Back Clinic Treatments. There are various treatments for all types of injuries and conditions here at Injury Medical & Chiropractic Clinic. The main goal is to correct any misalignments in the spine through manual manipulation and placing misaligned vertebrae back in their proper place. Patients will be given a series of treatments, which are based on the diagnosis. This can include spinal manipulation, as well as other supportive treatments. And as chiropractic treatment has developed, so have its methods and techniques.
Why do chiropractors use one method/technique over another?
A common method of spinal adjustment is the toggle drop method. With this method, a chiropractor crosses their hands and pressed down firmly on an area of the spine. They will then adjust the area with a quick and precise thrust. This method has been used for years and is often used to help increase a patient’s mobility.
Another popular method takes place on a special drop table. The table has different sections, which can be moved up or down based on the body’s position. Patients lie face down on their back or side while the chiropractor applies quick thrusts throughout the spinal area as the table section drops. Many prefer this table adjustment, as this method is lighter and does not include twisting motions used in other methods.
Chiropractors also use specialized tools to assist in their adjustments, i.e., the activator. A chiropractor uses this spring-loaded tool to perform the adjustment/s instead of their hands. Many consider the activator method to be the most gentle of all.
Whichever adjustment method a chiropractor uses, they all offer great benefits to the spine and overall health and wellness. If there is a certain method that is preferred, talk to a chiropractor about it. If they do not perform a certain technique, they may recommend a colleague that does.
Dr. Jimenez, D.C., presents how to implement exercise as part of your daily routine. Many factors and lifestyle habits tend to take over our daily lives, and in this 2-part series, we will look at how to implement exercise in a clinical setting. Part 2 will continue the presentation. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with Lyme disease. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
How To Implement Strategies?
Dr. Alex Jimenez, D.C., presents: Today we will discuss how to implement strategies using exercise as a prescription. Remember, just like we talked about how a healthy diet full of nutritious, whole foods can be used as a prescription, we want this science to make it to the patient and create outcomes because otherwise, this is just a bunch of things you know and not something that you know how to put into practice. So we’ve listened; we know that’s what you’re up to, so let’s get started. We will discuss some general aspects of implementing exercise as a prescription and some ideas we use in our practice. And then, of course, share the brilliant ideas with some of the other colleagues who also are figuring out ways to make this work in their practice. The first thing we want to share with you is when you’re approaching a patient with an exercise prescription, assuming the patient’s interested, you should ascertain first how this person is motivated.
Because it always makes sense to ride their motivation wave than to come from the standpoint that this is what I want from you, and this is why you need to do it. The first thing we want to put out there is that you want to ensure that this patient has a reason to want to exercise. So it’s less about a doctor’s orders or a provider’s recommendation, and you want to partner with our patients therapeutically, which means understanding their motivation. So for most people, there are two ways we can reinforce the outcome of a positive implementation of the exercise. First, we want to optimize those factors related to one-on-one communication with our patients. And then, number two, optimize the environment in our practice for success. Okay, so we’ll go over these things in detail now.
It only sometimes works if we give them a prescription and assume they want to do it. So if Joan Rivers was your patient in the past, this might have been her reason for not wanting to exercise, and you must be able to roll with it. Let’s talk about how we can do that. This works with patients, spouses, and children; it is wise to persuade people to do things and make them think it is their idea. So, with much bigger goals in mind, Nelson Mandela used the same principle. So we want you to think about who you are working with and who you are partnering with; these are some common functional medicine personas that you may come across, especially if you’re in more of a private practice, whether it’s cash or membership type of practice, you might see this persona in people.
Look For The Personas
Dr. Alex Jimenez, D.C., presents: Are these all personas the same? Not necessarily, as people have different reasons to exercise. For example, say you have a chronically ill individual who needs their hands to be held or have individuals who read many fitness magazines following these leaders through a whole lifestyle lens. And the way you engage with each of these personas is based on their goal for exercise. So, the unwell individual may have different goals, challenges, or limitations than the lifestyle lens individual. So make sure you know who you are working with, and if you need more clarification, have a conversation with them to find out.
Let’s say you’ve gotten through that step, and now you’re in the actual conversation of, “Hey, let’s figure out how to get this exercise thing to create benefits in your life.” As you’re having the conversation, you might learn to use some aspects of motivational interviewing. So rolling with resistance, for example, sometimes people say, “Nope, I don’t want to exercise.” So in this example, you might say, “Okay, if you don’t want to exercise at a gym, what other options have you heard of that you might want to consider?” Let’s say that’s how you opened it up and remember that there’s always a way to roll with the resistance, and it’s focused on acknowledging the patient’s input. You’re responding to them by saying, “Okay, fine. You don’t want to work at a gym. I get that,” while expressing empathy. Many individuals have tried to work at a gym, and the machines tend to injure them when used incorrectly, intimidate them, or the equipment is not made for their size structure.
Emphasize With Your Patients
Dr. Alex Jimenez, D.C., presents: Many people want to avoid exercising; this is one of the many frustrating things because you feel the equipment needs to be made for you. So notice that you can empathize without judging and then roll with resistance and ensure they understand that you acknowledge their input about the situation. These things are common sense to you. Many of us may not employ these to the fullest potential to motivate our patients to implement exercise as part of their daily routines. The important and obvious thing is to refrain from arguing with your patient. Because all that will go to create for most people is more resistance, so if they say, “Hey, I don’t want to exercise right now,” you can say, “Would you be willing to talk about exercising as a goal in the future?”
And if they say, “Yeah, I need to make it through December,” you can reply with, “Okay, great, let’s have you follow up with me in January. Does that work for you?” So again, avoiding arguing and expressing empathy can put people’s minds at ease and prevent resistance. Another factor that many people often do when it comes to implementing exercise as part of their routine is by developing discrepancy. So sometimes, people say things that conflict with the daily habits that they already follow. So they might say, “Yeah, I want to exercise because I don’t want to take a statin medication, but I don’t have time to exercise.” So this is where you help them understand like you recognize that exercise is one of the key ways to reduce your need for a statin medication. And you get that if we leave this cholesterol the way it is, it will cause more risks for your patients. But at the same time, time is a factor. So you come up with some ideas to benefit your patients and incorporate exercise as a routine.
Develop A Plan
Dr. Alex Jimenez, D.C., presents: Remember that you don’t have to solve everything for someone. You could put things out like developing discrepancies for the patient and then let the patient generate solutions that work. So also support self-efficacy. This means that we are not going to change the behavior. The patient is the one who has to change the behavior, and their understanding of their capacity to change their behavior is essential. So whatever you can do to point out the positives, acknowledge whatever they’ve done, even if it’s like, “Hey, it’s wonderful that you bought sneakers. I understand that you didn’t do anything we discussed; life happened. I want to acknowledge you for getting the sneakers because that makes it much easier to start the plan now.” So support self-efficacy whenever possible. Now other more tangible obstacles keep someone from wanting to implement exercise.
Many times it’s either on a mental or physical plane. So here are some solutions that we’ve listed for some of the common mental obstacles we’ve seen. Some people don’t want to be out in public because of concerns about body image. So, they can often go to a special kind of gym if they want to go to a gym, or they can do at-home videos or a personal trainer. Sometimes it gets boring, and they would often moan and groan about it when they are exercising; however, if they are doing fun exercises like dancing or swimming, they will become more motivated and start to change their exercise regime throughout the week. You could do these things despite needing more knowledge or confidence about doing it correctly or on time.
Incorporate A Trainer Or A Health Coach
Dr. Alex Jimenez, D.C., presents: That’s when you might want to bring in a health coach or personal trainer, and with physical obstacles which may be related to a person hasn’t been exercising for a long time and assuming that you’ve cleared them to be able to initiate an exercise plan, maybe there are ways that you can say, “Okay listen, I want you to walk at a low intensity to start with, and you know, over the next month I’d like you to build up two 5,000 steps a day.” This can be a routine set for three days a week, four days a week, or whatever you decide with them and does that work for the patient. That might be one way to work on physical or perceived physical limitations. And then there may be people who have real-time constraints. So the two ways to handle this; is to optimize NEAT or HIIT workouts.
These can be simple activities we do throughout the day, like taking the stairs, parking further away, walking during your lunch break, and having walking appointments and meetings. While watching TV in the evening, you could pump some free weights in your bedroom or your living room. Or if they are more avid exercisers and are open to taking on some HIIT training, that could be a way to get some concentrated cardio and strength training signals in the body. Next, we want to discuss the different scenarios we may have regarding our office structures that support implementing exercise. A common scenario would be that you need a dedicated person in-house to help people implement the exercise prescription.
