Sciatica can range from mild to severe. Most individuals are familiar with severe cases because of the intense shooting throbbing pain. On the other hand, mild cases can present with little to no discomfort or pain but involve tingling, pins and needles, electrical buzzing, and numbing sensations. This can make individuals think there is nothing wrong and their foot just fell asleep. It can come from nowhere, as there was no obvious back or leg trauma causing injury. However, somewhere along the nerve’s path, the nerve has become compressed, pinched, trapped, stuck, or twisted, most likely from a spasming muscle group in the low back, buttocks, or legs causing the sciatica foot symptoms. Chiropractic, massage, and decompression therapy can relax the muscles, relieve the symptoms, release the nerve, and restore function.
Sciatica Foot Symptoms
The sciatic nerve extends from the lower spine to the feet. Sciatica foot symptoms could be caused by several possibilities that range from piriformis syndrome to a developing slipped disc or spasming muscles. The symptoms travel through the nerve and can be felt anywhere along the nerve’s path, not necessarily at the source. This is why mild cases may only present with slight pricking/tingling sensations. However, left untreated, the cause can progress and develop into a severe case of sciatica.
Symptoms
The length of time that sciatica foot symptoms last will depend on the underlying cause. For example, if a herniated disc is the cause, the numbness may last for a few weeks or months until the disc heals. However, the numbness may be more long-lasting if sciatica is caused by degenerative disc disease. Sometimes, the nerve can be permanently damaged, leading to chronic pain and numbness. This is more likely to occur in individuals with diabetes or another condition that causes nerve damage.
A varying degree of leg weakness can present as the spinal nerve root issues interfere with effective signal communication between the brain and the leg muscles.
Leg weakness may also be interpreted as a pulling sensation in the leg.
Weakness in the foot or toe muscles can also present.
Leg movements such as walking, running, lifting the leg, or flexing the foot can also be affected.
The tingling and numbing sensations may worsen when sitting or standing for long periods or moving the back in certain ways.
Treatment
Chiropractic care is an excellent option for treating sciatica foot symptoms and starts with a personalized plan based on individual symptoms, injury, and medical history. Chiropractors are neuromusculoskeletal experts on the spine, vertebrae, surrounding muscles, tissues, and nerves. Treatment includes spinal and extremity adjustments to realign the body, decrease inflammation, relieve pressure, release the nerve, and ultimately allow the body to activate its natural healing processes.
Massage
Massage therapy can relieve muscle tension and spasms in the back and legs, reducing pressure on the sciatic nerve.
Massage also increases blood circulation and relaxes the muscles, speeding healing and recovery.
Electrical Stimulation
Electrical stimulation activates the nerves and muscles and reduces symptoms by blocking signals.
Physical Therapy
Physical therapy exercises can help stretch and strengthen the back and leg muscles.
Targeted exercises can be done at home to continue strengthening and maintaining the muscles.
Foot Orthotics
Using orthotic devices such as arch supports or heel cups can help relieve pressure on the feet.
Arch supports are especially helpful if sciatica foot symptoms are exacerbated by flat feet or other foot conditions.
Heel cups can help with the frequent use of high heels.
Emary, Peter C. “Evidence-based prognostication in a case of sciatica.” The Journal of the Canadian Chiropractic Association vol. 59,1 (2015): 24-9.
Frost, Lydia R et al. “Deficits in foot skin sensation are related to alterations in balance control in chronic low back patients experiencing clinical signs of lumbar nerve root impingement.” Gait & posture vol. 41,4 (2015): 923-8. doi:10.1016/j.gaitpost.2015.03.345
Shakeel, Muhammad, et al. “An uncommon cause of sciatica.” Journal of the College of Physicians and Surgeons–Pakistan: JCPSP vol. 19,2 (2009): 127-9.
Tampin, Brigitte, et al. “Disentangling ‘sciatica’ to understand and characterize somatosensory profiles and potential pain mechanisms.” Scandinavian journal of pain vol. 22,1 48-58. 2 Aug. 2021, doi:10.1515/sjpain-2021-0058
Dr. Jimenez, D.C., presents how to find the best diet approach to hypertension and cardiometabolic risk factors in this 2-part series. Many factors often play a role in our health and wellness. In today’s presentation, we will look at how a cardiometabolic diet is personalized for every body type and how genes play with the cardiometabolic diet. Part 2 will continue with how genes play their role in a cardiometabolic diet. We mention our patients to certified medical providers that provide available therapy treatments for individuals suffering from chronic conditions associated with metabolic connections. We encourage each patient when it is appropriate by referring them to associated medical providers based on their diagnosis or needs. We understand and accept that education is a marvelous way when asking our providers’ crucial questions at the patient’s request and acknowledgment. Dr. Alex Jimenez, D.C., uses this information as an educational service. Disclaimer
What Is A Cardiometabolic Diet?
