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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 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 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.
Bicycle riding is a form of transportation and a popular leisure and exercise activity. It helps with brain, heart, and whole body health. Whether recreational or pro cyclist, road or mountain biking, injuries are most often caused by overuse, repetitive strain, or a traumatic fall. If not treated properly by a medical professional, bicycle riding injuries can develop into long-term problems. Chiropractic care, sports massage, and decompression therapy combined with functional medicine can alleviate symptoms, rehabilitate the muscles, release compressed nerves, and restore mobility and function.
Bicycle Riding Injuries
Long-term cycling can cause muscle fatigue, leading to various injuries.
Overuse injuries occur when performing the same motion over and over again.
Musculoskeletal injuries range from sprains, torn ligaments, and tendons to fractures from crashes and falls.
Bicycle Setup
Not having the correct bike setup for the individual affects posture.
A seat that is too high causes the hips to rotate, leading to hip, back, and knee pain.
A seat that is too low causes over-flexion of the knees and pain.
Improper footwear not set in the right position can lead to pain in the calves and feet.
Handlebars that are too far forward can cause neck, shoulder, and back problems.
If any discomfort symptoms result from cycling, it’s recommended to get checked by a medical professional as soon as possible. After a correct diagnosis, resolving the issue/s could involve altering the bike setup to reduce the strain on certain body parts. Conversely, a condition could be developing that needs a personalized treatment program consisting of chiropractic care, physical therapy, steroid injections, or, if necessary, surgery.
Injuries
Hips
Tightness develops at the front of the hip/hip flexors from prolonged sitting and can lead to decreased flexibility and cause irritation of the bursa (fluid-filled sacs between the muscle and bone to reduce friction) at the front of the hip.
Symptoms at the front and outer side of the hip can travel down the thigh toward the knees.
Checking that the saddle height is correct can help.
Knees
The knee is the most common site for overuse injuries. Common knee overuse injuries include:
Patellofemoral syndrome
Patella and quadriceps tendinitis
Medial plica syndrome
Iliotibial band friction syndrome
The first four involve discomfort and pain around the kneecap. The last condition results in outer knee pain. Shoe insoles, wedges, and positioning can help prevent some of these injuries.
Feet
Foot tingling, numbness, burning sensations, or pain on the underside of the foot are common.
This occurs from pressure on the nerves that travel through the ball of the foot and toward the toes.
Shoes that are poorly fitted, too tight, or narrow are often the cause.
This comes from increased pressure in the lower leg and results in compressed nerves.
Neck and Back
Discomfort and pain in the neck result from staying in one riding position for too long.
Usually, if the handlebars are too low, the rider has to round their back, adding strain to the neck and back.
Tight hamstrings and/or hip flexor muscles can also cause riders to round/arch the back, causing the neck to be hyperextended.
Doing shoulder shrugs and neck stretches will help relieve neck tension. Regular stretching will create flexibility and make it easier to maintain proper form.
Shoulders
Shoulder overuse injuries cause muscle weakness, stiffness, swelling, tingling or numbness in the fingers, and pain. Treatments depend on the severity of the condition.
Shoulder impingement/pinching
Swelling of soft tissues
Rotator cuff tears
Injuries to the ball-and-socket joint tend to be labral tears of the socket lining cartilage or damage to other structures. Damage to the cartilage can lead to arthritis if not treated effectively.
Falls can cause:
Minor fractures or dislocation.
Fractured collarbone/clavicle – must be immobilized for four to six weeks before rehabilitation exercises are started.
Damage to the joint on the top of the shoulder/acromioclavicular joint or ACJ.
Many of these impact-related injuries can be treated with chiropractic and targeted physical therapy to strengthen the muscles and improve mobility. However, some cases, like severely displaced fractures, require surgical reconstruction or repair.
Intense aching in the forearm can make gripping and ungripping the hands difficult and painful.
These can be prevented by changing hand positions and alternating the pressure from the inside to the outsides of the palms ensuring the wrists don’t drop below the handlebars.
Cyclists are recommended to ride with their elbows slightly bent, not with their arms locked or straight. Bent elbows act as shock absorbers when riding over bumps or rough terrain.
Using padded gloves and stretching the hands and wrists before riding can help. Changing the grip on the handlebars takes the stress off of over-used muscles and redistributes pressure to different nerves.