Use Resources
Dr. Alex Jimenez, D.C., presents: Okay, so if you are the provider, health coach, and personal trainer, we want you to consider using resources. You must recognize your boundaries in terms of not being able to be everything to everyone but using your resources effectively. Because we can’t create boundaries that are so tight that you’re not making the type of office that you want, meaning one that incorporates exercise prescriptions. So we’re going to talk about an office workout and exercise grid and how we will work with the local community, personal trainers, and gyms to refer out. And we have trained them to look at our exercise prescription as a guideline even though we are not legally partnered with them. They use these prescriptions as a way of communicating what our goals are. Here are some tools that we use that we are going to share out.
And then, especially in certain times like we’re having right now, we also referred to online resources. So this office workout prescription was created by our team, and we handed out this resource to our patients. We encourage them to find a buddy in their office or home because it is generally more fun. There are data to suggest that when you exercise in a social format, Like participating in team sports, it creates more benefits than doing an individual sport or being at the gym with your AirPods centered only on yourself. So there is this association where having a social element to your exercise regimen increases the benefits. Set up reminders on your phone when you’re at the office to do these hourly five-minute exercises.
And then we also have an online link where our trainers and health coaches demonstrate proper form and modifications for these office workouts. And then, of course, once you give any resource, whether it’s this office workout prescription or any other help, determine with the patient what we want to do about this. We don’t want to give out this prescription and say we hope it works. The main question is that do you want to have accountability? “Hey, can you come back to see us in a month, and let’s see where you are with it?” Or, “Hey, can you consider taking it to this next level after a month if you feel good and come back to see us in two months?” Or, “Hey, once you’re done with this, why don’t we talk in two months to recheck your lipids and know if you made a bump in your LDL particle number so that we can lower the dose of your statin or get you off the statin.”
So we don’t recommend just doing the exercise prescription and leaving it open-ended in terms of follow-up; make it like any other prescription; if you were to put someone on a statin, you would follow up with them. So just like that, you would follow up with someone you prescribe an exercise prescription. Again, it’s really practical. It can be done whether you work in an office, a home office, or you don’t work at an office but work in the house. So it’s in your IFM toolkit. And it has a Monday through Friday, an eight-to-five grid of what you do throughout the week. So it diversifies exercises and makes it, so all your muscle groups are incorporated using the stuff you have in an office or a typical home.
Delegate With Your Patients
Dr. Alex Jimenez, D.C., presents: So it is beautiful for the “I don’t know what to do” people, and it’s a great start for sedentary people. Then you can also consider any technology that is of interest to you. Here are some that our health coach and personal trainer have suggested based on what the patient’s goals are. They may be trying to run a 5k, then find an app that might work for them there. Or they may incorporate yoga to work on their mind-body access or flexibility. You can personalize it to the type of workout if they’re interested in HIIT, yoga, or Pilates. Again, find technologies you enjoy, and check them out yourself. Or you can make a little cheat sheet that can be given out or put as a template. Here’s something important that we want you to consider if you still need to do it.
It’s called delegation. This can not be done alone; this is a group effort to allow the individual to have a team to back them up and help improve their health and wellness journey. Now, this is done in healthcare all over the place. For respiratory therapists, many people will do delegated work from the healthcare provider. So it’s just a transfer of responsibility for the performance of patient care. Now, remember that it’s still done under the provider’s responsibility. You should consider that different states and insurance contracts may have little nuances on how they would want you to do delegation. Still, we know habits have changed, and we need help to keep up with them to meet the requirement.
So how would we delegate a patient? We would go through a thorough examination, like taking their BMIS/BIAs with the Inbody Machine, and then go through a series of functional medicine tests to determine what issues or overlapping risk profiles are affecting them. Then the doctor and their associated medical providers will develop a personalized treatment plan for that patient that incorporates a healthy diet and exercise regime for them to follow.
Conclusion
Dr. Alex Jimenez, D.C., presents: Making these small changes is beneficial in the long haul regarding a person’s health and wellness journey. It may take a while to get accustomed to the routine, and sometimes it can be frustrating. However, finding what works and doesn’t work with the patient and making these changes can result in a better solution that benefits the person.
Dr. Jimenez, D.C., presents how Lyme disease can cause referred pain to the body in this 3-part series. Many environmental factors can cause numerous issues in the body that can lead to overlapping risk profile symptoms in the muscles and joints. In today’s presentation, we examine the different treatment protocols for Lyme disease. Part 1 looks at the body’s genes and looks at the right questions to ask. Part 2 looks at how Lyme disease is associated with chronic infections and how it affects the body. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with Lyme disease. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
The Biofilm In The Body
Dr. Alex Jimenez, D.C., presents: The elimination of all biofilms makes no more sense than trying to sterilize the gut. So biofilms are this adherent polysaccharide matrix. We like to think of it as a fruit cocktail jello. So you’ve got the jello and all the different pieces of fruit in there, and each other type of fruit might even be a different species of bacteria. And one of those bacteria can make penicillinase, and it can elaborate a cloud of penicillinase into the matrix, protecting even species that can’t make it. And we already talked about how these biofilms can be operant in probiotic colonization, but they are also part of several problematic infections.
So there are several strategies to modify biofilms, making them more porous to the immune system and antibiotics. So Lactoferrin is one, Colostrum, which contains Lactoferrin in a bunch of other products as well. Serum-derived bovine immune globulin is egg divide-derived immune globulin for your sensitive patients. Probiotics and prebiotics can have biofilm activity. And then enzymes, as we mentioned before, are a carbohydrate structure, and enzymes can break down that matrix and make it more porous. So can Xylitol and EDTA be strong anti-film actors and stevia?
Lyme Serology Test
Dr. Alex Jimenez, D.C., presents: So Lyme serology testing needs to be more sensitive for diagnosis, especially during the early or late stages. And we’ll see why in a minute. So the standard two-tiered test requires a screening test of either an ELISA test or an IFA and then a confirmation test of a Western blot. The International Lyme and Associated Disease Society or ILADS and others argue that this two-tiered test should be only for surveillance or research purposes but not for diagnosis in individuals. So here’s what that scheme looks like, you either get an EIA or an IFA, and if it’s positive or equivocal, you go onto a Western blot. If you’ve had symptoms for less than 30 days, you get both an IGM and an IGG. If you’ve had symptoms for more than 30 days, you only get an IGG. Now, there are special criteria for reading the Western blot. They require multiple positive bands depending on whether it’s an IGM or an IGG blot. If your screening test is negative and you’ve been sick for less than 30 days, you should be retested in, you know, at some recovery point. You should consider a different diagnosis if you have been sick for more than 30 days. And we are going to talk about why this scheme is problematic.
So it’s highly specific. This two-tiered test is 99 to hundred percent specific, but its sensitivity is rather poor, perhaps even lower than 50%. So, here’s the data on that. We see the number of patients in the study, the patients versus controls, and the sensitivity and specificity. We also see totals, and the total sensitivity was 46%, while the total specificity was 99%. So as a test, think about it; we all learned about appendicitis in med school. You must take out a few normal appendices to ensure you get all the bad ones. If you’re missing half of the Lyme disease cases, many people will go onto tertiary disease.
Testing For Lyme Disease
Dr. Alex Jimenez, D.C., presents: So what about seronegative Lyme? So people who had the test and it was negative. Well, here’s a female patient who had what appeared to be Lyme arthritis despite recurrent negative Borrelia Burgdorferi tests. So she was found to have a different species of Borrelia garinii, and multiple courses of antibiotics didn’t do the tricks. So she had more courses of antibiotics and synovectomy, which eventually did help. This test says that Lyme borreliosis patients with live spirochetes in body fluids have a low or negative level of Borrelia antibodies in their serum. This indicates that an efficient diagnosis of Lyme borreliosis must be based on various techniques such as serology, PCR, and culture. And in this study, spirochetes were isolated from skin cultures obtained from multiple lesions. These spirochetes were identified as not Borrelia Bergdorferi but instead as Borrelia Afzelii.
