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Astaxanthin and Its Benefits

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine, Health, Metabolic Syndrome, Natural Health, Nutrition, Supplements, Wellness

Do you feel:

Inflammation?
Unpredictable body swelling?
Tired or sluggish?
Weight gain?
Gastrointestinal digestive issues?

If you are experiencing any of these situations, then you might want to try astaxanthin.

The body needs specific vitamins, minerals, and supplements from food, in order to function correctly. The variety of these nutrients can be found in healthy foods like fruits, vegetables, lean meats, and whole grains are precisely what the body needs. One of the essential nutrients that the body needs is antioxidants. Antioxidants help the body get rid of free radicals that can cause the body to become overly stressed and leading it to develop chronic illnesses. There is an antioxidant that can help the body and can be found in berries and pomegranates, and it is called astaxanthin.

Astaxanthin

Astaxanthin is a xanthophyll carotenoid that can be found in various microorganisms and marine animals. Astaxanthin is common for humans to apply and consume into the body while also being different. This red, fat-soluble pigment is quite different from the other kinds of food that contain carotenoids. Astaxanthin surprising does not contain vitamin A like all the other food containing carotenoids, and astaxanthin is an impressive antioxidant. Studies have shown that astaxanthin can not only be beneficial for the eyes but can provide nutritional support as well as having potential health-promoting effects in preventing and treating various diseases that can harm the body. Some of the various diseases that can harm the body when there is an excessive amount of free radicals can include:

Various cancers
Chronic inflammatory diseases
Metabolic syndrome
Diabetes
Gastrointestinal diseases

Another study found that astaxanthin was superior to fish oil due to astaxanthin having the ability to enhance the body’s immune response and thus lowering the risk of vascular and infectious diseases that can harm the body, causing it to dysfunction.

A Powerful Antioxidant

There are some fantastic beneficial properties that astaxanthin can provide for the body and help improve the body�s systems as well.

Astaxanthin is a powerful antioxidant since various chronic diseases are rooted in a disproportionate balance of reactive oxygen and nitrogen species to antioxidants. Studies have shown�that astaxanthin has been known to scavenge free radicals more effectively out of the body than beta-carotene. There was another study showing how the body�s DNA was damage due to low plasma 8 -OHdG (8-hydroxy-2′-deoxyguanosine) levels.

Boosts the Immune System

The publication of the immunomodulatory effects of astaxanthin is not getting enough attention as they should be. A test study has reported that dietary astaxanthin was able to stimulate mitogen-induced lymphocyte proliferation. This will help increase the natural killer cell cytotoxicity and even delay the hypersensitivity response in the body while also increasing the numbers of total T and B cells in the peripheral blood in the body. Another study showed how astaxanthin could help significantly enhanced lymphocyte proliferation in vitro and ex vivo. The studies also found that astaxanthin can be consumed in high concentrations without the risk of cytotoxicity.

Controls Glucose and Lipids

Surprisingly there has been new research that has been revealing about another unique but vital role that astaxanthin has. The studies show that it can modulate peroxisome proliferator-activated receptors or PPARs. What this function does is that it may have various applications in human health, including producing glucose and lipid homeostasis. Since PPARs are members of the nuclear hormone receptors in the body, they are a superfamily that plays roles in the expression of many genes that are regulating cellular differentiation and many other functions in the body.

There are at least three subtypes of PPARs that helps the major organs and help the metabolism of glucose and lipids. PPAR? can primarily be expressed in the liver, kidney, heart, and skeletal muscle, where it can be involved in lipid metabolism and insulin sensitivity to the body. Another subtype of PPARs is PPAR?, which plays a role in glucose and lipid homeostasis but also is the site of action in the adipose tissue in the body. When astaxanthin is being involved, astaxanthin is a PPAR? agonist but can act as either an agonist or antagonist to PPAR? receptors. Studies have found that PPAR? agonist and PPAR? antagonist in astaxanthin can decrease cholesterol and triglycerides in loaded HepG2 cells, while changing several enzymes expressions that are being involved in lipid and glucose metabolism pathways, thus resulting in a hypolipidemic effect in the body.

Exercise Enhancement

Surprisingly astaxanthin can be used to prevent exercise-induced free radical production and is a lesser-known application. Astaxanthin can enhance exercise performance and even improve the recovery process. The increase in the reactive oxygen and nitrogen species or RONS are being produced during an exercise regime is deleterious to the health. It is often combated with a matching increase in the endogenous antioxidant enzymes. However, when a person is doing excessive exercises, it can cause RONS to rise above the body’s natural capacity to eliminate them. This will cause an increased risk of oxidative damage in lipids, protein, and DNA molecules. In a review study, it showed the ability of astaxanthin to squelch the RONS generating during exercising. It reported that the antioxidant effects of astaxanthin could provide a variety of benefits to athletes.

Conclusion

Astaxanthin is a powerful immunomodulatory antioxidant that can support numerous biological pathways that are in the body. It can dampen the effects of a variety of chronic diseases and illnesses that can harm the body. Astaxanthin is useful for being a therapeutic and powerful nutraceutical while also being an excellent addition for someone who needs supplements to support their general health and well-being. Some of the products here are beneficial to the body as they help support the immune system while providing more excellent stability.

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

References:

Ambati, Ranga Rao, et al. �Astaxanthin: Sources, Extraction, Stability, Biological Activities and Its Commercial Applications–a Review.� Marine Drugs, MDPI, 7 Jan. 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC3917265/.

Brown, Daniel R, et al. �Astaxanthin in Exercise Metabolism, Performance and Recovery: A Review.� Frontiers in Nutrition, Frontiers Media S.A., 18 Jan. 2018, www.ncbi.nlm.nih.gov/pmc/articles/PMC5778137/.

Choi, Chang-Ik. �Astaxanthin as a Peroxisome Proliferator-Activated Receptor (PPAR) Modulator: Its Therapeutic Implications.� Marine Drugs, MDPI, 23 Apr. 2019, www.ncbi.nlm.nih.gov/pmc/articles/PMC6521084/.

Lin, Kuan-Hung, et al. �Astaxanthin, a Carotenoid, Stimulates Immune Responses by Enhancing IFN-? and IL-2 Secretion in Primary Cultured Lymphocytes in Vitro and Ex Vivo.� International Journal of Molecular Sciences, MDPI, 29 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4730289/.

Park, Jean Soon, et al. �Astaxanthin Decreased Oxidative Stress and Inflammation and Enhanced Immune Response in Humans.� Nutrition & Metabolism, BioMed Central, 5 Mar. 2010, www.ncbi.nlm.nih.gov/pmc/articles/PMC2845588/?report=reader.

Team, DFH. �Applications of the Antioxidant, Astaxanthin.� Designs for Health, 27 June 2019, blog.designsforhealth.com/node/1047.

Yuan, Jian-Ping, et al. �Potential Health-Promoting Effects of Astaxanthin: a High-Value Carotenoid Mostly from Microalgae.� Molecular Nutrition & Food Research, U.S. National Library of Medicine, Jan. 2011, www.ncbi.nlm.nih.gov/pubmed/21207519.

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Ketogenic Diet for Metabolic Syndrome

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Basal Metabolic Index (BMI), Chiropractic, Diets, Functional Medicine, Health, Ketogenic Diet Explained, Metabolic Syndrome, Nutrition, Weight Loss, Wellness

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

What is the Ketogenic Diet?

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

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

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

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

How the Keto Diet Helps Improve Metabolic Syndrome

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

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

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

Type 2 Diabetes

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

Obesity

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

Metabolic Syndrome

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

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

Curated by Dr. Alex Jimenez

References:

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

Dr. Alex Jimenez Podcast: Metabolic Syndrome

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

Neural Zoomer Plus for Neurological Disease

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

Food Sensitivity for the IgG & IgA Immune Response

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

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

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

Formulas for Methylation Support

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

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

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

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

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

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

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

Berberine and Metabolic Syndrome

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine, Health, Metabolic Syndrome, Nutrition, Wellness

Do you feel:

Weight gain?
Hormones imbalances?
Craving sweet during the day?
Difficulty losing weight?
Eating sweets does not relieve the craving for sugar?

If you are experiencing any of these situations, then you might be experiencing an imbalance of your blood glucose. Why not try adding berberine into your daily diet and lifestyle.

