Back Clinic Functional Medicine Team. Functional medicine is an evolution in the practice of medicine that better addresses the healthcare needs of the 21st century. By shifting the traditional disease-centered focus of medical practice to a more patient-centered approach, functional medicine addresses the whole person, not just an isolated set of symptoms.
Practitioners spend time with their patients, listening to their histories and looking at the interactions among genetic, environmental, and lifestyle factors that can influence long-term health and complex, chronic disease. In this way, functional medicine supports the unique expression of health and vitality for each individual.
By changing the disease-centered focus of medical practice to this patient-centered approach, our physicians are able to support the healing process by viewing health and illness as part of a cycle in which all components of the human biological system interact dynamically with the environment. This process helps to seek and identify genetic, lifestyle, and environmental factors that may shift a person’s health from illness to well-being.
As individuals try to avoid sugar as best as possible, alternative sweeteners are becoming more popular. A new addition is monk fruit sweetener, also called monk fruit extract. Monk fruit is a small, round fruit native to southern China. Unlike some chemically based sugar alternatives, monk fruit extract is considered natural. The sweetener has been around for decades but has become more available in the United States. The zero-calorie extract can be used as a standalone sweetener in foods and drinks and as a flavor enhancer.
Monk Fruit Sugar Alternative
Manufacturers remove the seeds and skin, crush the fruit, and extract the juice, which is then dried into a concentrated powder. Unlike most fruits, the natural sugars in monk fruit are not what gives it its sweetness. Instead, the intense sweetness comes from antioxidants (commonly found in plant foods, antioxidants fight off free radicals that can cause health problems like cancer and heart disease) called mogrosides. The mogroside is the sweetest part of the fruit, with a taste over 100 times sweeter than sugar and no calories.
Safe For Consumption
Monk fruit has the generally recognized as safe -GRAS label from the U.S. Food and Drug Administration with no reported side effects. However, it is advised to read the ingredients label before buying this sweetener. Some of the cheaper products combine other sweeteners with monk fruit extract. Some contain erythritol, a sugar alcohol that can cause stomach bloating or upset stomach.
Use
It has been found to be a healthy option for lowering overall sugar intake. However, consuming monk fruit or any sweetener should be done in moderation and with a healthy nutrition plan. It comes in powder or liquid form. As a natural alternative, it can be used:
As s sugar substitute for favorite baking, cooking, soup, sauce recipes, etc.
For drinks like coffee, tea, lemonade, smoothies, etc.
Added on breakfast dishes like oatmeal or yogurt.
Whipped into frosting or a mousse.
The ultra-sweetness means that little is required as it goes a long way. It is recommended to drink regular water or tea and eat foods without the sweetener because, over time, the taste buds adjust and do not need the sweetener as much. Consult a doctor, dietician, or nutritionist to determine if this sugar alternative is right for you and the benefits.
What Is It?
References
Chen, W J et al. “The antioxidant activities of natural sweeteners, mogrosides, from fruits of Siraitia grosvenori.” International journal of food sciences and nutrition vol. 58,7 (2007): 548-56. doi:10.1080/09637480701336360
EFSA Panel on Food Additives and Flavourings (FAF) et al. “Safety of use of Monk fruit extract as a food additive in different food categories.” EFSA journal. European Food Safety Authority vol. 17,12 e05921. 11 Dec. 2019, doi:10.2903/j.efsa.2019.5921
Lobo, V et al. “Free radicals, antioxidants, and functional foods: Impact on human health.” Pharmacognosy reviews vol. 4,8 (2010): 118-26. doi:10.4103/0973-7847.70902
Pawar, Rahul S et al. “Sweeteners from plants–with emphasis on Stevia rebaudiana (Bertoni) and Siraitia grosvenorii (Swingle).” Analytical and bioanalytical chemistry vol. 405,13 (2013): 4397-407. doi:10.1007/s00216-012-6693-0
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.
High Blood Pressure and Physical Activity: Blood pressure flows throughout the body to meet metabolic demands. During periods of physiological stress like physical activity, exercise, or feeling overwhelmed, blood pressure can increase for a short period but is not considered dangerous or unhealthy. However, when an individual’s baseline resting blood pressure readings stay high, the risk of developing serious health conditions increases. High blood pressure is reversible with lifestyle adjustments and physical activity for a more healthy and sustainable level.
High Blood Pressure and Physical Activity
Everything individuals need to know and understand about high blood pressure includes:
Common causes
Healthy readings
Monitoring pressure
Beneficial activities to lower blood pressure and improve health.
Blood pressure measures the force exerted on the circulatory system. Blood pressure changes throughout the day, depending on the following:
Nutrition
Activity levels
Stress levels
Medical comorbidities
Unlike heart rate or temperature, blood pressure is two separate measurements. Typically seen as a fraction, for example – 120/80 mmHg, each number gives the medical provider information about the function and health of the vascular system:
Systolic
Written as the top number of the measurement, systolic blood pressure refers to the force exerted against the blood vessels during a heartbeat.