Dr. Alex Jimenez, D.C., presents: Regarding cardiovascular disorders, some terms we look for are: actual heart disease or stroke risk, or they’re on the metabolic side. Insulin, blood sugar, metabolic dysfunction. These words capture the themes we’ve been talking about lipids, glucose, inflammation, and insulin. Those are the people that you’re thinking about for this plan. And what you’re doing is building a lifestyle prescription. And for our patients who have cardiometabolic issues, we’re going to really take advantage of those features of our cardiometabolic food plan and then take them a step further to not only give a low glycemic impact, anti-inflammatory, plant-based kind of nutrient source but then how can we tailor it according to other parameters of this patient and then how can we help this patient implement it when they step outside your office and have to enter into their environment, which may or may not be set up for success.
So first things first. There is a practitioner guide that you must take advantage of, and this is like the scriptures of nutrition, and it has so many resources in here, but of course, they are of use to you once you know about them. So this is going to give you the how-to. So in case you miss something or want more detail, please refer to this practitioner guide for the cardiometabolic food plan. Now, let’s say you want to do the first entry-level use of this food plan. Well, we would grab the one that tells a cardiometabolic food plan. You’ll notice that all these specialized foods are selected to help with cardiometabolic conditions.
Personalizing A Plan
Dr. Alex Jimenez, D.C., presents: And it’s much better than saying, “Hey, eat fewer carbs, eat more plants. You know, eat healthier and exercise more.” That needs to be more specific. So taking it a step further, give them a blank food plan. It doesn’t have to be personalized to another level. Handing them a food plan and telling them to start eating from this list is only sometimes going to work. Sometimes we have to take it a step further to give them food choices in terms of quality and quantity. To that point, you have the ability right now with your patient to guesstimate size and caloric targets.
We can estimate size and weight and put small, medium, and large portions on food consumption. An example will be if we look at the different sizes of body types. For a petite adult body, it is best to ensure they consume about 1200-1400 calories. A medium adult body must consume about 1400-1800 calories, and a large adult body must consume about 1800-2200 calories. That might be the first kind of personalization.
Let’s give you some caloric-guided, quantity-guided food plan options. So what’s beautiful is that we have those already built out, and if you look closely at them, it tells you how many servings of each category should be in each specific small, medium, and large food plan. So you don’t have to do that calculation. Now if you want to take it to the next level and you have a BIA or a bioimpedance analysis machine, you can understand specifically their caloric burn rate and then if you want to modify it. An example would be a 40-year-old male who is unhappy with his weight and has been dealing with issues causing him ankle pain. So let’s see how we can change these things.
As we look at his body index, he is about 245 pounds and has been dealing with some cardiometabolic issues. Now when we look at his numbers and data from the BIA machine, we would develop a food plan that can help dampen the cardiometabolic issues effects that can help him. We would start to calculate come caloric recommendations and have a personalized diet and exercise plan to reduce the symptoms affecting his body and help promote muscle gain and weight loss. This customized plan allows him to keep track of his progress to see what works that is helping him lose weight or what needs improvement. Making these small changes can be beneficial in the long hall, as it will take some time to develop healthy habits.
How To Cater a Cardiometabolic Diet?
Dr. Alex Jimenez, D.C., presents: Now, what do you do with that information and cater it to become a diet for cardiometabolic disorders? Well, you would work with a health coach and other associated medical providers like a nutritionist to pull out a personalized food plan to help your patients understand what’s in each category and how to personalize the servings per day if you decide to get a bit more personalized with the caloric targets. And remember that some MVPs are the most valuable players with super nutrient powers within this food plan. It is also important to make time with the patient to discuss foods that benefit their health and wellness. Remember that this cardiometabolic food plan’s goal is to be able to personalize for unique clinical cases and unique patients. However, it still serves the general need for cardiometabolic food signals for our patients with these issues.