For many individuals reclaiming their health, the incidence of metabolic syndrome, and type 2 diabetes along with many other conditions that can be related to insulin resistance. Many local healthcare practitioners need all the tools to inform their patients as a powerful supplement that has been receiving recognition for its efficacy in improving the multiple parameters for metabolic health and improving glycemic control. This supplement is known as berberine, and the studies have shown that berberine is as effective as metformin and can help patients who have type 2 diabetes.

What Is Berberine?

Berberine is an alkaloid compound that is found in several plants like goldenseal, barberry, and tree turmeric. When berberine is crushed, it has a yellow color hue that is similar to curcumin and has been part of Chinese and Ayurvedic traditional medicine that has been used for thousands of years. Surprisingly berberine has worked in multiple ways and has been able to make some changes within the body�s cells and metabolic system. There has been research showing that berberine can transport in the bloodstream once it has been ingested and can activate the AMPK (AMP-activated protein kinase) enzyme. Once this happens, the enzyme is referred to as a “metabolic master switch” and can help regulate the significant organs and regulating the body’s metabolism.

The Health Benefits from Berberine

Research shows that berberine can provide many health benefits to the body, especially those who have been affected with type 2 diabetes and have metabolic syndrome. Here are some of the health benefits that berberine has to offer.

Bacterial Infections

Studies have found that berberine is an active antimicrobial agent. Studies have shown that berberine can enhance the inhibitory efficacy of antibiotics against the bacteria Staphylococcus aureus. This type of bacteria can cause many health problems in the body, like sepsis, pneumonia, and meningitis. There is even another study that shows that when a person consumes a high concentration of berberine could kill the Staphylococcus aureus bacteria more quickly. The berberine effects can dissociate the bacteria protein into individual chains and separate them into their molecular weight.

Regulates Blood Glucose

Type 2 diabetes is a common disease that can make a person’s blood sugar to either rise or fall, causing them to DKA (diabetic ketoacidosis). With berberine, it can help regulate blood glucose in the body. Studies have shown that type 2 diabetes has become a worldwide health threat for people, and finding treatment for this disease is limited due to the availability of effective medications that can help control the blood glucose levels. With berberine, it can help reduce insulin resistance and surprisingly, regulate the blood glucose to healthy levels like metformin. The research even shows that berberine can also help regulate the body�s lipid metabolism as well.

More results showed that berberine could do the following:

Lower the insulin resistance to make the blood sugar to lower the hormone insulin more effectively.
It helps increase the glycolysis so the body can break down the sugars.
Decease the sugar produced in the liver.
It helps break down the carbohydrates in the gut microbiome.
It helps increase the beneficial bacteria in the gut to prevent inflammation.

Help Losing Weight

Studies have shown that berberine is an effective weight loss supplement for anyone who may be obese. There was a twelve-week study that showed that the participates took about 500 mg of berberine, and they lost about five pounds of body fat. While another study stated that about 37 participants that have metabolic syndrome took about 300 mg of berberine, and the results showed that the participants have dropped their BMI (body mass index) levels go from obese to overweight in three months. The participants even improved many of their health markers and lose their belly fat.

Many researchers believed that when people take berberine and see that they are losing their excess weight, it can help improve their fat-regulating hormones like insulin, adiponectin, and leptin in their body. There is still more research being done about berberine and how its beneficial weight loss effects can help anyone with metabolic syndrome and might be overly obese.

Conclusion

Berberine is a compound that is found in plants like tree turmeric, goldenseal, and barberry. It has a yellow color cue and has many beneficial properties. Berberine can help anyone who has type 2 diabetes and metabolic syndrome. For the beneficial properties, berberine can help regulate the body�s glucose hormones and has the same effects as the pharmaceutical drug, metformin. When people consume berberine, their metabolic system will begin to function correctly and begun to live a healthier life. Some products can help the metabolic system and the immune system by supporting sugar metabolism as well as reducing the glutathione for providing more excellent stability, bioavailability, and digestive comfort in the body.

References:

Berry, Jennifer. �Everything You Need to Know about Berberine.� MedicalNewsToday, 19 July 2019, www.medicalnewstoday.com/articles/325798.php.

Chu, Ming, et al. �Role of Berberine in the Treatment of Methicillin-Resistant Staphylococcus Aureus Infections.� Scientific Reports, Nature Publishing Group, 22 Apr. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4840435/.

Gunnars, Kris. �Berberine � A Powerful Supplement With Many Benefits.� Healthline, 14 Jan. 2017, www.healthline.com/nutrition/berberine-powerful-supplement.

Hu, Yueshan, et al. �Lipid-Lowering Effect of Berberine in Human Subjects and Rats.� Phytomedicine, Urban & Fischer, 25 June 2012, www.sciencedirect.com/science/article/abs/pii/S0944711312001870.

Li, Zheng, et al. �Antioxidant and Anti-Inflammatory Activities of Berberine in the Treatment of Diabetes Mellitus.� Evidence-Based Complementary and Alternative Medicine, Hindawi, 11 Feb. 2014, www.hindawi.com/journals/ecam/2014/289264/.

Peng, Lianci, et al. �Antibacterial Activity and Mechanism of Berberine against Streptococcus Agalactiae.� International Journal of Clinical and Experimental Pathology, e-Century Publishing Corporation, 1 May 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4503092/.

Team, DFH. �Berberine: Boon for Metabolic Syndrome.� Designs for Health, 5 Jan. 2018, blog.designsforhealth.com/berberine-boon-for-metabolic-syndrome.

Yang, Jing, et al. �Berberine Improves Insulin Sensitivity by Inhibiting Fat Store and Adjusting Adipokines Profile in Human Preadipocytes and Metabolic Syndrome Patients.� Evidence-Based Complementary and Alternative Medicine: ECAM, Hindawi Publishing Corporation, 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3310165/.

Yin, Jun, et al. �Efficacy of Berberine in Patients with Type 2 Diabetes Mellitus.� Metabolism: Clinical and Experimental, U.S. National Library of Medicine, May 2008, www.ncbi.nlm.nih.gov/pmc/articles/PMC2410097/.

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What Is Metabolic Syndrome?

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Chiropractic, Functional Medicine, Gastro Intestinal Health, Gut and Intestinal Health, Health, Health Coaching, Ketogenic Diet Explained, Metabolic Syndrome, Nutrition, Wellness

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

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

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

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

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

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

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

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

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

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

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

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

References:

Mayo Clinic Staff. �Metabolic Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 14 Mar. 2019, www.mayoclinic.org/diseases-conditions/metabolic-syndrome/symptoms-causes/syc-20351916.

Sherling, Dawn Harris, et al. �Metabolic Syndrome.� Journal of Cardiovascular Pharmacology and Therapeutics, vol. 22, no. 4, 2017, pp. 365�367., doi:10.1177/1074248416686187.

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Three Metabolic Energy Systems

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Basal Metabolic Index (BMI), Fitness, Metabolic Syndrome, Power & Strength, PUSH-as-Rx

Personal Training 101

How You Get Energy & How You Use It

We usually talk of energy in general terms, as in �I don�t have a lot of energy today� or �You can feel the energy in the room.� But what really is energy? Where do we get the energy to move? How do we use it? How do we get more of it? Ultimately, what controls our movements? The three metabolic energy pathways are the�phosphagen system, glycolysis�and the�aerobic system.�How do they work, and what is their effect?

Albert Einstein, in his infinite wisdom, discovered that the total energy of an object is equal to the mass of the object multiplied by the square of the speed of light. His formula for atomic energy, E = mc², has become the most recognized mathematical formula in the world. According to his equation, any change in the energy of an object causes a change in the mass of that object. The change in energy can come in many forms, including mechanical, thermal, electromagnetic, chemical, electrical or nuclear. Energy is all around us. The lights in your home, a microwave, a telephone, the sun; all transmit energy. Even though the solar energy that heats the earth is quite different from the energy used to run up a hill, energy, as the first law of thermodynamics tells us, can be neither created nor destroyed. It is simply changed from one form to another.

ATP Re-Synthesis

The energy for all physical activity comes from the conversion of high-energy phosphates (adenosine�triphosphate�ATP) to lower-energy phosphates (adenosine�diphosphate�ADP; adenosine�monophosphate�AMP; and inorganic phosphate, P_i). During this breakdown (hydrolysis) of ATP, which is a water-requiring process, a proton, energy and heat are produced: ATP + H₂O �^��ADP + P_i�+ H⁺�+ energy + heat. Since our muscles don�t store much ATP, we must constantly resynthesize it. The hydrolysis and resynthesis of ATP is thus a circular process�ATP is hydrolyzed into ADP and P_i, and then ADP and P_i�combine to resynthesize ATP. Alternatively, two ADP molecules can combine to produce ATP and AMP: ADP + ADP �^��ATP + AMP.