However, Serum Borellia Burgdorferi tests were repeatedly negative. One of the problems with these tests is that the kit that comes approved is based on Borelli Burgdorferi, B-31 strain. And we see from these seronegative Lyme tests that some other strains and species may be involved. So the IDSA guidelines state that there is no convincing biological evidence for symptomatic chronic Borrelia Burgdorferi infection among patients after recommended treatment regimens for Lyme disease. This was noted in a culture-proven case of antibiotic failure with Borrelia Burgdorferi infections in 1989.
So, what about the animal model? There was an antibiotic failure in an animal model, this mouse model. In this dog model, there’s an antibiotic failure. In this Macaque monkey model, there’s an antibiotic failure. And in this particular study, Borrelia Burgdorferi can withstand antibiotic treatment when administered post-dissemination in primates. And as we’ll see in a little bit, many patients with Lyme disease are diagnosed post-dissemination. So these findings raises important questions to discuss with patients about the pathogenicity of antibiotic-tolerant persisters and whether or not they can contribute to symptoms post-treatment in Lyme disease. Human studies suggest that 25 to as many as 80% of patients have persistent symptoms after two to four weeks of antibiotic therapy. In this study, up to 40% of patients were found to have a persistent infection after the recommended IDSA treatment. So in this study, the patient’s condition deteriorated despite receipt of repeat courses of antibiotic therapy over two years.
The Protocols
Dr. Alex Jimenez, D.C., presents: They then received 12 months of intravenous antibiotics and 11 months of oral inter condition improved significantly. You’re going to see that we don’t have to resort to these long courses of antibiotics so much anymore because we have different tools. But this suggests that a longer duration may be helpful. Our study substantiates Borrelia persistence in some erythema migraine patients at the site of the infectious lesion site, despite antibiotic treatment over reasonable periods. And this was not because of rising MIC (minimal borreliacidal concentrations) levels. Therefore, resistance mechanisms other than the acquired resistance to antimicrobial agents should be considered in patients with Lyme Borrelia resistant to treatment. And in this study, a declining antibody response, which has been noted following antibiotic treatment in mice and in antibiotic-treated dogs, occurs despite low levels of persistent spirochetes. Our results show spirochetes are viable and transmissible and express antigens following antibiotic treatment.
This is a biostatistical review of the papers that the IDSA used to argue that there’s no compelling evidence of persistent symptoms after treatment and that repeated antibiotic treatment does not work. And they conclude that this biostatistical review reveals that re-treatment can be beneficial. Primary outcomes originally reported as statistically insignificant were likely underpowered. The positive treatment effects of Ceftriaxone are encouraging and consistent with persistent infection, a hypothesis deserving additional study. All right, so now we are going to start applying appropriate sequence diagnostic steps for Lyme disease.
What Symptoms To Look For?
Dr. Alex Jimenez, D.C., presents: The International Lyme and Associated Disease Society, or ILADS, has published evidence-based guidelines for managing and treating LymeLyme, and they’ve done something unique in the practice guidelines space. They publish an appendix, and then in this appendix, they compare the ILADS versus the IDSA guidelines for every single recommendation. So we see the management of an exodus species bite. So exodus tick bites typically have many useful symptoms, but the best treatment for chronic Lyme disease is early treatment of acute Lyme disease. But this is hard because the erythema migraines rash only shows up in about half of the patients with Lyme disease. And the central clearing makes it look like the bullseye rash, which is the stereotypical or classical erythema migraines rash. That central clearing only shows up in about half of the rashes. In fact, in one case series of 11 erythema migraine rashes, they were misdiagnosed as cellulitis, even though all 11 patients showed clinical evidence of Lyme disease progression.
To that point, making it even more difficult is that only about half of the patients with Lyme disease remember a tick bite. So it’s important to think about Lyme disease anytime you’re evaluating somebody suffering from flu-like symptoms off-season. So if they have the summer flu, they feel Lyme disease. So what are some symptoms? Severe unrelenting, life-altering fatigue. Now we’re talking about chronic Lyme disease here, not acute Lyme disease. Acute Lyme disease symptoms include low-grade to even significant fever, chills, body aches, and sweating. But we’re talking about chronic Lyme disease and its symptoms, which include severe unrelenting, life-altering fatigue, migrating arthralgias, and myalgias which can progress over time. What is this migrating business? It means that the left knee hurts so bad a person can hardly walk, but now three days have gone by, their left knee doesn’t hurt at all, but their left shoulder is killing them. This is known as referred pain, where one location in the body is dealing with pain instead of the main source that has been affected. This causes the sensory nerves to top go haywire in the body and, over time, develop overlapping symptoms that can affect the vital organs, muscles, joints, and tissues.
These symptoms correlate with joint inflammation going on here. Memory impairment, brain fog, mood swings, and anxiety all progress. What about the patient’s history? Living in or traveling to a tick-infested area is an important piece of history. A known tick bite, even though half the patients don’t know about it, that’d be useful. A rash, even though half the patients don’t have one, that’d be useful. And then the symptoms we described.
So what about the physical exam? Unfortunately, it’s generally non-specific, but you must carefully consider neurological, rheumatological, and cardiac symptoms when suspicious of Lyme disease. You know, you might find arthritic kinds of symptoms. You might discover meningitic signs. And anyone who has Bell’s Palsy should be ruled out for Lyme disease. Bell’s Palsy is Lyme disease until proven otherwise.
Another interesting thing is doing vibratory sense evaluation by confrontation. And what’s interesting is you do it, put your finger on the bottom of the metatarsal and put the tuning fork on the top of the metatarsal or metacarpal. And you wait until you can’t feel it transmitting the bone, right, and if the patient says that they don’t feel it, and you still do, that’s probably not normal.
Conclusion
Dr. Alex Jimenez, D.C., presents: When treating Lyme disease associated with chronic infections, if the immune system is not responding in a way that we would expect a healthy person’s immune system to respond, then providing additional tests to figure out the symptoms causing overlapping risk factors are useful. Remember that treating chronic infection is a master’s class in functional medicine. We must use all of our tools and do laps around the matrix. Every time you get a new piece of data, it is interesting. We need to think about the matrix in total. We need to consider the five modifiable factors of psychosocial, spiritual, mental, emotional, and spiritual aspects of what the patient is going through. And remember that your ATMs are not your destiny. And that infectious agents often modify the local and systemic immune response displaying self-stealth pathology, which can be in the body for years. Talking with your patient about what is happening in their genes and providing a personalized treatment plan to give them the tools for their health and wellness.
Dr. Jimenez, D.C., presents how chronic infections are associated with Lyme disease in this 3-part series. Many environmental factors often play a role in our health and wellness. In today’s presentation, we look at genes and how to answer the right questions. Part 12 looked at what Lyme disease does to the body. Part 3 looks at treatment protocols for Lyme disease. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic infections associated with Lyme disease. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
Chronic Infections
Dr. Alex Jimenez, D.C., presents: We will have an interesting, brief discussion about evidence of an atomic force micrograph of a borrelia burgdorferi biofilm. This is a talk about stealth pathology and chronic infection in general, and we are using Lyme as a backdrop, but this is far from a comprehensive course on Lyme disease. So, let’s dive in because we are going to learn a lot about stealth pathology and a lot about Lyme disease. How do you begin thinking about chronic occult infection and stealth pathology? It starts with the basic functional medicine model.
It would help if you dealt with the phenotype. You know, your genes are not your destiny. Well, your phenotype isn’t your destiny either because it’s malleable. And how do we change your phenotype by dealing with the exposome, internal exposome, lifestyle issues, air, water, food pollution, medications, environmental toxins, xenobiotics, those kinds of things? Other exposomes include internal metabolic byproducts, lipid peroxides, oxidative stress, protein addicts, inflammation, the microbiome, et cetera. And then cognitive thoughts, beliefs, fears, phobias, isolation stressors, et cetera. And these cognitive processes have profound effects on immune responses. And then, on top of that, you have to deal with the pathogen. You must understand the biology, life cycle, and genetics of the pathogen you’re dealing with. You must also understand the pathophysiology, stealth pathology, cooperation, biofilm production, and interactions with the host immune system. And it’s important to remember that we’re talking about chronic infection here, not acute infection.
Acute Infections
Dr. Alex Jimenez, D.C., presents: If your patient has an acute infection, like pneumonia or meningitis, get them on IV antibiotics immediately, and don’t wait for your functional medicine workup. So how do you even begin to think about this? Well, you start with a comprehensive physical exam and look carefully at the question, when was the last time your patient was truly well? We like to think of it like this. If wellness is a straight line at some point, it broke right at that place, right around there. This can happen several times, so it might have broken ten years ago. And they came along with this new normal, but it broke numerous times again. And so, at each of those breaks in the overall health, what happened? What were the antecedents? What were the triggers?