There’s something in here for everybody; remember, you must get started on something. So please consider how you can make this available to your patients so that they have it to a couple of recipes; it’s got menu plans, shopping guides, and recipe indexes. It’s chalked full of the things that slow us down in getting nitty gritty about the cardiometabolic food plan or nutrition in general. Something is always better than nothing. So by starting with the cardiometabolic food plan for your patients, you will start seeing the science be beautifully put into action. We will talk about how to use genetics with diet prescription.
Cardiometabolic Diet & Genes
Dr. Alex Jimenez, D.C., presents: Going a bit deeper, we will discuss how we tailor the cardiometabolic food plan in patients based on their APO-E genotypes. How do we customize it a little bit further? So what is APO-E? APO-E is a class of APO lipoproteins produced in the liver macrophages in astrocytes. It is required for the chylomicrons and IDLs while mediating cholesterol metabolism and is the principal cholesterol carrier in the brain. Now, there are three possible genotypes. There’s APO-E2, APO-E3, and APO-E4. And what happens is you’re going to get one from each parent. So you’re going to end up with a combination at the end. So you’ll be either APO-E3 with APO-E4 or APO-E2 with APO-E3. So based on what you got from your mother and what you got from your father, you’re going to have that combination.
APO-E Explained
Dr. Alex Jimenez, D.C., presents: So APO-E2 two and APO-E3, there’s a lot of information online, but there’s not good evidence on making specific dietary changes in these particular genotypes. So unfortunately, we don’t have the data to confidently say how to modulate, change or customize the food plan based on these genotypes. The best we can tell you is to follow the biomarkers; every patient is an individual. But what about APO-E4? Around 20% of Americans have at least one APO-E4 allele, and if you have APO-E4, you have an increased risk of mild cognitive impairment, Alzheimer’s, hyperlipidemia, diabetes, and coronary heart disease. And if you smoke or drink, you have a worse outcome with this genotype. Interestingly, being relevant to the times increases the risk of infections that can affect your body.
So usually, something helps one thing, but it will, and it can hurt others. So with your patients that you already have their genetics on, this might be a nice way to look at if you know their APO-E4 risk stratified them even more when protecting them. So this was independent of whether they had dementia, underlying cardiovascular disease, or diabetes.
If you have APO-E4, it may be protective against malaria, and who knows what other benefits it would have? An interesting fact about APO-E4 is that, in a study where they tried to give them DHA supplementation, they found it harder to get the DHA in the brain higher with APO-E4. They could elevate it, but not as well as if you had APO-E2 or APO-E3. And this was like supplementing with DHA. Other studies showed that the levels did not respond well if you did DHA and EPA together. So you didn’t get as high of a response of the omega-3s with APO-E4 versus if you had APO-E2 or APO-E3.
How Omega-3 Play Their Role?
Dr. Alex Jimenez, D.C., presents: So the interesting thing, though, is that the study looked at the omegas in the brain that was supplemented with DHA. We have all kinds of new research on the benefit of EPA-only omega-3s; there’s even a main name brand product that is EPA-only. If you look at, if you look to the right, you see that EPA ends up becoming DHA. So if you start increasing, both EPA and DHA will go up. What about APO-E in your diet or the food that you’re consuming? When they looked at genetically modified mice where they took APO-E out, they found extreme hypercholesterolemia with a high-fat food plan.
So when the mice were fed higher fat diets, they had this extreme rise in high cholesterol. Why is this relevant? Because APO-E4 does not function as well as APO-E3 and APO-E2. That hinted that this could affect us if we consumed a higher-fat food plan. So in a U.K. study, they found out that if they gave patients APO-E4 and switched it from saturated fats, they decreased their saturated fats while increasing their lower glycemic index carbohydrates; they found that it lowered their LDL and APO-B. This is a clue that we may want to decrease saturated fats, even healthier saturated fats, in these patients.
So the Berkeley Heart Study from the Berkeley Heart Lab was bought by Quest. It’s now called Cardio iq. It’s one of the original advanced lipid testing labs. And they had an observational study where they saw different effects in these patients with APO-E4 and other products based on various dietary modifications. So what did they find? They found that giving them fish oil lowered their triglycerides, reduced their small density LDL and HDL, and increased their LDL. So their HDL decreased, but the small density LDL went down, and their triglycerides went down.