Like many other animals, humans produce ATP through three metabolic pathways that consist of many enzyme-catalyzed chemical reactions: the phosphagen system, glycolysis and the aerobic system. Which pathway your clients use for the primary production of ATP depends on how quickly they need it and how much of it they need. Lifting heavy weights, for instance, requires energy much more quickly than jogging on the treadmill, necessitating the reliance on different energy systems. However, the production of ATP is never achieved by the exclusive use of one energy system, but rather by the coordinated response of all energy systems contributing to different degrees.

1. Phosphagen System

During short-term, intense activities, a large amount of power needs to be produced by the muscles, creating a high demand for ATP. The phosphagen system (also called the ATP-CP system) is the quickest way to resynthesize ATP (Robergs & Roberts 1997). Creatine phosphate (CP), which is stored in skeletal muscles, donates a phosphate to ADP to produce ATP: ADP + CP �^��ATP + C. No carbohydrate or fat is used in this process; the regeneration of ATP comes solely from stored CP. Since this process does not need oxygen to resynthesize ATP, it is anaerobic, or oxygen-independent. As the fastest way to resynthesize ATP, the phosphagen system is the predominant energy system used for all-out exercise lasting up to about 10 seconds. However, since there is a limited amount of stored CP and ATP in skeletal muscles, fatigue occurs rapidly.

2. Glycolysis

Glycolysis is the predominant energy system used for all-out exercise lasting from 30 seconds to about 2 minutes and is the second-fastest way to resynthesize ATP. During glycolysis, carbohydrate�in the form of either blood glucose (sugar) or muscle glycogen (the stored form of glucose)�is broken down through a series of chemical reactions to form pyruvate (glycogen is first broken down into glucose through a process called�glycogenolysis). For every molecule of glucose broken down to pyruvate through glycolysis, two molecules of usable ATP are produced (Brooks et al. 2000). Thus, very little energy is produced through this pathway, but the trade-off is that you get the energy quickly. Once pyruvate is formed, it has two fates: conversion to lactate or conversion to a metabolic intermediary molecule called acetyl coenzyme A (acetyl-CoA), which enters the mitochondria for oxidation and the production of more ATP (Robergs & Roberts 1997). Conversion to lactate occurs when the demand for oxygen is greater than the supply (i.e., during anaerobic exercise). Conversely, when there is enough oxygen available to meet the muscles� needs (i.e., during aerobic exercise), pyruvate (via acetyl-CoA) enters the mitochondria and goes through aerobic metabolism.

When oxygen is not supplied fast enough to meet the muscles� needs (anaerobic glycolysis), there is an increase in hydrogen ions (which causes the muscle pH to decrease; a condition called acidosis) and other metabolites (ADP, P_i�and potassium ions). Acidosis and the accumulation of these other metabolites cause a number of problems inside the muscles, including inhibition of specific enzymes involved in metabolism and muscle contraction, inhibition of the release of calcium (the trigger for muscle contraction) from its storage site in muscles, and interference with the muscles� electrical charges (Enoka & Stuart 1992; Glaister 2005; McLester 1997). As a result of these changes, muscles lose their ability to contract effectively, and muscle force production and exercise intensity ultimately decrease.

3. Aerobic System

Since humans evolved for aerobic activities (Hochachka, Gunga & Kirsch 1998; Hochachka & Monge 2000), it�s not surprising that the aerobic system, which is dependent on oxygen, is the most complex of the three energy systems. The metabolic reactions that take place in the presence of oxygen are responsible for most of the cellular energy produced by the body. However, aerobic metabolism is the slowest way to resynthesize ATP. Oxygen, as the patriarch of metabolism, knows that it is worth the wait, as it controls the fate of endurance and is the sustenance of life. �I�m oxygen,� it says to the muscle, with more than a hint of superiority. �I can give you a lot of ATP, but you will have to wait for it.�

The aerobic system�which includes the�Krebs cycle�(also called the�citric acid cycle or TCA cycle) and the�electron transport chain�uses blood glucose, glycogen and fat as fuels to resynthesize ATP in the mitochondria of muscle cells (see the sidebar �Energy System Characteristics�). Given its location, the aerobic system is also called�mitochondrial respiration.�When using carbohydrate, glucose and glycogen are first metabolized through glycolysis, with the resulting pyruvate used to form acetyl-CoA, which enters the Krebs cycle. The electrons produced in the Krebs cycle are then transported through the electron transport chain, where ATP and water are produced (a process called�oxidative phosphorylation) (Robergs & Roberts 1997). Complete oxidation of glucose via glycolysis, the Krebs cycle and the electron transport chain produces 36 molecules of ATP for every molecule of glucose broken down (Robergs & Roberts 1997). Thus, the aerobic system produces 18 times more ATP than does anaerobic glycolysis from each glucose molecule.

Fat, which is stored as triglyceride in adipose tissue underneath the skin and within skeletal muscles (called�intramuscular triglyceride), is the other major fuel for the aerobic system, and is the largest store of energy in the body. When using fat, triglycerides are first broken down into free fatty acids and glycerol (a process called�lipolysis). The free fatty acids, which are composed of a long chain of carbon atoms, are transported to the muscle mitochondria, where the carbon atoms are used to produce acetyl-CoA (a process called�beta-oxidation).

Following acetyl-CoA formation, fat metabolism is identical to carbohydrate metabolism, with acetyl-CoA entering the Krebs cycle and the electrons being transported to the electron transport chain to form ATP and water. The oxidation of free fatty acids yields many more ATP molecules than the oxidation of glucose or glycogen. For example, the oxidation of the fatty acid palmitate produces 129 molecules of ATP (Brooks et al. 2000). No wonder clients can sustain an aerobic activity longer than an anaerobic one!

Understanding how energy is produced for physical activity is important when it comes to programming exercise at the proper intensity and duration for your clients. So the next time your clients get done with a workout and think, �I have a lot of energy,� you�ll know exactly where they got it.

Energy System Characteristics

Energy System Workouts

Have clients warm up and cool down before and after each workout.

Phosphagen System

An effective workout for this system is short, very fast sprints on the treadmill or bike lasting 5�15 seconds with 3�5 minutes of rest between each. The long rest periods allow for complete replenishment of creatine phosphate in the muscles so it can be reused for the next interval.

2 sets of 8 x 5 seconds at close to top speed with 3:00 passive rest and 5:00 rest between sets
5 x 10 seconds at close to top speed with 3:00�4:00 passive rest

Glycolysis

This system can be trained using fast intervals lasting 30 seconds to 2 minutes with an active-recovery period twice as long as the work period (1:2 work-to-rest ratio).

8�10 x 30 seconds fast with 1:00 active recovery
4 x 1:30 fast with 3:00 active recovery

Aerobic System

While the phosphagen system and glycolysis are best trained with intervals, because those metabolic systems are emphasized only during high-intensity activities, the aerobic system can be trained with both continuous exercise and intervals.

60 minutes at 70%�75% maximum heart rate
15- to 20-minute tempo workout at lactate threshold intensity (about 80%�85% maximum heart rate)
5 x 3:00 at 95%�100% maximum heart rate with 3:00 active recovery

by�Jason Karp, PhD

References:

Brooks, G.A., et al. 2000.�Exercise Physiology: Human Bioenergetics and Its Applications.Mountain View, CA: Mayfield.

Enoka, R.M., & Stuart, D.G. 1992. Neurobiology of muscle fatigue.�Journal of Applied Physiology, 72�(5), 1631�48.

Glaister, M. 2005. Multiple sprint work: Physiological responses, mechanisms of fatigue and the influence of aerobic fitness.�Sports Medicine, 35�(9), 757�77.

Hochachka, P.W., Gunga, H.C., & Kirsch, K. 1998. Our ancestral physiological phenotype: An adaptation for hypoxia tolerance and for endurance performance?�Proceedings of the National Academy of Sciences, 95,�1915�20.

Hochachka, P.W., & Monge, C. 2000. Evolution of human hypoxia tolerance physiology.�Advances in Experimental and Medical Biology, 475,�25�43.