This value represents the highest pressure on the arteries, veins, and capillaries.
Diastolic
The bottom number/measurement, the diastolic reading, represents the pressure the vascular system is subjected to between heartbeats.
In most cases, elevated diastolic blood pressure values are seen in individuals with high systolic blood pressure.
Readings
According to the CDC, a healthy blood pressure reading is 120/80 mmHg. As blood pressure changes throughout the day, it is recommended to have a baseline level/when at rest to remain as close as possible to these values. When baseline levels remain high, the risk of developing serious medical complications increases. Criteria for different stages of diagnosis include:
Elevated blood pressure – 120-129 mmHg / 80 or less mmHg.
Stage 1 hypertension – 130-139 mmHg / 80-89 mmHg.
Stage 2 hypertension – 140 or higher mmHg / 90 or higher mmHg.
Prolonged exposure to high pressure damages the vessels and heart.
Measurements
The first step to assessing baseline blood pressure is taking regular and accurate readings. An automatic blood pressure cuff and monitor at home can record readings to determine baseline values. Various factors can contribute to inaccurate readings. Here are a few tips for avoiding inaccuracy:
Keep the arm being measured at the height of the heart.
Avoid taking blood pressure after exercise or stress.
Double-check readings on the opposite arm when possible.
Try to take readings at a similar time during a rest period.
After each reading, record values in a journal for the primary care provider.
Performing daily blood pressure readings for a few weeks can be beneficial to determine baseline levels.
Physical Activity
Aerobic activities increase the body’s need for oxygen. Getting the muscles active and moving during physical activity increases the demand for oxygen, which is why breathing and heart rate increase. The cardiovascular system includes the heart, arteries, and veins. Additional stress is added when the system goes through aerobic activity to maintain metabolic levels, improving strength and endurance. Regular aerobic exercise can decrease high baseline pressure because a stronger heart and vascular system do not need to exert as much energy to maintain cell function. Aerobic activities include:
Brisk Walking
A low-impact aerobic exercise, brisk walking, has been shown to reduce baseline systolic blood pressure in individuals who participated in supervised walking sessions over six months.
Gardening
Gardening activities like digging and lifting are considered moderate-intensity exercises. It is a recommended low-impact option for individuals of all ages.
Bicycle Riding
Cycling has been shown to offer short and long-term benefits for managing blood pressure.
It is common for pressure to increase while biking; studies have shown that regular cycling can reduce baseline systolic and diastolic blood pressure over six months.
It is recommended to start slow. As confidence builds and cardiovascular endurance increases, longer and more regular bike rides become easier to integrate into a routine.
Dancing
All forms of dancing can help to improve cardio endurance and strength, which has been shown to reduce systolic and diastolic blood pressure readings.
Whether line dancing, partner dancing, or dancing alone, dancing regularly can help reduce stress and blood pressure levels.
Hypertension Nutrition
References
Cardoso, Crivaldo Gomes Jr, et al. “Acute and chronic effects of aerobic and resistance exercise on ambulatory blood pressure.” Clinics (Sao Paulo, Brazil) vol. 65,3 (2010): 317-25. doi:10.1590/S1807-59322010000300013
Conceição, Lino Sergio Rocha, et al. “Effect of dance therapy on blood pressure and exercise capacity of individuals with hypertension: A systematic review and meta-analysis.” International journal of cardiology vol. 220 (2016): 553-7. doi:10.1016/j.ijcard.2016.06.182
Hollingworth, M et al. “Dose-response associations between cycling activity and risk of hypertension in regular cyclists: The UK Cycling for Health Study.” Journal of human hypertension vol. 29,4 (2015): 219-23. doi:10.1038/jhh.2014.89
Mandini, Simona, et al. “Walking and hypertension: greater reductions in subjects with higher baseline systolic blood pressure following six months of guided walking.” PeerJ vol. 6 e5471. 30 Aug. 2018, doi:10.7717/peerj.5471
Sapra A, Malik A, Bhandari P. Vital Sign Assessment. [Updated 2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: www.ncbi.nlm.nih.gov/books/NBK553213/
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.