Mediators For Genes
Dr. Alex Jimenez, D.C., presents: What were the mediators? And then, look at a physical and nutritional exam and, again, for antecedent triggers and mediators. And then create a timeline to look for the antecedent triggers and mediators. People come with baggage. They’ve been given this diagnosis and that diagnosis. And the other diagnosis, you know, they might have seronegative, rheumatoid arthritis, they might have fibromyalgia, chronic fatigue syndrome, maybe somebody said they had Epstein-Barr virus. Whatever it is, we need to look at those diagnoses critically and do whatever’s necessary. More tests, consultations, whatever’s required to rule it in or out. And from there, we populate a matrix. And this matrix is a living document because every time a new bit of data comes in, we need to fit that into the matrix.
The functional medicine workup has a layer on the bug’s biology and pathophysiology. And here is what we call the infectious Denee disease conundrum in these five areas where these bacteria seem to be able to figure out how to evade antibiotic and antimicrobial herbs and pharmaceuticals and our immune system. And then always remember the fundamental functional medicine adage, which is, unless there is a compelling reason to do otherwise, start in the gut. So start in the gut unless there’s a compelling reason to do otherwise, and here is why. So baseline nutritional deficiencies can be caused by many different antecedences and triggers. Let’s take just one as an example. People are in autonomic dysregulation, causing fight-or-flight responses. Fight or flight shunts blood away from your gut, which means you are not digesting or absorbing efficiently.
How Do Chronic Infections Affect The Body
Dr. Alex Jimenez, D.C., presents: That means that you’re functionally malnourished. Also, you’re shunting blood away from your gall. So the gut-associated lymphoid tissue comprises 70% of your entire immune system, intimately associated with the gut; you’re shunting blood away from that. So you’re functionally immune compromised just from autonomic balance issues. So what does cause increased baseline oxidative stress, impaired immune function, and impaired mucosal defenses that result in the proliferation of some of these endogenous viruses? In middle teens, you are colonized or dormant, infected with Epstein-Barr, cytomegalovirus, and some herpes simplex viruses may bloom. That increases your susceptibility to infection. These things increase the frequency, severity, and duration of infection. And here’s where amplification loops begin. This causes exacerbations in oxidative stress in your mucosal damage.
And then sick behaviors of anorexia and so on result in these amplification loops. And now, the problem is getting bigger and bigger, and the body’s ability to solve this problem is shrinking. And that’s where functional medicine interventions are so powerful and important. And the question always comes up, “Do I have enough time? Do I have enough data, if you will, to even begin treatment?” We want to simplify functional medicine to show you how powerful it is. Let’s say assimilation is an example. We’re just going to pick four ways to intervene in assimilation. We’re going to say there’s no problem in assimilation, so we’re not going to do anything. Or there’s a mild problem. So we’re going to put them on an elimination diet; maybe there’s a more moderate problem.
Conclusion
Dr. Alex Jimenez, D.C., presents: So we’re going to add to that elimination diet, say, colostrum. And then, for a severe problem, we’re going to layer on top of that a GI-focused medical food. So this is a more complex medical food. So we have these four interventions. Now, we’re considering intervening at all the functional medicine matrix nodes. In that case, we have the, you know, the seven physiologic nodes, what we think are often overlooked, the mental, emotional, and spiritual domains of wellness, the five modifiable lifestyle factors, and so on. So you end up with about 19 and more if you’re doing labs because you’ll intervene on all those. But four to the 19th power is the number of different combinations or ways this can happen. This becomes unique in the world intervention for your patient. So never be afraid to start and do another lap around the matrix by adding more information, and think about the next step. Now, we want to talk about the quality of evidence that we find in evidence-based medicine. A 2005 research paper published by Dr. Iondas titled “Why Most Published Research Finds Are False?” The research shows an increasing concern that most current published research findings are false, as studies show that many claims are more false than true for many designs and settings. The research is more or less an accurate measure of the prevailing bias.
Dr. Jimenez, D.C., presents how to find the right diet for cardiometabolic syndrome in this 2-part series. Many environmental factors often play a role in our health and wellness. In today’s presentation, we continue discussing how genes play with the cardiometabolic diet. Part 1 looked at how every body type is different and how the cardiometabolic diet plays its role. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with metabolic connections. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
Omega-3s & Genes
Dr. Alex Jimenez, D.C., presents: We’ve found that fish oils or omega-3s can lower triglycerides, small-density LDL, and sometimes lower LDL and keep HDL regulated. But these studies were back when they were supplementing with more of an even DHA/EPA ratio. But that’s something to be observant of; the study showed that giving them fish oil lowers their small density LDL and triglycerides. They also found that if they gave them a lower fat food plan, and a lower fat diet, they found it lowered their LDL and small density LDL. A moderate fat diet reduced their LDL, but it increased their small density LDL. And they found that average alcohol consumption lowered their HDL and increased their LDL. So that’s not a good sign when that happens. So the opposite of what you want to occur with a moderate alcohol consumption diet or food plan.
So going back to APO-E4 in the body, how would this gene be affected when dealing with viral infections like herpes or cold sores? So research studies have revealed that APO-E4 and herpes simplex one viruses can affect the brain’s cerebral tissues. So the research also indicates that patients with APO-E4 are more susceptible to getting the herpes virus. And remember, herpes simplex one virus is what causes cold sores. What about HSV and dementia? How would that correlate with the body? The research indicates that HSV increases the risk of dementia. And what the thought is is that just like the herpes virus can come out and cause cold sores, it can internally manifest, and you can get these episodes where HSV becomes active in the brain, which can cause some of the pathogenesis of dementia or Alzheimer’s disease.
APO-E & Finding The Right Diet
Dr. Alex Jimenez, D.C., presents: And there was a study that showed that if you gave patients with dementia antivirals, it decreased the risk of getting dementia. So what do we do with the APO-E genotype? If you have APO-E2, APO-E3, or APO-E4, you can start them on the cardiometabolic food plan. If they’re on the SAD diet, the standard American diet, then putting them on the cardiometabolic food plan is just a good idea. It’s going to start shifting them in the right direction. What about additional consideration if they have APO-E3/4 and APO-E4/4? There are a couple of reasons you should jump in on this. They like it more when you customize a diet to a patient’s genetics. So if you can say, listen, we have your genes, and we know that you would do better if you had lower saturated fat, or if you don’t do so well on alcohol X, Y, or Z, it makes them pay attention more.
Because now it’s personalized. It’s not like, “Hey, everybody, just eat healthily.” It’s more personalized to your genetics. So, that would be a reason to start this from the get-go. But get them on the cardiometabolic food plan, and they should begin to feel better. But we would start by putting the whole thing in perspective that this APO-E3/4 and APO-E4/4 is not a death sentence. It’s a clue of how you respond to your environment and what we need to watch out for. It does not mean that you are going to get Alzheimer’s. The majority of people with Alzheimer’s do not have APO-E4. You have a higher risk of getting Alzheimer’s if you have APO-E4. And that’s where functional medicine comes in to risk-stratify them.
Finding The Right Diet For You
Dr. Alex Jimenez, D.C., presents: We recommend a lower simple carbohydrate diet or a higher glycemic index diet. And diet and food plan interchangeably, but patients call it a food plan because diet has negative connotations. So we avoid the word diet because when people hear or speak it, some people are triggered by it. You have people with food disorders and people with bad experiences with diets. A lower fat and a lower saturated fat food plan or recommendation is something to consider and be more aggressive with omega-3s. And if you start giving omega-3s to the patients, it is best to check their omega-3 levels and see if they begin to fluctuate. If they start shifting for the better, then we strongly advise against alcohol and monitor these patients for cognitive decline; there are different tools that you can use.
When it comes to omega-3s, it is best to do a cognitive test to keep an eye on their mentation. So if it starts to decline, you’re jumping in way before you have a major problem. And because of the issue of them not being able to deal with viral infections like herpes. And because the herpes virus may play a role in getting dementia, you may consider lysine supplementation. Arginine can deplete lysine. So if you end up eating a lot of pumpkin seeds and a lot of almonds and whatnot that have higher amounts of arginine, you can counteract that with lysine. And the research suggested that you need about two grams of lysine daily. But remember, every patient is different, so don’t just throw everybody on lysine if they have APO-E3/4, APO-E4, or APO-E44 3 but just something to consider.