McLester, J.R. 1997. Muscle contraction and fatigue: The role of adenosine 5′-diphosphate and inorganic phosphate.�Sports Medicine, 23�(5), 287�305.

Robergs, R.A. & Roberts, S.O. 1997.�Exercise Physiology: Exercise, Performance, and Clinical Applications.�Boston: William C. Brown.

Dietary Strategies: Treatment Of Metabolic Syndrome

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Basal Metabolic Index (BMI), Functional Medicine, Metabolic Syndrome, Nutrition, Wellness

Dietary Strategies:

Abstract: Metabolic syndrome (MetS) is established as the combination of central obesity and different metabolic disturbances, such as insulin resistance, hypertension and dyslipidemia. This cluster of factors affects approximately 10%�50% of adults worldwide and the prevalence has been increasing in epidemic proportions over the last years. Thus, dietary strategies to treat this heterogenic disease are under continuous study. In this sense, diets based on negative-energy-balance, the Mediterranean dietary pattern, n-3 fatty acids, total antioxidant capacity and meal frequency have been suggested as effective approaches to treat MetS. Furthermore, the type and percentage of carbohydrates, the glycemic index or glycemic load, and dietary fiber content are some of the most relevant aspects related to insulin resistance and impaired glucose tolerance, which are important co-morbidities of MetS. Finally, new studies focused on the molecular action of specific nutritional bioactive compounds with positive effects on the MetS are currently an objective of scientific research worldwide. The present review summarizes some of the most relevant dietary approaches and bioactive compounds employed in the treatment of the MetS to date.

Keywords: metabolic syndrome; dietary strategies; bioactive compounds

1. Metabolic Syndrome

dietary healthy unhealthy food It was during the period between 1910 and 1920 when it was suggested for the first time that a cluster of associated metabolic disturbances tended to coexist together [1]. Since then, different health organisms have suggested diverse definitions for metabolic syndrome (MetS) but there has not yet been a well-established consensus. The most common definitions are summarized in Table 1. What is clear for all of these is that the MetS is a clinical entity of substantial heterogeneity, commonly represented by the combination of obesity (especially abdominal obesity), hyperglycemia, dyslipidemia and/or hypertension [2�6].

dietary table 1

Obesity consists of an abnormal or excessive fat accumulation, for which the main cause is a chronic imbalance between energy intake and energy expenditure [7,8]. The excess of energy consumed is primarily deposited in the adipose tissue as triglycerides (TG) [9].

Dyslipidemia encompasses elevated serum TG levels, increased low density lipoprotein- cholesterol (LDL-c) particles, and reduced levels of high density lipoprotein-cholesterol (HDL-c) [10]. It is associated with hepatic steatosis [11], dysfunction of pancreatic ?-cells [12] and elevated risk of atherosclerosis [13], among others.

Another main modifiable MetS manifestation is hypertension, which is mainly defined as a resting systolic blood pressure (SBP) ? 140 mmHg or diastolic blood pressure (DBP) ? 90 mmHg or drug prescription to lower hypertension [14]. It usually involves narrowed arteries and is identified as a major cardiovascular and renal risk factor, related to heart and vascular disease, stroke and myocardial infarction [13,15�17].

Hyperglycemia, related insulin resistance and type 2 diabetes mellitus are characterized by an impaired uptake of glucose by the cells, that lead to elevated plasma glucose levels, glycosuria and ketoacidosis [18]. It is responsible for different tissue damage that shortens the life expectancy of diabetics, involving cardiovascular diseases (CVD), atherosclerosis, hypertension [19], ?-cell dysfunction [12], kidney disease [20] or blindness [21]. Currently, diabetes is considered the leading cause of death in developed countries [22].

Moreover, oxidative stress and low grade inflammation are two important mechanisms implicated in the etiology, pathogenesis, and development of MetS [23]. Oxidative stress is defined as an imbalance between the pro-oxidants and antioxidants in the body [24]. It plays a key role in the development of atherosclerosis by different mechanisms such as the oxidation of LDL-c particles [25] or impairment of HDL-c functions [26]. Inflammation is an immune system response to injury hypothesized to be a major mechanism in the pathogenesis and progression of obesity related disorders and the link between adiposity, insulin resistance, MetS and CVD [27].

Although the prevalence of the MetS varies broadly around the word and depends on the source used for its definition, it is clear that over the last 40�50 years the number of people presenting with this syndrome has risen in epidemic proportions [28]. Moreover, the frequency of this syndrome is increased in developed countries, sedentary people, smokers, low socioeconomic status population, as well as in individuals with unhealthy dietary habits [29,30].

For all of this, there is currently a wide concern to find effective strategies to detect, treat and control the comorbidities associated with MetS. This is a complex challenge as MetS is a clinical entity of substantial heterogeneity and therefore, the different cornerstones implicated in its development should be addressed. In this review we compiled and examined different dietary patterns and bioactive compounds that have pointed out to be effective in MetS treatment.

2. Dietary Patterns

dietary Several dietary strategies and their potential positive effects on the prevention and treatment of the different metabolic complications associated to the MetS, are described below and summarized in Table 2.

2.1. Energy-Restricted Diet Strategies

dietary

Energy restricted diets are probably the most commonly used and studied dietary strategies for combating excess weight and related comorbidities. They consist in personalized regimes that supply less calories than the total energy expended by a specific individual [31].

A hypocaloric diet results in a negative energy balance and subsequently, in body weight reduction [31]. Weight loss is achieved via fat mobilization from different body compartments as a consequence of the lipolysis process necessary to provide energy substrate [32,33]. In people who are overweight or suffering from obesity, as is the case of most people with MetS, weight loss is important as it is associated with improvement of related disorders such as abdominal obesity (visceral adipose tissue), type 2 diabetes, CVD or inflammation [32�36].

Moreover, as described above, low grade inflammation is associated with MetS and obesity. Therefore, of particular importance is the fact that in obese individuals following a hypocaloric diet, a depletion of plasma inflammatory markers such as interleukin (IL)-6 has been observed [34]. Thus, caloric restriction in obese people suffering MetS may improve the whole-body pro-inflammatory state.

At the same time, body weight reduction is associated with improvements in cellular insulin signal transduction, increments in peripheral insulin sensitivity and higher robustness in insulin secretory responses [32,36]. People with excess body weight who are at risk of developing type 2 diabetes, may benefit from a hypocaloric regime by improving plasma glucose levels and insulin resistance.

In addition, different intervention trials have reported a relationship between energy restricted diets and lower risk of developing CVD. In this sense, in studies with obese people following a hypocaloric diet, improvements in lipid profile variables such as reductions of LDL-c and plasma�TG levels, as well as improvements in hypertension via depletion of SBP and DBP levels have been observed [35,37].

Among the different nutritional intervention trials, a reduction of 500�600 kcal a day of the energy requirements is a well-established hypocaloric dietary strategy, which has demonstrated to be effective in weight reduction [38,39]. However, the challenge lies in maintaining the weight loss over time, as many subjects can follow a prescribed diet for a few months, but most people have difficulty in maintaining the acquired habits over the long term [40,41].

2.2. Diets Rich in Omega-3 Fatty Acids

dietary foods omega 3 infographic The very long-chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are essential omega-3 polyunsaturated fatty acids (n-3 PUFAs) for human physiology. Their main dietary sources are fish and algal oils and fatty fish, but they can also be synthesized by humans from ?-linolenic acid [40].

There is a moderate body of evidence suggesting that n-3 PUFAs, mainly EPA and DHA, have a positive role in the prevention and treatment of the pathologies associated to MetS [42].

In this context, it has been described that EPA and DHA have the ability to reduce the risk of developing CVD and cardiometabolic abnormalities as well as CVD-related mortality [42]. These beneficial effects are thought to be mainly due to the ability of these essential fatty acids to reduce plasma TG levels [43].

Moreover, different studies have shown that people following an increased n-3 PUFA diet have reduced plasma levels of the pro-inflammatory cytokines IL-6 and tumor necrosis factor-alpha (TNF?), as well as plasma C-reactive protein (CRP) [44]. These effects are probably mediated by resolvins, maresins and protectins, which are EPA and DHA metabolic products with anti-inflammatory properties [44].

There are some studies that have observed an association between n-3 ingestion and improvements or prevention of type 2 diabetes development. However, other studies found opposite results [44]. Thus, it cannot be made any specific affirmation in this respect.