Nowadays, many individuals are incorporating various fruits, vegetables, lean portions of meat, and healthy fats and oils into their diet to get all the vitamins and minerals that their bodies need. The body needs these nutrients biotransformed into energy for the muscles, joints, and vital organs. When normal factors like eating unhealthy foods, not getting enough exercise, and underlying conditions affect the body, it can cause somato-visceral issues that correlate with disorders that push many individuals to feel unwell and miserable. Luckily, some supplements and vitamins like magnesium help with overall health and can reduce the effects of these environmental factors that are causing pain-like symptoms in the body. In this 3-part series, we will look at the impact of magnesium helping the body and what foods contain magnesium. Part 1 looks at how magnesium correlates with heart health. Part 2 looks at how magnesium helps with blood pressure. We refer our patients to certified medical providers that provide many available therapy treatments for individuals suffering from underlying conditions associated with low magnesium levels affecting the body and correlated to many underlying conditions affecting a person’s health and wellness. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis. We accept that education is a marvelous way when asking our providers’ hard-hitting questions at the patient’s request and acknowledgment. Dr. Jimenez, D.C., only utilizes this information as an educational service. Disclaimer
An Overview Of Magnesium
Have you been experiencing muscle numbness in different locations in your body? What about muscle cramps or fatigue? Or have you been experiencing issues with your heart? Suppose you have been dealing with these overlapping issues that are affecting not only your body but your overall health. In that case, it could correlate with your body’s low magnesium levels. Studies reveal that this essential supplement is the body’s fourth most abundant cation when it comes to magnesium since it is a co-factor for multiple enzymic reactions. Magnesium helps with cellular energy metabolism, so the muscles and vital organs can function properly and helps replenish intracellular and extracellular water intake. Magnesium helps with the body’s metabolism, but it can also help reduce the effects of chronic conditions affecting the body.
How Magnesium Helps The Body
Additional studies reveal that magnesium is important in lowering chronic conditions’ effects on the body. Magnesium could help many individuals dealing with cardiovascular issues or chronic diseases associated with the heart or the muscles surrounding the upper and lower extremities of the body. How can magnesium help with overlapping health disorders that can affect the body? Studies show that taking magnesium can help prevent and treat many common health conditions:
Metabolic syndrome
Diabetes
Headaches
Cardiac arrhythmias
Many of these conditions are associated with everyday factors that can affect the body and lead to chronic disorders that can cause pain to the muscles, joints, and vital organs. So, taking magnesium can reduce pre-existing conditions from elevating the body and causing more harm.
Magnesium In Food
Biomedical physiologist Alex Jimenez mentions that magnesium supplementation usually causes diarrhea and explains what foods are high in magnesium. Surprisingly, avocados and nuts have a chaulk full of magnesium. One medium avocado has about 60 milligrams of magnesium, while nuts, especially cashews, have approximately 83 milligrams of magnesium. One cup of almonds has about 383 milligrams of magnesium. It also has 1000 milligrams of potassium, which we covered in an earlier video, and around 30 grams of protein. So this is a good snack to break up the cup into about half-cup serving throughout the day and snack on as you’re going. The second one is beans or legumes; for example, one cup of black beans cooked has around 120 milligrams of magnesium. And then wild rice is also a good source of magnesium. So what are the signs of low magnesium? The symptoms of low magnesium are muscle spasms, lethargy, irregular heartbeat, pins and needles in the hands or legs, high blood pressure, and depression. This video was informative for you regarding magnesium, where to find it, and the best supplemental forms to take it in. Thank you again, and tune in next time.
Foods Containing Magnesium
When it comes to taking magnesium, there are many ways to incorporate magnesium into the body’s system. Some people take it in supplemental form, while others eat healthy, nutritious foods with a chaulk full of magnesium to get the recommended amount. Some of the foods that are riched in magnesium include:
Dark Chocolate=65 mg of magnesium
Avocados=58 mg of magnesium
Legumes=120 mg of magnesium
Tofu= 35 mg of magnesium
What is great about getting these magnesium riched foods is that they can be in any dishes we consume for breakfast, lunch, and dinner. Incorporating magnesium in a healthy diet can help boost the body’s energy levels and help support the major organs, joints, and muscles from various disorders.
Conclusion
Magnesium is an essential supplement that the body needs to boost energy levels and help reduce the effects of pain-like symptoms that can cause dysfunction in the body. Whether it is in supplemental form or eating it in healthy dishes, magnesium is an important supplement that the body needs to function properly.
References
Fiorentini, Diana, et al. “Magnesium: Biochemistry, Nutrition, Detection, and Social Impact of Diseases Linked to Its Deficiency.” Nutrients, U.S. National Library of Medicine, 30 Mar. 2021, www.ncbi.nlm.nih.gov/pmc/articles/PMC8065437/.
Schwalfenberg, Gerry K, and Stephen J Genuis. “The Importance of Magnesium in Clinical Healthcare.” Scientifica, U.S. National Library of Medicine, 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5637834/.
Having and maintaining flexibility in the joints depends on the connective tissues surrounding the muscles. Proper lubrication in the connective tissues enables the fibers to slide over one another easily. Naturally occurring proteins collagen and elastin are key components of connective tissue that provide strength and elasticity. The more elastic the connective tissue, the more flexibility around the joint. If it is becoming difficult to stretch out or there is chronic stiffness and tightness, there are foods that help maintain flexibility and enhance overall health.