So final thoughts on APO-E and nutrition. There are many pieces to the puzzle. Do not be dogmatic and say you have these genes, so you must do this. Just realize there are so many different genes, so many other variabilities, and recognize that it’s not that race can have something to do with how APO-E is affected. For example, they did a study that found that people in Nigeria had higher amounts of APO-E4, and the APO-E4 four did not increase their risk of dementia. So there are other pieces of the puzzle, monitor biomarkers and continue to adjust the plan. Next, we will discuss dealing with people with high triglycerides and high LDL.
What To Do With Abnormal Lipids?
Dr. Alex Jimenez, D.C., presents: So how do you take the abnormal lipid findings that you see on your profiles of your patients, those biomarkers, as all of us check? And how do you adjust the cardiometabolic food plan? What of the highlights of a cardiometabolic food plan that you will do for your patient in response to their lipids? Let’s first review a few things we know about how to modulate the diet’s lipids. First, we know that if you go from a standard American diet to the cardiometabolic food plan. You remove the trans fatty acids, and if you remove the trans fatty acids, then you will see a decrease in LDL cholesterol triglycerides. You’ll get an improvement in HDL; to say it another way, if your diet is high in trans fatty acids, you’ll have a higher LDL you have, you’ll have more elevated triglycerides, and you’ll have lower HDL.
How To Modulate Your Diet
Dr. Alex Jimenez, D.C., presents: What else about modulating the diet? If you have longer chain fatty acids that are not polyunsaturated, you’ll have an increase in your LDL and triglycerides and an increase or no change in your HDL cholesterol. On the other hand, we focus a lot on the shorter chain fatty acids and functional medicine. So if you have shorter chain fatty acids that are less than ten carbons, you’ll have lower LDL cholesterol triglycerides and increased HDL. So you can see with the cardiometabolic food plan, by addressing with the patient, their fat source, you can begin to impact LDL cholesterol without anti-triglycerides, without any other modulation other than dietary habit. And then finally, we know the data early and some of the most recent meta-analyses of changing simple sugars in the diet.
We know that that can, in its own right, increase LDL cholesterol triglycerides, and you get a lowering of HDL. So let’s put this all in context. What do we want to do for our patients to decrease the risk of coronary artery disease or atherosclerosis fat disease? We want their LDL cholesterol to be in a lower range. We do not wish for that LDL to be oxidized. We want the HDL to be higher. And if we can get triglycerides down through dietary change, then that gives us a clue that they might not be dysfunctional in the insulin metabolism. Then finally, with omega-3 fatty acids or adding omega-3 fatty acids or mono-concentrated fatty acids, we’ll lower LDL cholesterol triglycerides, and we’ll get an increase in HDL cholesterol. This is associated with a reduction in cardiovascular risk independent of lipid levels.
Conclusion
Dr. Alex Jimenez, D.C., presents: How is that affecting the body? It is because you have inflammatory drivers independent of your serum lipids that will increase your risk of atherosclerosis disease. It comes to saturated fat and fat content. Balancing the proteins, and the fat, you don’t have as much oxidative stress associated with inflammation after a meal. Thus, even if you have an elevated LDL level, you have less chance of having an increased oxidized LDL. Incorporating fibrous foods, antioxidants, lean meats, dark leafy greens, and supplements into a healthy diet can help lower LDL and fatty acids in the body and reduce all these comorbidities causing issues to your health and wellness.
So, those are just some tips and tricks for diet prescription to reduce cardiometabolic syndrome. And we encourage your patients to add more greens, legumes, nuts, and seeds, making the plant-based diet a mainstay for their heart health.
Dr. Jimenez, D.C., presents how to find the best diet approach to hypertension and cardiometabolic risk factors in this 2-part series. Many factors often play a role in our health and wellness. In today’s presentation, we will look at how a cardiometabolic diet is personalized for every body type and how genes play with the cardiometabolic diet. Part 2 will continue with how genes play their role in a cardiometabolic diet. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with metabolic connections. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
What Is A Cardiometabolic Diet?
Dr. Alex Jimenez, D.C., presents: Regarding cardiovascular disorders, some terms we look for are: actual heart disease or stroke risk, or they’re on the metabolic side. Insulin, blood sugar, metabolic dysfunction. These words capture the themes we’ve been talking about lipids, glucose, inflammation, and insulin. Those are the people that you’re thinking about for this plan. And what you’re doing is building a lifestyle prescription. And for our patients who have cardiometabolic issues, we’re going to really take advantage of those features of our cardiometabolic food plan and then take them a step further to not only give a low glycemic impact, anti-inflammatory, plant-based kind of nutrient source but then how can we tailor it according to other parameters of this patient and then how can we help this patient implement it when they step outside your office and have to enter into their environment, which may or may not be set up for success.
So first things first. There is a practitioner guide that you must take advantage of, and this is like the scriptures of nutrition, and it has so many resources in here, but of course, they are of use to you once you know about them. So this is going to give you the how-to. So in case you miss something or want more detail, please refer to this practitioner guide for the cardiometabolic food plan. Now, let’s say you want to do the first entry-level use of this food plan. Well, we would grab the one that tells a cardiometabolic food plan. You’ll notice that all these specialized foods are selected to help with cardiometabolic conditions.
Personalizing A Plan
Dr. Alex Jimenez, D.C., presents: And it’s much better than saying, “Hey, eat fewer carbs, eat more plants. You know, eat healthier and exercise more.” That needs to be more specific. So taking it a step further, give them a blank food plan. It doesn’t have to be personalized to another level. Handing them a food plan and telling them to start eating from this list is only sometimes going to work. Sometimes we have to take it a step further to give them food choices in terms of quality and quantity. To that point, you have the ability right now with your patient to guesstimate size and caloric targets.
We can estimate size and weight and put small, medium, and large portions on food consumption. An example will be if we look at the different sizes of body types. For a petite adult body, it is best to ensure they consume about 1200-1400 calories. A medium adult body must consume about 1400-1800 calories, and a large adult body must consume about 1800-2200 calories. That might be the first kind of personalization.
Let’s give you some caloric-guided, quantity-guided food plan options. So what’s beautiful is that we have those already built out, and if you look closely at them, it tells you how many servings of each category should be in each specific small, medium, and large food plan. So you don’t have to do that calculation. Now if you want to take it to the next level and you have a BIA or a bioimpedance analysis machine, you can understand specifically their caloric burn rate and then if you want to modify it. An example would be a 40-year-old male who is unhappy with his weight and has been dealing with issues causing him ankle pain. So let’s see how we can change these things.
As we look at his body index, he is about 245 pounds and has been dealing with some cardiometabolic issues. Now when we look at his numbers and data from the BIA machine, we would develop a food plan that can help dampen the cardiometabolic issues effects that can help him. We would start to calculate come caloric recommendations and have a personalized diet and exercise plan to reduce the symptoms affecting his body and help promote muscle gain and weight loss. This customized plan allows him to keep track of his progress to see what works that is helping him lose weight or what needs improvement. Making these small changes can be beneficial in the long hall, as it will take some time to develop healthy habits.
How To Cater a Cardiometabolic Diet?
Dr. Alex Jimenez, D.C., presents: Now, what do you do with that information and cater it to become a diet for cardiometabolic disorders? Well, you would work with a health coach and other associated medical providers like a nutritionist to pull out a personalized food plan to help your patients understand what’s in each category and how to personalize the servings per day if you decide to get a bit more personalized with the caloric targets. And remember that some MVPs are the most valuable players with super nutrient powers within this food plan. It is also important to make time with the patient to discuss foods that benefit their health and wellness. Remember that this cardiometabolic food plan’s goal is to be able to personalize for unique clinical cases and unique patients. However, it still serves the general need for cardiometabolic food signals for our patients with these issues.
There’s something in here for everybody; remember, you must get started on something. So please consider how you can make this available to your patients so that they have it to a couple of recipes; it’s got menu plans, shopping guides, and recipe indexes. It’s chalked full of the things that slow us down in getting nitty gritty about the cardiometabolic food plan or nutrition in general. Something is always better than nothing. So by starting with the cardiometabolic food plan for your patients, you will start seeing the science be beautifully put into action. We will talk about how to use genetics with diet prescription.