Head Injuries
Head injuries can range from scrapes, contusions, concussions, or traumatic brain injury.
Wearing a helmet can reduce the risk of head injury by 85 percent.
Chiropractic Treatment
Chiropractic for cyclists can relieve symptoms, rehabilitate and strengthen muscles, improve posture, and prevent future injuries. Cyclists have also reported enhanced:
Respiration
Range of motion
Heart rate variability
Muscle strength
Athletic ability
Neurocognitive functions such as reaction time and information processing.
Common Bicycle Riding Injuries
References
Mellion, M B. “Common cycling injuries. Management and prevention.” Sports medicine (Auckland, N.Z.) vol. 11,1 (1991): 52-70. doi:10.2165/00007256-199111010-00004
Olivier, Jake, and Prudence Creighton. “Bicycle injuries and helmet use: a systematic review and meta-analysis.” International journal of epidemiology vol. 46,1 (2017): 278-292. doi:10.1093/ije/dyw153
Silberman, Marc R. “Bicycling injuries.” Current sports medicine reports vol. 12,5 (2013): 337-45. doi:10.1249/JSR.0b013e3182a4bab7
When everyday factors affect how many of us function, our back muscles begin to suffer. The back muscles in the cervical, thoracic, and lumbar section surround the spine and spinal cord, which helps the body stay upright and promotes good posture. The muscles allow the upper portions of the body to bend down and twist without pain while providing stability to the lower parts of the body. However, when the body ages or everyday activities cause issues, it can develop low back pain associated with weak back muscles. There are many ways to prevent these issues from escalating with various hyperextension exercises for low back pain. This 2-part series examines how low back pain affects the body and how different hyperextension exercises can help strengthen the back. Part 1 examines how hyperextension affects the body and how it is associated with low back pain. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic low back pain. 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
Low Back Pain Affecting The Body
Have you been dealing with aches and pains when bending down? Do you feel stiffness in your torso when twisting? Or have you experienced limited mobility in your hips? Many of these symptoms correlate with low back pain. Studies reveal that back pain is one of the most common issues in the emergency room. Low back pain is associated with many factors that put pressure on the various muscles in the back and can lead to underlying conditions that can cause symptoms to make the body dysfunctional. Additional studies have revealed that chronic low back pain can have influenced overlapping risk profiles, which include:
Stress
Dietary habits
Lifting heavy objects
Musculoskeletal disorders
When these factors affect the back, many individuals will be in constant pain and take medication to relieve their pain. However, medicine can only go so far as it only masks the pain, but there are other ways to reduce low back pain and help strengthen the various muscles surrounding the low back.
An Overview Of Hyperextension (Part 2)
Biomedical physiologist Alex Jimenez explains how there are a couple of different variations that you can do to prevent low back pain. The first one is the elbows in front. The second one is the elbows in front while pointing them forward and keeping them pointed forward throughout the entire movement. The third one is the hands behind the head. And then the fourth variation is putting weight behind your back once you work up to this level. And then using that weight to put more stress on a pivot point. You can also hold the weight to your chest, but putting it behind your head gives you a further pivot point or a further point on the fulcrum, which are your hips putting more stress on your spinal rectors. The repetitions and frequency should be performed at the beginning of most workouts, before or after your abdominal exercises on leg days. You can use this exercise as a warmup before deadlifting or squatting. I’ll remember you don’t have to go as much weight or as many reps when you’re doing this on leg days. So we recommend starting with four sets of 20 reps and slowly working up to four sets of 40 reps. This seems like a lot, but it will be beneficial in the end.
Various Hyperextension Exercises For The Back
When it comes to low back pain, the various muscles are weak, which can lead to multiple symptoms affecting a person’s mobility. Luckily making small changes in a daily structure, like incorporating exercises that target the back, can be beneficial. Studies reveal that exercises targeting the back muscles can help strengthen the targeted muscles to have mobility and stability in the back. As a bonus, exercises combined with chiropractic treatments can help restore the body and allow the spine to be realigned. When it comes to back exercises, hyperextension exercises can help prevent low back symptoms from reoccurring and strengthen weak back muscles. Here are some of the various hyperextension exercises that benefit the back.
Reverse Flys
There are different variations of how to do reverse flys. You can pick a moderate or lightweight dumbbell or a resistance band. This exercise is great for the upper back muscles and rear deltoids.