Foods That Help Maintain Flexibility
Joint flexibility means functioning connective tissues that join the skeleton and muscles and the ability of different body parts to extend and complete motions. Connecting tissues assists with movement and stabilization. These issues include:
Ligaments
Ligamentscan be band-shaped or string-shaped collagen fibers that connect bones.
Tendons
Tendonsare similar to ligaments and are band or string shaped but connect muscles to the bones.
Fascia
Fascia is a densely woven mesh that wraps around the blood vessels, bones, muscles, organs, and nerves.
Flexibility keeps the muscles active and mobile as they are necessary for daily physical activities. When these tissues become stiff from inactivity or an unhealthy diet, it limits the body’s range of movement and increases the risk of injury. Stretching improves flexibility, and adding foods to a nutrition plan will help maintain limberness.
Nutrition
A nutrition plan full of vitamins, minerals, and antioxidants will nourish connecting tissues and cells and increase collagen production. Foods rich in essential fatty acids/EFAs, vitamin C, sulfur, and water will promote healthy connective tissue for enhanced flexibility.
Fatty Acids
Essential fatty acids include omega-3 and omega-6, primarily found in fish, flax seeds, and liquid oils.
These fatty acids are essential because they cannot be made in the body.
Foods likefatty fish, flax seeds, walnuts, or supplements, can help achieve the proper ratio.
For individuals not too keen on fish, consider omega-3 supplements.
Collagen
Collagen is the main protein from connective tissue, and vitamin C is essential for collagen production.
Vitamin C-rich foods – oranges, bell peppers, broccoli, strawberries, tomatoes, leafy green vegetables, raspberries, pineapple, cruciferous vegetables, parsley, and watermelon.
Make various smoothie recipes for breakfast or an afternoon snack.
Sulfur helps maintain the flexible bonds in connective tissues.
Animal proteins that provide sulfur include fish, poultry, beef, and eggs.
Vegetable sources include Brussels sprouts, cabbage, broccoli, cauliflower, onions, and garlic.
Hydration
Water is not considered food as it contains no calories, but it is vital as it makes up 76 percent of the muscles. A high percentage of water content is the key to muscle elasticity. When the body is dehydrated, it holds onto water, causing fluid retention and stiffness. The more the muscles stay dehydrated, the more they have trouble recovering from physical activities, fatigue levels increase, the range of motion decreases, and the risk of injury increases. Don’t wait until you are thirsty. Stay hydrated throughout the day to keep the joints lubricated and energy levels high.
Fruits high in water include:
Strawberries
Watermelon
Cantaloupe
Peaches
Grapefruit
Pineapple
Apples
Pears
Vegetables high in water include:
Cucumber
Lettuce
Zucchini
Celery
Eggplant
Limit Salt and Sugar Intake
Processed foods tend to have a high salt content.
Too much salt causes the joints to swell as the body retains fluid.
Keeping sugar intake low is important in enhancing flexibility.
This is because sugar breaks down the collagen in the skin and connective tissues.
This means avoiding processed foods, ready meals, and junk food.
Flexibility can be improved by eliminating foods that destroy collagen, focusing on foods that reduce insulin spikes, and maintaining hydration in the connective tissues. A nutritionist can develop a personalized nutrition plan for optimal neuromusculoskeletal health.
Foods That Help Maintain Flexibility
References
Beba, Mohammad et al. “The effect of curcumin supplementation on delayed-onset muscle soreness, inflammation, muscle strength, and joint flexibility: A systematic review and dose-response meta-analysis of randomized controlled trials.” Phytotherapy research: PTR vol. 36,7 (2022): 2767-2778. doi:10.1002/ptr.7477
Kviatkovsky, Shiloah A et al. “Collagen peptide supplementation for pain and function: is it effective?.” Current opinion in clinical nutrition and metabolic care vol. 25,6 (2022): 401-406. doi:10.1097/MCO.0000000000000870
MacKay, Douglas, and Alan L Miller. “Nutritional support for wound healing.” Alternative medicine review: a journal of clinical therapeutic vol. 8,4 (2003): 359-77.
Shaw, Gregory, et al. “Vitamin C-enriched gelatin supplementation before intermittent activity augments collagen synthesis.” The American journal of clinical nutrition vol. 105,1 (2017): 136-143. doi:10.3945/ajcn.116.138594
Zdzieblik, Denise, et al. “Improvement of activity-related knee joint discomfort following supplementation of specific collagen peptides.” Applied physiology, nutrition, and metabolism = Physiologie applique, nutrition et metabolism vol. 42,6 (2017): 588-595. doi:10.1139/apnm-2016-0390
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