Cardiometabolic Diet & Genes
Dr. Alex Jimenez, D.C., presents: Going a bit deeper, we will discuss how we tailor the cardiometabolic food plan in patients based on their APO-E genotypes. How do we customize it a little bit further? So what is APO-E? APO-E is a class of APO lipoproteins produced in the liver macrophages in astrocytes. It is required for the chylomicrons and IDLs while mediating cholesterol metabolism and is the principal cholesterol carrier in the brain. Now, there are three possible genotypes. There’s APO-E2, APO-E3, and APO-E4. And what happens is you’re going to get one from each parent. So you’re going to end up with a combination at the end. So you’ll be either APO-E3 with APO-E4 or APO-E2 with APO-E3. So based on what you got from your mother and what you got from your father, you’re going to have that combination.
APO-E Explained
Dr. Alex Jimenez, D.C., presents: So APO-E2 two and APO-E3, there’s a lot of information online, but there’s not good evidence on making specific dietary changes in these particular genotypes. So unfortunately, we don’t have the data to confidently say how to modulate, change or customize the food plan based on these genotypes. The best we can tell you is to follow the biomarkers; every patient is an individual. But what about APO-E4? Around 20% of Americans have at least one APO-E4 allele, and if you have APO-E4, you have an increased risk of mild cognitive impairment, Alzheimer’s, hyperlipidemia, diabetes, and coronary heart disease. And if you smoke or drink, you have a worse outcome with this genotype. Interestingly, being relevant to the times increases the risk of infections that can affect your body.
So usually, something helps one thing, but it will, and it can hurt others. So with your patients that you already have their genetics on, this might be a nice way to look at if you know their APO-E4 risk stratified them even more when protecting them. So this was independent of whether they had dementia, underlying cardiovascular disease, or diabetes.
If you have APO-E4, it may be protective against malaria, and who knows what other benefits it would have? An interesting fact about APO-E4 is that, in a study where they tried to give them DHA supplementation, they found it harder to get the DHA in the brain higher with APO-E4. They could elevate it, but not as well as if you had APO-E2 or APO-E3. And this was like supplementing with DHA. Other studies showed that the levels did not respond well if you did DHA and EPA together. So you didn’t get as high of a response of the omega-3s with APO-E4 versus if you had APO-E2 or APO-E3.
How Omega-3 Play Their Role?
Dr. Alex Jimenez, D.C., presents: So the interesting thing, though, is that the study looked at the omegas in the brain that was supplemented with DHA. We have all kinds of new research on the benefit of EPA-only omega-3s; there’s even a main name brand product that is EPA-only. If you look at, if you look to the right, you see that EPA ends up becoming DHA. So if you start increasing, both EPA and DHA will go up. What about APO-E in your diet or the food that you’re consuming? When they looked at genetically modified mice where they took APO-E out, they found extreme hypercholesterolemia with a high-fat food plan.
So when the mice were fed higher fat diets, they had this extreme rise in high cholesterol. Why is this relevant? Because APO-E4 does not function as well as APO-E3 and APO-E2. That hinted that this could affect us if we consumed a higher-fat food plan. So in a U.K. study, they found out that if they gave patients APO-E4 and switched it from saturated fats, they decreased their saturated fats while increasing their lower glycemic index carbohydrates; they found that it lowered their LDL and APO-B. This is a clue that we may want to decrease saturated fats, even healthier saturated fats, in these patients.
So the Berkeley Heart Study from the Berkeley Heart Lab was bought by Quest. It’s now called Cardio iq. It’s one of the original advanced lipid testing labs. And they had an observational study where they saw different effects in these patients with APO-E4 and other products based on various dietary modifications. So what did they find? They found that giving them fish oil lowered their triglycerides, reduced their small density LDL and HDL, and increased their LDL. So their HDL decreased, but the small density LDL went down, and their triglycerides went down.
Dr. Jimenez, D.C., presents how chronic metabolic connections like inflammation and insulin resistance are causing a chain reaction in the body in this 2-part series. Many factors often play a role in our health and wellness. In today’s presentation, we will continue on how these chronic metabolic diseases affect the vital organs and organ systems. It can lead to overlapping risk factors associated with pain-like symptoms in the muscles, joints, and vital organs. Part 1 examined how overlapping risk profiles like insulin resistance and inflammation affect the body and cause muscle and joints pain-like symptoms. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with metabolic connections. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
How The Liver Associated With Metabolic Diseases
So we can look to the liver to find earlier cues of cardiovascular risk. How can we do that? Well, let’s understand some liver biochemistry. So in a healthy liver cell hepatocyte, when you have increased insulin being secreted because there was a meal that required glucose to be absorbed, what you expect if the insulin receptor works is that the glucose would go in. Then the glucose would get oxidized and turned into energy. But here’s the problem. When the hepatocyte has insulin receptors that don’t work, you’ve got that insulin on the outside, and the glucose never made it in. But what also happens on the inside of the hepatocyte is it was assumed that the glucose was going to get in. So what it does is it turns off fatty acid oxidation, thinking, “Guys, we don’t need to burn our fatty acids. We’ve got some glucose coming in.”
So when the glucose is not there, and you’re not burning off fatty acids, very common for people to feel fatigued because nothing is burning for energy. But here is the secondary sequela; where are all those fatty acids going, right? Well, the liver may try to repackage them as triglycerides. Sometimes, they stay in the hepatocyte or get shifted out of the liver into the bloodstream as VLDL or very low-density lipoprotein. You might see it as a high triglyceride shift in a standard lipid panel. So, when all of us are talking about getting a triglyceride level to around 70 as your 8+ goal, when I start seeing triglycerides rising, we wait until they’re 150, even though that’s the cutoff for our labs. When we see it at 150, we know they are shunting triglycerides out of the liver.
So that will happen many times before we find impaired fasting glucose. So look at your triglycerides, fasting triglycerides, as an emerging or early biomarker of insulin dysfunction. So this is another diagram that says that if the triglycerides are being created because the fatty acids are being oxidized, they can stay in the liver. Then that makes steatosis or the fatty liver, or they can be pushed out, and they turn into lipoproteins. We’re going to talk about that in just a second. The body is like, “What are we going to do with these fatty acids?” We can’t try to shove them into places because nobody wants them. To that point, the liver is like, “I don’t want them, but I will keep some with me.” Or the liver would have these fatty acids transported and stuck to the blood vessel walls.
And then the blood vessels and arteries are like, “Well, I don’t want them; I’ll put them underneath my endothelium.” And so that’s how you get atherogenesis. The muscles are like, “I don’t want them, but I’ll take some.” That’s how you get the fatty streaks in your muscles. So when the liver is getting bogged down with steatosis, inflammation occurs in the body and produces this feed-forward cycle inside the hepatocyte, damaging the liver. You’re getting cellular death; you’re getting fibrosis, which is just an extension of what happens when we don’t address the core issues for fatty liver: inflammation and insulin resistance. So, we look for subtle rises in AST, ALT, and GGT; remember that it is a liver-based enzyme.
Hormone Enzymes & Inflammation
GGT enzymes in the liver are smoke detectors and tell us how much oxidative stress is going on. Will we look at HSCRP and APOB to see the output of this liver? Is it starting to dump excess fatty acids through VLDL, APOB, or triglycerides? And how it picks that is just genetics, honestly. So I look for liver markers to tell me what’s going on in the liver as a sign of what’s happening everywhere. Because that might be the genetic weak spot of the person, some people are genetically vulnerable just in terms of their lipid profiles. To that point, we can look for something called metabolic dyslipidemia. You know this as high triglycerides and low HDL. You can specifically look for a ratio; an optimal balance is three and lower. It starts going from three to five and then five to eight, like eight is almost pathognomonic of insulin resistance. You’re just reaching becoming more and more insulin resistant.
As the number increases for that trig over HDL ratio, that is a simple, easy way to screen for insulin resistance. Now some people look 3.0 on this but still have insulin resistance. So there are other tests you do. This is a way to find those who show insulin resistance through lipids. And remember, everybody is different. Women with PCOS could have amazing lipids but could express an increase or decrease of hormones associated with insulin, estrogen, and inflammation. So look for something other than one test or ratio to indicate whether they’ve got it. You’re looking to see what could be the place where we will find the clue.