Sit in a chair where the dumbbells are in front of you. *For resistance bands, make sure the bands are under your feet.
Pick up the dumbbells/resistance bands with the palms of your hands and bend forward.
Squeeze the shoulder blades together, lift the arms to shoulder level with slightly bent elbows, and lower them.
Repeat for three sets of 12 reps and rest in between.
Hip Thrust
Different variations to this exercise can help with the posterior muscles in the lower back. You can use barbells, dumbbells, resistance bands, or your body weight to strengthen your core back muscles.
Lean against a bench with the knees bent and the feet flat on the floor.
Rest the shoulder blades on the bench for support and have the weight placed near your core.
Raise your body slightly by pushing your heels down to the floor and walking out slowly beyond your knees.
Push through your heels to have your hips at shoulder level, hold for a second, and lower your hips back down.
Repeat for three sets of 12 reps and rest in between.
Supermans
This exercise has two different variations and makes you aware of your back muscles. This exercise helps improve muscle mobility in all three sections of the back.
Lay on the mat face down with your arms in front and your legs straight.
Keep the head in a neutral position and raise both the arms and legs off the mat. This allows the body to be in a banana shape in a comfortable position. *If you want more challenge, lift the opposite arms and legs simultaneously.
Hold for a couple of seconds for the upper and lower back and hamstrings to maintain their positions.
Lower down with control.
Repeat for three sets of 12 reps and rest in between.
Fire Hydrants
This exercise helps the lower back and glute muscles reduce the effects of low back pain and make it more challenging to use a resistance band.
Be in a cat/cow position on your mat, allowing the wrist to be aligned under the shoulders and the knees to be aligned under the hips.
Maintain a neutral spine while engaging the core.
Squeeze the glutes and lift your right leg off the mat, keeping the knee at 90 degrees. *The hips should be the only ones moving to keep the core and pelvis stable.
Lower the right leg down with control.
Repeat for three sets of 12 reps and rest before repeating the motion on the left leg.
Conclusion
All in all, having low back pain doesn’t mean your life is over. Incorporating hyperextension exercises as part of your daily routine can help strengthen your back muscles and ensure that you won’t have reoccurring symptoms from low back pain. Making these small changes can lead to beneficial results in the long run for your health and wellness journey.
References
Allegri, Massimo, et al. “Mechanisms of Low Back Pain: A Guide for Diagnosis and Therapy.” F1000Research, U.S. National Library of Medicine, 28 June 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4926733/.
Casiano, Vincent E, et al. “Back Pain – Statpearls – NCBI Bookshelf.” In: StatPearls [Internet]. Treasure Island (FL), StatPearls Publishing, 4 Sept. 2022, www.ncbi.nlm.nih.gov/books/NBK538173/.
Koes, B W, et al. “Diagnosis and Treatment of Low Back Pain.” BMJ (Clinical Research Ed.), U.S. National Library of Medicine, 17 June 2006, www.ncbi.nlm.nih.gov/pmc/articles/PMC1479671/.
The body is an amazingly complex machine as it allows the individual to move each section, like the back, arms, legs, torso, neck, and head, without feeling any pain. Each section has various muscles, ligaments, and tissues that surround the skeletal joint and allow mobility, stability, and range of motion when the host is active. However, when underlying conditions start to affect the body, each section can be affected and cause pain-like symptoms associated with the muscles, ligaments, and tissues. Sometimes it can even cause referred pain in the vital organs, leading to more problems when not treated immediately. To that point, various exercises combined with therapy can help prevent pain-like symptoms from affecting the body and restore mobility to the upper and lower portions. This 2-part series will look at an exercise called hyperextension, which can help strengthen these muscles in the upper and lower portions. Part 1 will examine how hyperextension affects the body and how it is associated with low back pain. Part 2 will look at the various hyperextension exercises that can help strengthen each muscle group. We refer our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic pain-like conditions associated with low back pain. 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
What Is Hyperextension?
Have you been experiencing pain-like symptoms in different areas of your body? Does it hurt when twisting and turning? Or do you constantly ache when bending over? Many of these symptoms are associated with muscle and joint pain that can affect the body and lead to hyperextension. Hyperextension is when a skeletal joint has a greater range of motion without feeling pain.