The European Food Safety Authority recommends and intake of 250 mg EPA + DHA a day, in the general healthy population as a primary prevention of CVD [45]. These amounts can be achieved with an ingestion of 1�2 fatty fish meals per week [45].

2.3. Diets Based on Low Glycemic Index/Load

dietary salad unconstructed Over the last ten years, the concern about the quality of the carbohydrates (CHO) consumed has risen [46]. In this context, the glycemic index (GI) is used as a CHO quality measure. It consists in a ranking on a scale from 0 to 100 that classifies carbohydrate-containing foods according to the postprandial glucose response [47]. The higher the index, the more promptly the postprandial serum glucose rises and the more rapid the insulin response. A quick insulin response leads to rapid hypoglycemia, which is suggested to be associated with an increment of the feeling of hunger and to a subsequent higher caloric intake [47]. The glycemic load (GL) is equal to the GI multiplied by the number of grams of CHO in a serving [48].

There is a theory which states that MetS is a consequence of an elevated intake of high GI foods over time, among others unhealthy dietary habits [49]. In this sense, following a diet rich in high GI CHO has been associated with hyperglycemia, insulin resistance, type 2 diabetes, hypertriglyceridemia, CVD, and obesity [47,50,51], abnormalities directly related to MetS.

On the contrary, a low GI diet has been associated with slower absorption of the CHO and subsequently smaller blood glucose fluctuations, which indicate better glycemic control [46]. In patients with type 2 diabetes, diets based on low GI are associated with reductions in glycated hemoglobin (HbA1c) and fructosamine blood levels, two biomarkers used as key monitoring factors in diabetes management [52,53].

For all of this, it is common to find the limitation of CHO at high GI among the advice for MetS treatment [28], in particular with respect to �ready-to-eat processed foods� including sweetened beverages, soft drinks, cookies, cakes, candy, juice drinks, and other foods which contain high amounts of added sugars [54].

2.4. Diets with High Total Antioxidant Capacity

dietary antioxidant foods Dietary total antioxidant capacity (TAC) is an indicator of diet quality defined as the sum of antioxidant activities of the pool of antioxidants present in a food [55]. These antioxidants have the capacity to act as scavengers of free radicals and other reactive species produced in the organisms [56]. Taking into account that oxidative stress is one of the remarkable unfortunate physiological states of MetS, dietary antioxidants are of main interest in the prevention and treatment of this multifactorial disorder [57]. Accordingly, it is well-accepted that diets with a high content of spices, herbs, fruits, vegetables, nuts and chocolate, are associated with a decreased risk of oxidative stress-related diseases development [58�60]. Moreover, several studies have analyzed the effects of dietary TAC in individuals suffering from MetS or related diseases [61,62]. In the Tehran Lipid and Glucose Study it was demonstrated that a high TAC has beneficial effects on metabolic disorders and especially prevents weight and abdominal fat gain [61]. In the same line, research conducted in our institutions also evidenced that beneficial effects on body weight, oxidative stress biomarkers and other MetS features were positively related with higher TAC consumption in patients suffering from MetS [63�65].

In this sense, the World Health Organization (WHO) recommendation for fruit and vegetables consumption (high TAC foods) for the general population is a minimum of 400 g a day [66]. Moreover, cooking with spices is recommended in order to increase the TAC dietary intake and, at the same time, maintain flavor while reducing salt [67].

2.5. Moderate-High Protein Diets

dietary Protein rich Foods The macronutrient distribution set in a weight loss dietary plan has commonly been 50%�55% total caloric value from CHO, 15% from proteins and 30% from lipids [57,68]. However, as most people have difficulty in maintaining weight loss achievements over time [69,70], research on increment of protein intake (>20%) at the expense of CHO was carried out [71�77].

Two mechanisms have been proposed to explain the potential beneficial effects of high-moderate protein diets: the increment of diet-induced thermogenesis [73] and the increase of satiety [78]. The increment of the thermogenesis is explained by the synthesis of peptide bonds, production of urea and gluconeogenesis, which are processes with a higher energy requirement than the metabolism of lipids or CHO [75]. An increment of different appetite-control hormones such as insulin, cholecystokinin or glucagon-like peptide 1, may clarify the satiety effect [79].

Other beneficial effects attributed to moderate-high protein diets in the literature are the improvement of glucose homeostasis [80], the possibility of lower blood lipids [81], the reduction of blood pressure [82], the preservation of lean body mass [83] or the lower of cardiometabolic disease risk [84,85]. However, there are other studies that have not found benefits associated to a moderate-high protein diet [76]. This fact may be explained by the different type of proteins and their amino acid composition [80], as well as by the different type of populations included in each study [85]. Therefore, more research in the field is needed in order to make these results consistent.

In any case, when a hypocaloric diet is implemented, it is necessary to slightly increase the amount of proteins. Otherwise it would be difficult to reach the protein energy requirements, established as 0.83 g/kg/day for isocaloric diets and which should probably be at least 1 g/kg/day for energy-restricted diets [86].

2.6. High Meal Frequency Pattern

dietary eating time

The pattern of increasing meal frequency in weight loss and weight control interventions has currently become popular among professionals [87,88]. The idea is to distribute the total daily energy�intake into more frequently and smaller meals. However, there is no strong evidence about the efficacy of this habit yet [89]. While some investigations have found an inverse association between the increment of meals per day and body weight, body mass index (BMI), fat mass percentage or metabolic diseases such as coronary heart disease or type 2 diabetes [71,88,90�92], others have found no association [93�95].

Different mechanisms by which high meal frequency can have a positive effect on weight and metabolism management have been proposed. An increment of energy expenditure was hypothesized; however, the studies carried out in this line have concluded that total energy expenditure does not differ among different meal frequencies [96,97]. Another postulated hypothesis is that the greater the number of meals a day, the higher the fat oxidation, but again no consensus has been achieved [89,98]. An additional suggested mechanism is that increasing meal frequency leads to plasma glucose levels with lower oscillations and reduced insulin secretion which is thought to contribute to a better appetite control. However, these associations have been found in population with overweight or high glucose levels but in normal-weight or normoglycaemic individuals the results are still inconsistent [93,99�101].

2.7. The Mediterranean Diet

dietary Mediterranean Diet The concept of the Mediterranean Diet (MedDiet) was for the first time defined by the scientific Ancel Keys who observed that those countries around the Mediterranean Sea, which had a characteristic diet, had less risk of suffering coronary heart diseases [102,103].

The traditional MedDiet is characterized by a high intake of extra-virgin olive oil and plant foods (fruits, vegetables, cereals, whole grains, legumes, tree nuts, seeds and olives), low intakes of sweets and red meat and moderate consumption of dairy products, fish and red wine [104].

There is a lot of literature supporting the general health benefits of the MedDiet. In this sense, it has been reported that a high adherence to this dietary pattern protects against mortality and morbidity from several causes [105]. Thus, different studies suggested the MedDiet as a successful tool for the prevention and treatment of MetS and related comorbidities [106�108]. Moreover, recent meta-analysis concluded that the MedDiet is associated with less risk of developing type 2 diabetes and with a better glycemic control in people with this metabolic disorder [107,109,110]. Other studies have found a positive correlation between the adherence to a MedDiet pattern and reduced risk of developing CVD [111�114]. In fact, many studies have found a positive association between following a MedDiet and improvements in lipid profile by reduction of total cholesterol, LDL-c and TG, and an increase in HDL-c [111�115]. Finally, different studies also suggest that the MedDiet pattern may be a good strategy for obesity treatment as it has been associated with significant reductions in body weight and waist circumference [108,116,117].

The high amount of fiber which, among other beneficial effects, helps to weight control providing satiety; and the high antioxidants and anti-inflammatory nutrients such as n-3 fatty acids, oleic acid or phenolic compounds, are thought to be the main contributors to the positive effects attributed to the MedDiet [118].

For all these reasons, efforts to maintain the MedDiet pattern in Mediterranean countries and to implement this dietary habits in westernized countries with unhealthy nutritional patterns should be made.