So let’s use the word healthy. A healthy person has VLDL that looks to be a healthy normal size in their bodies, and they have normal LDL and HDL. But now look at what happens when you get insulin resistance. These VLDL ls start to pump up with triglycerides. That’s why they’re fattening up. It’s lipotoxicity. So if you start looking at the VLDL three numbers in a lipoprotein profile, you’ll see that that number is creeping up, and there are more of them, and their size is bigger. Now with LDL, what happens is that the cholesterol amount within the top and the bottom is the same. If I pop all these water balloons, it’s the same amount of LDL cholesterol. However, that amount of LDL cholesterol in insulin resistance is repackaged in small dense LDL.
How Does Functional Medicine Play Its Part?
Now we understand that there may be some of you who cannot or do not have access to this testing, or your patients cannot afford it, and that’s why we answered the questions and looked for other clues of insulin resistance and treat the root cause that is affecting the body. Look for signs of inflammation and other overlapping profiles of insulin resistance. The particle number is higher when they’re insulin resistance. So cholesterol is the same, whereas the particle number is more elevated, and small dense LDL is more atherogenic. Treat it because whether or not you have access to knowing the LDL particle, there should be something in your head that says, “Man, even though this person’s LDL cholesterol looks good, they have tons of inflammation and insulin resistance; I can’t be sure that they don’t have higher particle number.” You might assume that they do this just to be safe.
The other thing that happens in insulin resistance is that the HDL or the healthy cholesterol tends to become small. So that’s not very good because the efflux capacity of HDL is lessened when it’s smaller. So we like the larger HDL, if you will. Access to these tests would give you a solid indication of what’s going on with your patient from a cardiometabolic perspective.
When it comes to these tests, it is important to utilize them to determine the patient’s timeline when they have inflammation or insulin resistance in their bodies, affecting their quality of life. However, many people would often express that these tests are expensive and would go with the gold standard of testing for affordability and be able to decide if it is worth it to better their health and wellness.
Look For Cardiometabolic Risk Patterns
So when it comes to cardiometabolic risk factor patterns, we look at the insulin aspect and how it correlates with mitochondrial dysfunction associated with insulin resistance and inflammation. A research article mentions how two mitochondrial dysfunctions can affect the body. Okay, let’s talk about the first issue, which is the quantity issue. One could be endotoxins that we encounter in our environment, or two; it can be genetically passed along from generation to generation. So the two types could indicate that you don’t have enough mitochondria. So that’s a quantity issue. The other problem is it’s a quality issue. You got plenty of them; they don’t work well, so they don’t have high output or at least normal results. Now how does this play out in the body? So out in the periphery, your muscles, adipocytes, and liver, you have mitochondria in those cells, and it’s their job to energize that lock and jiggle. So if your mitochondria are in the right number, you’ve got plenty to energize the insulin cascade lock and jiggle.
Interesting, right? So here it is in summary, if you don’t have enough mitochondria, which is the problem in the periphery, you get insulin resistance because the lock and jiggle aren’t working well. But if you do not have the mitochondria working well in the pancreas, especially in the beta cell, you don’t secrete insulin. So you still get hyperglycemia; you don’t have high insulin state. When this happens, we know your brain should be hurting, but hopefully, it will come together slowly.
Another article mentions that it connects mitochondrial dysfunction with type two diabetes, and poor maternal nutrition can prime it. This one talks about how fatty liver is associated with lipotoxicity, right? That’s that increased fatty acid, and oxidative stress, which, remember, is the byproduct of inflammation. ATP depletion and mitochondrial dysfunction. When this happens, it can affect the liver, which then turns into the fatty liver, and can also be associated with gut dysfunction, which leads to chronic inflammation, elevated insulin resistance, mitochondrial dysfunction, and many more. These chronic metabolic diseases are connected, and there are ways to reduce these symptoms from affecting the body.
Conclusion
When having a conversation with their doctors, many patients know that the same drivers affect a whole host of other phenotypes, all commonly rooted in inflammation, insulin, and toxicity. So when many people realize these factors are the root cause, doctors will work with many associated medical providers to develop personalized functional treatment plans. So remember, you always have to use the timeline and the matrix to kind of help you know where do you start with this patient, and for some people, it might be you’re just going to tweak a little bit of lifestyle because all they’re working on is changing their body count. So it’s one of the blessings of functional medicine that we were able to turn off the inflammation in the gut, which helps reduce the toxic impact burdening the liver. It also allows the individual to find out what works or doesn’t work with their bodies and take these small steps to improve their health.
We hope you have fresh eyes about inflammation, insulin, and toxicity and how it is at the root of so many conditions that your patients are facing. And how through very simple and effective lifestyle and nutraceutical interventions, you can change that signaling and change the course of their symptoms today and the risks they have tomorrow.
Dr. Alex Jimenez, D.C., presents how metabolic connections are causing a chain reaction to major chronic diseases in this 2-part series. Many factors often play a role in our health and wellness. It can lead to overlapping risk factors associated with pain-like symptoms in the muscles, joints, and vital organs. Part 2 will continue the presentation on metabolic connections with major chronic diseases. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with metabolic connections. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Jimenez, D.C., makes use of this information as an educational service. Disclaimer
How Inflammation Affects The Body
Dr. Alex Jimenez, D.C., presents: So here you have a lean set of adipocytes on the left, and then as they start to plump up with more cellular weight, you can see those macrophages, the green boogies come around looking, saying, “Hey, what’s going on here? It doesn’t look right.” So they are investigating, and this causes local cell death; it’s just a part of the inflammatory cascade. So there is also another mechanism happening here. Those adipocytes are not just getting plumper by accident; it’s often related to a calorie surfette. So this nutrient overload damages the endoplasmic reticulum, leading to more inflammation. What these cells and the adipocytes are trying to do is protect themselves from glucose and lipo toxicity.
And the whole cell, the adipocyte cell, is creating these caps that are trying to say, “Please stop, we can’t take any more glucose, we can’t take any more lipids.” It’s a protection mechanism known as insulin resistance. It’s not just some random thing happening. It is the body’s way of trying to prevent glucose and lipotoxicity. Now that the inflammation alarm is occurring more than just in the adipocytes, it’s getting systemic. Other tissues and organs are starting to feel the same burden of the calorie surfette, causing inflammation and cell death. So glucose and lipotoxicity look like fatty liver when dealing with the liver. And you can also have it just like fatty liver progresses to cirrhosis with hepatocyte death. The same mechanism that’s happening in muscle cells. So our skeletal muscle cells specifically see cell death after inflammation and see fatty deposition.
The best way to think about it is, for example, the cows raised for food consumption and how they have marbled. So that’s the fatty deposition. And in humans, you can think about how people become sarcopenic as they become more and more insulin resistant. It’s the same phenomenon when body tissue tries to protect itself from glucolipotoxicity, causing a local inflammatory response. It becomes an endocrine response when it starts targeting other tissues in the periphery, whether the liver, muscle, bone, or brain; it’s just whatever is happening; they’re in the visceral adipocytes that can occur in other tissues. So that’s your paracrine effect. And then it can go viral, if you will.
Inflammation Associated With Insulin Resistance
Dr. Alex Jimenez, D.C., presents: You’re getting this local and systemic pro-inflammatory response coupled with insulin resistance, returning to this protection mechanism against glucose and lipotoxicity. Here you see how the blood vessels in our arteries get caught in the loop of fatty deposition and cell death. So you’ll see leaky blood vessels and fatty deposits, and you’ll see damage and pro-atherogenesis. Now, this is something we explained in AFMCP for the cardiometabolic module. And that is the physiology behind the insulin receptor. This is known as the lock and jiggle technique. So you have to have insulin lock into the insulin receptor up at the top., which is known as the lock.
And then there’s a phosphorylation cascade called the jiggle that then creates this cascade that ultimately causes the glucose-4 channels to open up the glucose-4 receptors to go into the cell so that it can be then the glucose, which is then utilized for energy production by the mitochondria. Of course, insulin resistance is where that receptor isn’t sticky or as responsive. And so not only do you fail to get glucose into the cell for energy production, but you are also rendering a hyper insulin state in the periphery. So you get hyperinsulinemia as well as hyperglycemia in this mechanism. So what can we do about that? Well, many nutrients have been shown to improve the lock and jiggle things that can improve the glucose-4 transporters coming up towards the periphery.