When a person suffers from a traumatic injury or has a chronic condition, it can cause the various muscles in the body to extend their range of motion and cause more pain that can affect their quality of life. A perfect example would be a person who is double-jointed in their hands, knee, elbows, and back. Even though many double-jointed people can further extend their joints, it can lead to various issues that can impact the body and lead to pain-like symptoms. For example, studies reveal that if a person has been in an auto accident and suffers from whiplash, the hyper-extended muscles can cause pain-like symptoms in the soft tissues, leading to neck pain. When this happens, it can cause symptoms of limited mobility and affect the individual.
Now if it is chronic conditions like EDS (Ehlers-Danlos syndrome) or chronic back conditions, it can affect the lower extremity muscles while affecting the mobility and stability of the body. Studies reveal that low back pain associated with hyperextension is developed when various factors can cause the spine to be in subluxation and compress the different vertebrate discs, muscles, ligaments, and tissues, which can cause pain over time. Additional studies have also found that when there are injuries in the thoracolumbar and lumbar spine, it is often combined with various forces that can cause mobility issues which leads to spinal subluxation and spinal compression.
An Overview Of Hyperextension
Biomedical physiologist Alex Jimenez will be explaining a specific exercise called Hyperextensions. Hyperextensions are an exercise that is designed to strengthen the erectors of the spine. They usually involve an extension type of maneuver for the concentric portion and AF flexion for the eccentric portion. Hyperextension relies on a pivot point, usually at the hips, which stresses the lower back muscles. It also allows you to work on the lower back muscles, which we said, the glutes, hamstrings, and even the mid back, depending on the arc of the movement. So why are hyperextensions important? They strengthen the lower back muscles, also known as the spinal rectors, and are responsible for stabilizing the spine. It can help decrease the chances of lower back pain or injuries, and it also helps strengthen your deadlift and squats. And it does this by allowing you to have better stabilization throughout these dynamic movements. So what muscles are involved? Numerous muscles are involved in the upper and lower body extremities, allowing hyperextension exercises to provide more range of motion without pain. The next part will show different variations of hyperextension exercises that can help each muscle.
Hyperextension Associated With Low Back Pain
Spinal subluxation often leads to low back pain and can affect a person’s ability to move. So how is hyperextension associated with low back pain? Some factors leading to low back pain, like incorrect posture or excessive lifting of heavy objects, can affect the low back muscles. The low back muscles support the low back, stabilize the spine, and help maintain good posture. When these muscles have been overused, it can lead to various injuries. All is not lost, as studies reveal that hyperextension exercises for low back pain, when done slowly, can provide isometric endurance improvement to the back muscles and allow flexibility back to the spine. Hyperextension exercises can strengthen the lower back muscles and reduce pain. However, exercise combined with chiropractic care can enable the body to restore itself and reduce the pain-like symptoms associated with spinal subluxation to allow the range of motion back in the muscles.
Conclusion
Hyperextension in the body allows the various muscle groups to extend their full range of motion. When multiple factors or chronic conditions begin to affect the different muscles in the body, it can lead to pain-like symptoms associated with the upper and lower extremities. Fortunately, the combination of exercises and chiropractic care can restore the body and the muscles to relax. In part 2 of this series, we will look at the various hyperextension exercises for low back pain and how they can help increase the body’s range of motion.
References
Johnson, G. “Hyperextension Soft Tissue Injuries of the Cervical Spine–a Review.” Journal of Accident & Emergency Medicine, U.S. National Library of Medicine, Jan. 1996, www.ncbi.nlm.nih.gov/pmc/articles/PMC1342595/.
MACNAB, I. “Low Back Pain. the Hyperextension Syndrome.” Canadian Medical Association Journal, U.S. National Library of Medicine, 15 Sept. 1955, www.ncbi.nlm.nih.gov/pmc/articles/PMC1826142/.
Manniche, C, et al. “Intensive Dynamic Back Exercises with or without Hyperextension in Chronic Back Pain after Surgery for Lumbar Disc Protrusion. A Clinical Trial.” Spine, U.S. National Library of Medicine, Apr. 1993, pubmed.ncbi.nlm.nih.gov/8484146/.
Oh, In-Soo, et al. “Pure Hyperextension Injury of the Lower Lumbar Spine with an Ureteral Impingement.” European Spine Journal : Official Publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society, U.S. National Library of Medicine, May 2013, www.ncbi.nlm.nih.gov/pmc/articles/PMC3641240/.
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