3. Dietary: Single Nutrients and Bioactive Compounds

dietary Nutrition single nutrient New studies focused on the molecular action of nutritional bioactive compounds with positive effects on MetS are currently an objective of scientific research worldwide with the aim of designing more personalized strategies in the framework of molecular nutrition. Among them, flavonoids and antioxidant vitamins are some of the most studied compounds with different potential benefits such as antioxidant, vasodilatory, anti-atherogenic, antithrombotic, and anti-inflammatory effects [119]. Table 3 summarizes different nutritional bioactive compounds with potential positive effects on MetS, including the possible molecular mechanism of action involved.

dietary table 3

3.1. Ascorbate

dietary Ascorbate Vitamin C, ascorbic acid or ascorbate is an essential nutrient as human beings cannot synthesize it. It is a water-soluble antioxidant mainly found in fruits, especially citrus (lemon, orange), and vegetables (pepper, kale) [120]. Several beneficial effects have been associated to this vitamin such as antioxidant and anti-inflammatory properties and prevention or treatment of CVD and type 2 diabetes [121�123].

This dietary component produces its antioxidant effect primarily by quenching damaging free radicals and other reactive oxygen and nitrogen species and therefore preventing molecules such as LDL-c from oxidation [122]. It can also regenerate other oxidized antioxidants like tocopherol [124].

Moreover, it has been described that ascorbic acid may reduce inflammation as it is associated with depletion of CRP levels [125]. This is an important outcome to take in consideration in the treatment of MetS sufferers, as they usually present low grade inflammation [27].

Supplementation with vitamin C have also been associated with prevention of CVD by improving the endothelial function [126] and probably by lowering blood pressure [121]. These effects are thought to be exerted by the ability of vitamin C to enhance the endothelial nitric oxide synthase enzyme (eNOS) activity and to reduce HDL-c glycation [127].

Additionally, several studies have attributed to ascorbate supplementation an antidiabetic effect by improving whole body insulin sensitivity and glucose control in people with type 2 diabetes [123]. These antidiabetic properties are thought to be mediated by optimization of the insulin secretory function of the pancreatic islet cells by increasing muscle sodium-dependent vitamin C transporters (SVCTs) [128].

Despite all of this, it should be taken into account that most people reach ascorbic acid requirements (established at 95�110 mg/day in the general population) from diet and do not need supplementation [122,129]. Besides, it should be considered that an excess of vitamin C ingestion leads to the opposite effect and oxidative particles are formed [130,131].

3.2. Hydroxytyrosol

dietary Hydroxytyrosol Hydroxytyrosol (3,4-dihydroxyphenylethanol) is a phenolic compound mainly found in olives [132].

It is considered the strongest antioxidant of olive oil and one of the main antioxidants in nature [133]. It acts as a powerful scavenger of free radicals, as a radical chain breaker and as metal chelator [134]. It has the ability of inhibiting LDL-c oxidation by macrophages [132]. In this sense, it is the only phenol recognized by the European Food Safety Authority (EFSA) as a protector of blood lipids from oxidative damage [135].

Hydroxytyrosol has also been reported to have anti-inflammatory effects, probably by suppressing cyclooxygenase activity and inducing eNOS expression [136]. Thus, enhancement of olives/olive oil intakes or hydroxytyroxol supplementation in people suffering from MetS may be a good strategy in order to improve inflammatory status.

Another beneficial effect attributed to this phenolic compound is its cardiovascular protective effect. It presents anti-atherogenic properties by decreasing the expression of vascular cell adhesion protein 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) [132,137], which are probably the result of an inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF?B), activator protein 1 (AP-1), GATA transcription factor and nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase [138,139]. Hydroxytyrosol also provides antidyslipidemic effects by lowering plasma levels of LDL-c, total cholesterol and TG, and by rising HDL-c [138].

Despite the beneficial effects attributed to hydfroxytyrosol as an antioxidant, for its antiinflamatory properties and as cardiovascular protector, it should be taken into account that most studies focused on this compound have been performed with mixtures of olive phenols, thus a synergic effect cannot be excluded [140].

3.3. Quercetin

dietary Quercetin is a predominant flavanol naturally present in vegetables, fruits, green tea or red wine. It is commonly found as glycoside forms, where rutin is the most common and important structure found in nature [141].

Many beneficial effects that can contribute to MetS improvement have been attributed to quercetin. Among them, its antioxidant capacity should be highlighted, as it has been reported to inhibit lipid peroxidation and increase antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) or glutathione peroxidase (GPX) [142].

Moreover, an anti-inflammatory effect mediated via attenuation of tumor necrosis factor ? (TNF-?), NF?B and mitogen-activated protein kinases (MAPK), as well as depletion of IL-6, IL-1?, IL-8 or monocyte chemoattractant protein-1 (MCP-1) gene expression has also been attributed to this polyphenol [143].

As most people with MetS are overweight or obese, the role of quercetin in body weight reduction and obesity prevention has been of special interest. In this sense, it stands out the capacity of quercetin to inhibit adipogenesis through inducing the activation of AMP-activated protein kinase (AMPK) and decreasing the expression of CCAAT-enhancer-binding protein-? (C/EBP?), peroxisome�proliferator-activated receptor gamma (PPAR?), and sterol regulatory element-binding protein 1 (SREBP-1) [141,144].

According to the antidiabetic effects, it is proposed that quercetin may act as an agonist of peroxisome proliferator-activated receptor gamma (PPAR?), and thus improve insulin-stimulated glucose uptake in mature adipocytes [145]. Moreover, quercetin may ameliorate hyperglycemia by inhibiting glucose transporter 2 (GLUT2) and insulin dependent phosphatidylinositol-3-kinase (PI3K) and blocking tyrosine kinase (TK) [142].

Finally, different studies observed that quercetin has the ability to reduce blood pressure [146�148]. However, the mechanisms of action are not clear, since some authors have suggested that quercetin increases eNOS, contributing to inhibition of platelet aggregation and improvement of the endothelial function [146,147], but there are other studies that have not come across these results [148].

3.4. Resveratrol

dietary

Resveratrol (3,5,4?-trihidroxiestilben) is a phenolic compound mainly found in red grapes and derived products (red wine, grape juice) [149]. It has shown antioxidant and anti-inflammatory activities, and cardioprotective, anti-obesity and antidiabetic capacities [150�156].

The antioxidant effects of resveratrol have been reported to be carried out by scavenging of hydroxyl, superoxide, and metal-induced radicals as well as by antioxidant effects in cells producing reactive oxygen species (ROS) [150].

Moreover, it has been reported that the anti-inflammatory effects of resveratrol are mediated by inhibiting NF?B signaling [151]. Furthermore, this polyphenol reduces the expression of proinflammatory cytokines such as interleukin 6 (IL-6), interleukin 8 (IL-8), TNF-?, monocyte chemoattractant protein-1 (MCP-1) and eNOS [152]. In addition, resveratrol inhibits the cyclooxygenase (COX) expression and activity, a pathway involved in the synthesis of proinflammatory lipid mediators [152].

Concerning the effects of resveratrol against development of type 2 diabetes, it has been reported that treatment of diabetes patients with this polyphenol provides significant improvements in the status of multiple clinically relevant biomarkers such as fasting glucose levels, insulin concentrations or glycated hemoglobin and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) [153,154].

Additionally, cardioprotective effects have been attributed to resveratrol. In this sense, it is suggested that resveratrol improves the endothelial function by producing nitric oxide (NO) through increasing the activity and expression of eNOS. This effect is thought to be conducted through activation of nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (Sirt 1) and 5? AMP-activated protein kinase (AMPK) [155]. Besides, resveratrol exerts endothelial protection by stimulation of NF-E2-related factor 2 (Nrf2) [156] and decreasing the expression of adhesion proteins such as ICAM-1 and VCAM-1 [152].

Finally, it has been described that resveratrol may have a role in preventing obesity as it has been related with energy metabolism improvement, increasing lipolysis and reducing lipogenesis [157]. However, more studies are needed in order to corroborate these findings.

3.5. Tocopherol

dietary vitamin e Tocopherol Tocopherols, also known as vitamin E, are a family of eight fat-soluble phenolic compounds whose main dietary sources are vegetable oils, nuts and seeds [130,158].

For a long time, it has been suggested that vitamin E could prevent different metabolic diseases as a potent antioxidant, acting as scavenger of lipid peroxyl radicals by hydrogen donating [159]. In this sense, it was described that tocopherols inhibit peroxidation of membrane phospholipids and prevent generation of free radicals in cell membranes [160].

