. R/S-1,3-butanediol is a non-toxic dialcohol that is readily oxidized in the liver to yield d/l-?OHB (Desrochers et al., 1992). In distinct experimental contexts, this dose has been administered daily to mice or rats for as long as seven weeks, yielding circulating ?OHB concentrations of up to 5 mM within 2 h of administration, which is stable for at least an additional 3h (D’Agostino et al., 2013). Partial suppression of food intake has been observed in rodents given R/S-1,3-butanediol (Carpenter and Grossman, 1983). In addition, three chemically distinct ketone esters (KEs), (i) monoester of R-1,3-butanediol and d-?OHB (R-3-hydroxybutyl R-?OHB); (ii) glyceryl-tris-?OHB; and (iii) R,S-1,3-butanediol acetoacetate diester, have also been extensively studied (Brunengraber, 1997; Clarke et al., 2012a; Clarke et al., 2012b; Desrochers et al., 1995a; Desrochers et al., 1995b; Kashiwaya et al., 2010). An inherent advantage of the former is that 2 moles of physiological d-?OHB are produced per mole of KE, following esterase hydrolysis in the intestine or liver. Safety, pharmacokinetics, and tolerance have been most extensively studied in humans ingesting R-3-hydroxybutyl R-?OHB, at doses up to 714 mg/kg, yielding circulating d-?OHB concentrations up to 6 mM (Clarke et al., 2012a; Cox et al., 2016; Kemper et al., 2015; Shivva et al., 2016). In rodents, this KE decreases caloric intake and plasma total cholesterol, stimulates brown adipose tissue, and improves insulin resistance (Kashiwaya et al., 2010; Kemper et al., 2015; Veech, 2013). Recent findings indicate that during exercise in trained athletes, R-3-hydroxybutyl R-?OHB ingestion decreased skeletal muscle glycolysis and plasma lactate concentrations, increased intramuscular triacylglycerol oxidation, and preserved muscle glycogen content, even when co-ingested carbohydrate stimulated insulin secretion (Cox et al., 2016). Further development of these intriguing results is required, because the improvement in endurance exercise performance was predominantly driven by a robust response to the KE in 2/8 subjects. Nonetheless, these results do support classical studies that indicate a preference for ketone oxidation over other substrates (GARLAND et al., 1962; Hasselbaink et al., 2003; Stanley et al., 2003; Valente-Silva et al., 2015), including during exercise, and that trained athletes may be more primed to utilize ketones (Johnson et al., 1969a; Johnson and Walton, 1972; Winder et al., 1974; Winder et al., 1975). Finally, the mechanisms that might support improved exercise performance following equal caloric intake (differentially distributed among macronutrients) and equal oxygen consumption rates remain to be determined. Clues may emerge from animal studies, as temporary exposure to R-3-hydroxybutyl R-?OHB in rats was associated with increased treadmill time, improved cognitive function, and an apparent energetic benefit in ex vivo perfused hearts (Murray et al., 2016).

Future Perspective

Once largely stigmatized as an overflow pathway capable of accumulating toxic emissions from fat combustion in carbohydrate restricted states (the �ketotoxic� paradigm), recent observations support the notion that ketone body metabolism serves salutary roles even in carbohydrate-laden states, opening a �ketohormetic� hypothesis. While the facile nutritional and pharmacological approaches to manipulate ketone metabolism make it an attractive therapeutic target, aggressively posed but prudent experiments remain in both the basic and translational research laboratories. Unmet needs have emerged in the domains of defining the role of leveraging ketone metabolism in heart failure, obesity, NAFLD/NASH, type 2 diabetes, and cancer. The scope and impact of ‘non-canonical� signaling roles of ketone bodies, including regulation of PTMs that likely feed back and forward into metabolic and signaling pathways, require deeper exploration. Finally, extrahepatic ketogenesis could open intriguing paracrine and autocrine signaling mechanisms and opportunities to influence co-metabolism within the nervous system and tumors to achieve therapeutic ends.

Acknowledgments

Ncbi.nlm.nih.gov/pmc/articles/PMC5313038/

Footnotes

Ncbi.nlm.nih.gov

In conclusion, ketone bodies are created by the liver in order to be used as an energy source when there is not enough glucose readily available in the human body. Ketogenesis occurs when there are low glucose levels in the blood, particularly after other cellular carbohydrate stores have been exhausted. The purpose of the article above was to discuss the multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

Referenced from:�Ncbi.nlm.nih.gov/pmc/articles/PMC5313038/

Green Call Now Button H .png

Additional Topic Discussion:�Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain attributes to the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief. �

blog picture of cartoon paper boy

EXTRA EXTRA | IMPORTANT TOPIC: Recommended El Paso, TX Chiropractor

***