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.
Getting healthy sleep can be difficult when dealing with back problems or recovering from surgery. It can be difficult, if not impossible, to get and stay comfortable long enough to sleep on a regular flat mattress. It is worth considering an adjustable bed as an alternative. Because of their lifestyle and health benefits, these beds are growing in popularity to meet an individual’s spine, posture, and sleeping needs.
Adjustable Bed
An adjustable bed can raise and lower a mattress’s orientation to different angles, allowing the upper body to rest at a slight incline, such as 30 to 45 degrees, with support under the knees as they bend at a slight angle. The body can feel better in an inclined or semi-upright position rather than lying flat. Individuals with back or neck problems or joint conditions like shoulder arthritis have reported feeling better in this position.
Features
The number of adjustments varies from model to model. Available features include:
Adjustable firmness for the low back/lumbar area.
Adjustments may be made by remote control.
Some offer massage options.
Zero gravity – NASA invented the zero gravity position to reduce pressure on astronauts during takeoff. In this position, the head and knees are raised above the heart, making the body feel weightless.
Adjustable beds are sold in single, queen, and king sizes.
Split queen and king sizes allow the settings to be customized for each side of the bed.
Benefits
Snoring
Over 90 million Americans snore during sleep.
The main cause of snoring is the blockage of the windpipe while sleeping, which can be caused by several factors, but most commonly by the weight of the neck on the windpipe, preventing the individual from breathing properly.
An adjustable bed allows for an inclined position, decreasing the pressure on the windpipe, reducing snoring, and allowing for a more relaxing sleep.
Asthma
Asthma can disrupt healthy sleep and make breathing difficult at night.
COPD and chronic lung conditions can worsen over time, impacting sleep quality.
Lying flat often irritates these lung conditions.
Sleeping with the head and feet in a raised position makes breathing easier.
Posture
Unhealthy posture causes soreness, stiffness, tightness, headaches, and other health issues.
Adjustable beds provide postural support to the spine and can improve posture and increase overall health.
Back Problems
80% of individuals deal with various back issues and symptoms.
Adjustable beds provide support and alignment to the spine by allowing the mattress to conform to the body’s contours.
This can prevent sciatica, enabling the nerves to relax and rest without added body pressure.
For those with sciatica, pain can be alleviated by using a raised leg position to take the stress off the nerves and increase circulation.
Lowering the bed up and down can help stretch the back.
Digestion
An adjustable bed can help with digestion issues.
An inclined position prevents indigestion and acid reflux and helps the body process food more efficiently.
A six-inch raise is recommended to increase digestion.
Individuals who go to bed on a full stomach should raise the incline as there is more digestive activity.
Inflammation, Swelling, and Injury Recovery
When dealing with neuromusculoskeletal injuries, doctors often recommend elevating the injured part of the body to speed up recovery.
An adjustable bed lifts or raises the mattress and elevates the limbs while maintaining a neutral/natural sleeping position.
Pregnancy
Physical and hormonal changes during pregnancy can cause back discomfort symptoms, sciatica, circulation issues, and swelling.
Pregnant women can use the zero gravity position to reduce swelling, alleviate back pain, and improve circulation.
This position also makes back sleeping safer for the mom and baby.
Individuals should research all the styles and features available to find what works for them.
Ten Benefits
References
Ancuelle, Victor, et al. “Effects of an adapted mattress in musculoskeletal pain and sleep quality in institutionalized elders.” Sleep science (Sao Paulo, Brazil) vol. 8,3 (2015): 115-20. doi:10.1016/j.slsci.2015.08.004
Söderback, I, and A Lassfolk. “The usefulness of four methods of assessing the benefits of electrically adjustable beds in relation to their costs.” International journal of technology assessment in health care vol. 9,4 (1993): 573-80. doi:10.1017/s0266462300005493
Tetley, M. “Instinctive sleeping and resting postures: an anthropological and zoological approach to the treatment of low back and joint pain.” BMJ (Clinical research ed.) vol. 321,7276 (2000): 1616-8. doi:10.1136/bmj.321.7276.1616
Verhaert, Vincent, et al. “Ergonomics in bed design: the effect of spinal alignment on sleep parameters.” Ergonomics vol. 54,2 (2011): 169-78. doi:10.1080/00140139.2010.538725
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
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