Moreover, it has been shown that supplementation with ?-tocopherol or ?-tocopherol, two of the different isoforms of vitamin E, could have an effect on inflammation status by reducing CRP levels [161]. Additionally, inhibition of COX and protein kinase C (PKC) and reduction of cytokines�such as IL-8 or plasminogen activator inhibitor-1 (PAI-1) are other mechanisms that may contribute to these anti-inflammatory effects [162,163].

However, the beneficial effects attributed to this vitamin previously have lately became controversial as different clinical trials have not come across such benefits, but ineffective or even harmful effects have been observed [164]. It has been recently suggested that this may be explained by the fact that vitamin E may lose most of the antioxidant capacity when ingested by human beings through different mechanisms [162].

3.6. Anthocyanins

dietary Anthocyanins

Anthocyanins are water-soluble polyphenolic compounds responsible for the red, blue and purple colors of berries, black currants, black grapes, peaches, cherries, plums, pomegranate, eggplant, black beans, red radishes, red onions, red cabbage, purple corn or purple sweet potatoes [165�167]. Actually, they are the most abundant polyphenols in fruits and vegetables [167]. Moreover, they can also be found in teas, honey, nuts, olive oil, cocoa, and cereals [168].

These compounds have high antioxidant capacity inhibiting or decreasing free radicals by donating or transferring electrons from hydrogen atoms [167].

Regarding clinical studies, it has been shown that these bioactive compounds may prevent type 2 diabetes development by improving insulin sensitivity [169]. The exact mechanisms by which anthocyanins exert their antidiabetic effect are not yet clear, but an enhancement of the glucose uptake by muscle and adipocyte cells in an insulin-independent manner has been suggested [169].

Moreover, it has been shown that anthocyanins may have the capacity to prevent CVD development by improving endothelial function via increasing brachial artery flow-mediated dilation and HDL-c, and decreasing serum VCAM-1 and LDL-c concentrations [170�173].

Finally, these polyphenolic compounds may exert anti-inflamatory effects via reducing proinflamatory molecules such as IL-8, IL-1? or CRP [172,174].

However, most studies have used anthocyanin-rich extracts instead of purified anthocyanins; thus, a synergic effect with other polyphenols cannot be discarded.

3.7. Catechins

dietary tea leaves Catechins Catechins are polyphenols that can be found in a variety of foods including fruits, vegetables, chocolate, wine, and tea [175]. The epigallocatechin 3-gallate present in tea leaves is the catechin class most studied [176].

Anti-obesity effects have been attributed to these polyphenols in different studies [176]. The mechanisms of action suggested to explain these beneficial effects on body weight are: increasing energy expenditure and fat oxidation, and reducing fat absorption [177]. It is thought that energy expenditure is enhanced by catechol-O-methyltransferase and phosphodiesterase inhibition, which stimulates the sympathetic nervous system causing an activation of the brown adipose tissue [178]. Fat oxidation is mediated by upregulation of acyl-CoA dehydrogenase and peroxisomal b-oxidation enzymes [178,179].

Moreover, catechin intake has also been associated with lower risk of CVD development by improving lipid biomarkers. Thus, it has been reported that consumption of this kind of polyphenols may increase HDL-c and decrease LDL-c and total cholesterol [180].

Finally, and antidiabetic effect has also been related to catechin comsumption, lowering fasting glucose levels [175] and improving insulin sensitivity [178].

4. Conclusions

As the prevalence of MetS reaches epidemic rates, the finding of an effective and easy-to-follow dietary strategy to combat this heterogenic disease is still a pending subject. This work recompiled different dietary nutrients and nutritional patterns with potential benefits in the prevention and�treatment of MetS and related comorbidities (Figure 1) with the aim of facilitating future clinical�studies in this area. The challenge now is to introduce precision bioactive compounds in personalized�nutritional patterns in order to gain the most benefits for prevention and treatment of this disease�through nutrition.

Conflicts of Interest: The authors declare no conflict of interest.

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Eur. J. Nutr. 2014, 53, 1299�1311. [CrossRef] [PubMed]

Close Accordion

Metabolic Syndrome And Chiropractic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Basal Metabolic Index (BMI), Chiropractic, Functional Medicine, Metabolic Syndrome, Nutrition, Wellness

Metabolic Syndrome:

Key indexing terms:

Metabolic syndrome X
Insulin resistance
Hyperglycemia
Inflammation
Weight loss

Abstract
Objective: This article presents an overview of metabolic syndrome (MetS), which is a collection of risk factors that can lead to diabetes, stroke, and heart disease. The purposes of this article are to describe the current literature on the etiology and pathophysiology of insulin resistance as it relates to MetS and to suggest strategies for dietary and supplemental management in chiropractic practice.

Methods: The literature was searched in PubMed, Google Scholar, and the Web site of the American Heart Association, from the earliest date possible to May 2014. Review articles were identified that outlined pathophysiology of MetS and type 2 diabetes mellitus (T2DM) and relationships among diet, supplements, and glycemic regulation, MetS, T2DM, and musculoskeletal pain.

Results: Metabolic syndrome has been linked to increased risk of developing T2DM and cardiovascular disease and increased risk of stroke and myocardial infarction. Insulin resistance is linked to musculoskeletal complaints both through chronic inflammation and the effects of advanced glycosylation end products. Although diabetes and cardiovascular disease are the most well-known diseases that can result from MetS, an emerging body of evidence demonstrates that common musculoskeletal pain syndromes can be caused by MetS.

Conclusions: This article provides an overview of lifestyle management of MetS that can be undertaken by doctors of chiropractic by means of dietary modification and nutritional support to promote blood sugar regulation.

Introduction: Metabolic Syndrome

Metabolic syndrome (MetS) has been described as a cluster of physical examination and laboratory findings�that directly increases the risk of degenerative metabolic disease expression. Excess visceral adipose tissue, insulin resistance, dyslipidemia, and hypertension are conditions that significantly contribute to the syndrome. These conditions are united by a pathophysiological basis in low-grade chronic inflammation and increase an individual’s risk of cardiovascular disease, type 2 diabetes mellitus (T2DM), and all-cause mortality.1

The National Health and Nutrition Examination Survey (NHANES) 2003-2006 estimated that approximately 34% of United States adults aged 20 years and more had MetS.2 The same NHANES data found that 53% had abdominal adiposity, a condition that is closely linked to visceral adipose stores. Excess visceral adiposity generates increased systemic levels of pro-inflammatory mediator molecules. Chronic, low- grade inflammation has been well documented as an associated and potentially inciting factor for the development of insulin resistance and T2DM.1

NHANES 2003-2006 data showed that 39% of subjects met criteria for insulin resistance. Insulin resistance is a component of MetS that significantly contributes to the expression of chronic, low-grade inflammation and predicts T2DM expression. T2DM costs the United States in excess of $174 billion in 2007. 3 It is estimated that 1 in 4 adults will have T2DM by the year 2050.3 Currently, more than one third of US adults (34.9%) are obese, 4 and, in 2008, the annual medical cost of obesity was $147 billion.4,5 This clearly represents a health care concern.

The pervasiveness of MetS dictates that doctors of chiropractic will see a growing proportion of patients who fit the syndrome criteria.6 Chiropractic is most commonly used for musculoskeletal complaints believed to be mechanical in nature;6 however, an emerging body of evidence identifies MetS as a biochemical promoter of musculoskeletal complaints such as neck pain, shoulder pain, patella tendinopathy, and widespread musculoskeletal pain. 7�13 As an example, the cross-linking of collagen fibers can be caused by increased advanced glycation end-product (AGE) formation as seen in insulin resistance.14 Increased collagen cross-linking is observed in both osteoarthritis and degenerative disc disease, 15 and reduced mobility in elderly patients with T2DM has also been attributed to AGE-induced collagen cross-linking. 16,17

A diagnosis of MetS is made from a patient having 3 of the 5 findings presented in Table 1. Fasting hyperglycemia is termed impaired fasting glucose and indicates insulin resistance. 18,19 An elevated hemoglobin A1c (HbA1c) level measures long-term blood glucose�regulation and is diagnostic for T2DM when elevated in the presence of impaired fasting glucose. 3,18

metabolic table 1

The emerging evidence demonstrates that we cannot view musculoskeletal pain as only coming from conditions that are purely mechanical in nature. Doctors of chiropractic must demonstrate prowess in identification and management of MetS and an understanding of insulin resistance as its main pathophysiological feature. The purposes of this article are to describe the current literature on the etiology and pathophysiology of insulin resistance as it relates to MetS and to suggest strategies for dietary and supplemental management in chiropractic practice.