Anti-Inflammatory Supplements Reduce Inflammation
Dr. Alex Jimenez, D.C., presents: You see these listed here: vanadium, chromium, cinnamon alpha lipoic acid, biotin, and another relatively new player, berberine. Berberine is a botanical that can dampen all primary pro-inflammatory signals. So what precedes these comorbidities often and it’s insulin dysfunction. Well, what precedes insulin dysfunction many times? Inflammation or toxicity. So if berberine is helping the primary inflammation issue, it will address the downstream insulin resistance and all the comorbidities that can happen. So consider berberine as your option. So again, this shows you that if you can reduce inflammation up here at the top, you can minimize many cascade effects downstream. Berberine specifically seems to act in the microbiome layer. It modulates the gut microbiota. It may create some immune tolerance, therefore not rendering as much inflammation.
So consider berberine as one of the tools you can use to support insulin dysfunction and insulin resistance-related comorbidities. Berberine seems to increase insulin receptor expression, so the lock and jiggle work more effectively and improve the cascade with the glucose-4 transporters. That’s one mechanism by which you can start to find the root cause of many of the conditions we discussed when you see paracrine and endocrine glucose toxicity, lipotoxicity organ damage. Now another mechanism for you to consider is leveraging NF kappa B. So the goal is to keep NF kappa B grounded because as long as they don’t translocate, a host of inflammation signals do not get triggered.
So our goal is to keep NF kappa B grounded. How can we do that? Well, we can use NF kappa B inhibitors. So in this presentation of treatment options for any comorbidities related to insulin dysfunction, there are many ways to reduce these overlapping conditions affecting our bodies. So you can directly affect insulin resistance through anti-inflammatory supplements or indirectly help insulin resistance or insulin dysfunction by leveraging things against inflammation. Cause if you remember, insulin dysfunction is what then causes all those comorbidities. But what causes insulin dysfunction is generally inflammation or toxins. So our goal is to address pro-inflammatory things. Because if we can address pro-inflammatory things and nip the insulin dysfunction in the bud, we can prevent all the downstream organ damage or organ dysfunction.
Reducing Inflammation In The Body
Dr. Alex Jimenez, D.C., presents: Let’s move on to the next section that you can leverage or reduce the inflammation and insulin soup damage if you will, that the genes bathe in the body. This is the one you’ll often hear in our presentation, and that’s because, actually, in functional medicine, we help fix the gut. That’s usually where you need to go. And this is the pathophysiology for why we do that in cardiometabolic medicine. So if you have that poor or sad diet, that modern western diet with bad fats, it will directly damage your microbiome. That change in the microbiome can render increased intestinal permeability. And now lipopolysaccharides can translocate or leak into the bloodstream. To that point, the immune system says, “Oh no way, buddy. You’re not supposed to be in here.” You’ve got these endotoxins in there, and now there is a local and systemic inflammatory response that inflammation will drive the insulin dysfunction, which will cause the metabolic disorders that come after that.
Whatever the person’s genetically prone to, it gets clicked on epigenetically. So remember, if you can quell the inflammation in the microbiome, meaning create this tolerant and strong microbiome, you can reduce the inflammatory tone of the entire body. And when you reduce that, it’s been shown that it sets the insulin sensitivity. So the lower the inflammation, the higher the insulin sensitivity related to the microbiome. So surprise, it’s been shown that probiotics are associated with improved insulin sensitivity. So the right probiotics will create immune tolerance. Microbiome strength and modulation occur with probiotics. And so insulin sensitivity is preserved or regained based on where you are. So please consider that as another indirect mechanism or treatment option for leveraging cardiometabolic health for patients.
Probiotics
Dr. Alex Jimenez, D.C., presents: So when it comes to probiotics, we will use them in someone who might also concurrently have irritable bowel syndrome or food allergies. We might pick probiotics over NF kappa B inhibitors if they also have insulin resistance issues. But if they have many neurocognitive problems, we might start with the NF kappa B. So, that’s the way you can decide which ones to pick. Now, remember, when talking with patients, it is important to discuss how their eating habits are causing inflammation in their bodies. It is also important to note that it’s not just a quality conversation; it’s a quantity conversation and an immune conversation.
This reminds you that when you fix the gut by feeding it well and reducing its inflammatory tone, you get a host of other preventative benefits; you stop or at least reduce the strength of the dysfunction. And you can see that, ultimately can reduce the overlapping risk of obesity, diabetes, and metabolic syndrome. We are trying to drive home that metabolic endotoxemia, or just managing the microbiome, is a powerful tool to help your insulin-resistant or cardiometabolic patients. So much data tells us that we cannot just make the conversation about eating right and exercising.
It’s so much beyond that. So the more we can improve the gut microbiota, we can change inflammation signals through proper diet, exercise, stress management, sleep, all the other things we’ve been talking about, and fixing the gums and the teeth. The less the inflammation, the less the insulin dysfunction and, therefore, the less all those downstream disease effects. So what we want to make sure you know is to go to the gut and make sure that the gut microbiome is happy and tolerant. It’s one of the most potent ways to influence a healthy cardiometabolic phenotype. And aside, although it was a bigger thing a decade ago, non-caloric artificial sweeteners do as they might be non-caloric. And so people may be tricked into thinking it’s zero sugar.
But here’s the problem. These artificial sweeteners can interfere with healthy microbiome compositions and induce more type two phenotypes. So, even though you think you’re getting the benefit with no calories, you’re going to increase your risk for diabetes more through its effect on the gut microbiome. All right, We’ve made it through objective one. Hopefully, you’ve learned that insulin, inflammation, adipokines, and all the other things that happen in the endocrine response affect many organs. So let’s now start to look at emerging risk markers. Okay, we’ve talked a bit about TMAO. Again, that’s still a relevant concept here with gut and insulin resistance. So we want to make sure that you look at TMAO not as the end all be all but as another emerging biomarker that could give you a clue about microbiome health in general.
Looking For The Inflammatory Markers
Dr. Alex Jimenez, D.C., presents: We look at elevated TMAO to help the patient recognize that they have changed their eating habits. Most of the time, we help patients reduce unhealthy animal proteins and increase their plant-based nutrients. It’s generally how many doctors use it in standard medical practice. Alright, now another emerging biomarker, okay, and it sounds funny to call it emerging because it seems so obvious, and that is insulin. Our standard of care is centralized around glucose, fasting glucose, to our postprandial glucose A1C as a measure of glucose. We are glucose so centric and need insulin as an emerging biomarker if we try to be preventative and proactive.
And as you remember, we talked yesterday that fasting insulin in the bottom of the first quartile of your reference range for fasting insulin might be where you want to go. And for us in the US, that tends to be between five and seven as a unit. So notice that this is the pathophysiology of type two diabetes. So type two diabetes can happen from insulin resistance; it can also occur from mitochondrial problems. So pathophysiology of type two diabetes could be because your pancreas is not secreting enough insulin. So again, this is that little 20% that we talk about the majority of the people who are getting type two diabetes; it’s from insulin resistance, as we would suspect, from a hyper insulin problem. But there is this group of people who have damaged mitochondria, and they are not outputting insulin.
So their blood sugar rises, and they get type two diabetes. Okay, then the question is, if there is a problem with pancreatic beta cells, why is there a problem? Is the glucose going up because the muscles have insulin resistance, so they cannot capture and bring in glucose? So is it the liver that’s hepatic insulin resistant that cannot take in glucose for energy? Why is this glucose running around in the bloodstream? That’s what this is paraphrasing. So contributing role, you have to look at the adipocytes; you have to look for visceral adiposity. You must see if this person is just a big belly fat inflammatory-like catalyst. What can we do to reduce that? Is the inflammation coming from the microbiome?
Conclusion
Dr. Alex Jimenez, D.C., presents: Even the kidney can play a role in this, right? Like perhaps the kidney has increased glucose reabsorption. Why? Could it be because of an oxidative stress hit to the kidney, or could it be in the HPA axis, the hypothalamus pituitary adrenal axis where you’re getting this cortisol response and this sympathetic nervous system response that’s generating inflammation and driving the blood insulin and blood sugar disturbances? In Part 2, we will talk here about the liver. It’s a common player for many people, even if they don’t have fulminant fatty liver disease; it’s generally a subtle and common player for people with cardiometabolic dysfunction. So remember, we’ve got the visceral adiposity causing inflammation and insulin resistance with atherogenesis, and the liver is like this innocent bystander caught up in the drama. It’s happening before sometimes the atherogenesis starts.
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