Methods

metabolic method arrows PubMed was searched from the earliest possible date to May 2014 to identify review articles that outlined the pathophysiology of MetS and T2DM. This led to further search refinements to identify inflammatory mechanisms that occur in the pancreas, adipose tissue, skeletal muscle, and hypothalamus. Searches were also refined to identify relationships among diet, supplements, and glycemic regulation. Both animal and human studies were reviewed. The selection of specific supplements was based on those that were most commonly used in the clinical setting, namely, gymnema sylvestre, vanadium, chromium and ?-lipoic acid.

Discussion

Insulin Resistance Overview

metabolic insulin resistance 1 Under normal conditions, skeletal muscle, hepatic, and adipose tissues require the action of insulin for cellular glucose entry. Insulin resistance represents an inability of insulin to signal glucose passage into insulin-dependent cells. Although a genetic predisposition can exist, the�etiology of insulin resistance has been linked to chronic low-grade inflammation.1 Combined with insulin resistance-induced hyperglycemia, chronic low-grade inflammation also sustains MetS pathophysiology.1

Two thirds of postprandial blood glucose metabolism occurs within skeletal muscle via an insulin-dependent mechanism.18,19 Insulin binding to its receptor triggers glucose entry and subsequently inhibits lipolysis within the target tissue.21,22 Glucose enters skeletal muscles cells by way of a glucose transporter designated Glut4. 18 Owing to genetic variability, insulin-mediated glucose uptake can vary more than 6-fold among non-diabetic individuals. 23

Prolonged insulin resistance leads to structural changes within skeletal muscle such as decreased Glut4 transporter number, intramyocellular fat accu- mulation, and a reduction in mitochondrial con- tent.19,24 These events are thought to impact energy generation and functioning of affected skeletal mus- cle.24 Insulin-resistant skeletal muscle is less able to suppress lipolysis in response to insulin binding.25 Subsequently, saturated free fatty acids accumulate and generate oxidative stress. 22 The same phenomenon within adipose tissue generates a rapid adipose cell expansion and tissue hypoxia.26 Both these processes increase inflammatory pathway activation and the generation of proinflammatory cytokines (PICs).27

Multiple inflammatory mediators are associated with the promotion of skeletal muscle insulin resistance. The PICs tumor necrosis factor ? (TNF-?), interleukin 1 (IL- 1), and IL-6 have received much attention because of their direct inhibition of insulin signaling.28�30 Since cytokine testing is not performed clinically, elevated levels of high- sensitivity C-reactive protein (hsCRP) best represent the low-grade systemic inflammation that characterizes insulin resistance.31,32

Insulin resistance�induced hyperglycemia can lead to irreversible changes in protein structure, termed glycation, and the formation of AGEs. Cells such as those of the vascular endothelium are most vulnerable to hyperglycemia due to utilization of an insulin-independent Glut1 transporter. 33 This makes AGE generation responsible for most diabetic complications, 15,33,34 including collagen cross-linking.15

If unchanged, prolonged insulin resistance can lead to T2DM expression. The relationship between chronic low-grade inflammation and T2DM has been well characterized. 35 Research has demonstrated that patients with T2DM also have chronic inflammation within the pancreas, termed insulitis, and it worsens hyperglycemia due to the progressive loss of insulin- producing ? cells.36�39

Visceral Adiposity And Insulin Resistance

metabolic Visceral Adiposity Insulin resistance Caloric excess and a sedentary lifestyle contribute to the accumulation of subcutaneous and visceral adipose tissue. Adipose tissue was once thought of as a metabolically inert passive energy depot. A large body of evidence now demonstrates that excess visceral adipose tissue acts as a driver of chronic low-grade inflammation and insulin resistance.27,34

It has been documented that immune cells infiltrate rapidly expanding visceral adipose tissue. 26,40 Infil- trated macrophages become activated and release PICs that ultimately cause a phenotypic shift in resident macrophage phenotype to a classic inflammatory M1 profile.27 This vicious cycle creates a chronic inflam- matory response within adipose tissue and decreases the production of adipose-derived anti-inflammatory cytokines.43 As an example, adiponectin is an adipose- derived anti-inflammatory cytokine. Macrophage- invaded adipose tissue produces less adiponectin, and this has been correlated with increasing insulin resistance. 26

Hypothalamic Inflammation And Insulin Resistance

metabolic Hypothalamic Inflammation And Insulin Resistance Eating behavior in the obese and overweight has been popularly attributed to a lack of will power or genetics. However, recent research has demonstrated a link between hypothalamic inflammation and increased body weight.41,41

Centers that govern energy balance and glucose homeostasis are located within the hypothalamus. Recent studies demonstrate that inflammation in the hypothalamus coincides with metabolic inflammation and an increase in appetite.43 These hypothalamic centers simultaneously become resistant to anorexigenic stimuli, leading to altered energy intake. It has been suggested that this provides a neuropathological basis for MetS and drives a progressive increase in body weight. 41

Central metabolic inflammation pathologically activates hypothalamic immune cells and disrupts central insulin and leptin signaling.41 Peripherally, this has been associated with dysregulated glucose homeostasis that also impairs pancreatic ? cell functioning.41,44 Hypothalamic inflammation contributes to hypertension through similar mechanisms, and it is thought that central inflammation parallels chronic low-grade systemic inflammation and insulin resistance.41�44

Clinical Correlates Diet-Induced Inflammation & Insulin Resistance

Fatty foods Feeding generally leads to a short-term increase in both oxidative stress and inflammation. 41 Total�calories consumed, glycemic index, and fatty acid profile of a meal all influence the degree of postprandial inflammation. It is estimated that the average American consumes approximately 20% of calories from refined sugar, 20% from refined grains and flour, 15% to 20% from excessively fatty meat products, and 20% from refined seed/legume oils.45 This pattern of eating contains a macronutrient composition and glycemic index that promote hyperglycemia, hyperlipemia, and an acute postprandial inflammatory response. 46 Collectively referred to as postprandial dysmetabolism, this pro-inflammatory response can sustain levels of chronic low-grade inflammation that leads to excess body fat, coronary heart disease (CHD), insulin resistance, and T2DM.28,29,47

Recent evidence suggests that several MetS criteria may not sufficiently identify all individuals with postprandial dysmetabolism. 48,49 A 2-hour oral glucose tolerance test (2-h OGTT) result greater than 200 mg/dL can be used clinically to diagnose T2DM. Although MetS includes a fasting blood glucose level less than 100 mg/dL, population studies have shown that a fasting glucose as low as 90 mg/dL can be associated with an 2-h OGTT level greater than 200 mg/dL.49 Further, a recent large cohort study indicated that an increased 2-h OGTT was independently predictive of cardiovascular and all-cause mortality in a nondiabetic population. 48 Mounting evidence indicates that post- prandial glucose levels are better correlated with MetS and predicting future cardiovascular events than fasting blood glucose alone.41,48

Fasting triglyceride levels generally correlate with postprandial levels, and a fasting triglyceride level greater than 150 mg/dL reflects MetS and insulin resistance. Contrastingly, epidemiologic data indicate that a fasting triglyceride level greater than 100 mg/dL influences CHD risk via postprandial dysmetabolism. 48 The acute postprandial inflammatory response that contributes to CHD risk includes an increase in PICs, free radicals, and hsCRP.48,49 These levels are not measured clinically but, monitoring fasting glucose, 2-hour postprandial glucose and fasting triglycerides can be used as correlates of postprandial dysmetabolic and low-grade systemic inflammation.

MetS And Disease Expression

metabolic diabetes related words Diagnosis of MetS has been linked to an increased risk of developing T2DM and cardiovascular disease over the following 5 to 10 years. 1 It further increases a patient’s risk of stroke, myocardial infarction, and death from any of the aforementioned conditions.1

Facchini et al47 followed 208 apparently healthy, non-obese subjects for 4 to 11 years while monitoring the incidence of clinical events such as hypertension, stroke, CHD, cancer, and T2DM. Approximately one fifth of participants experienced clinical events, and all of these subjects were either classified as intermediately or severely insulin resistant. It is important to note that all of these clinical events have a pathological basis in chronic low-grade inflammation,50 and no events were experienced in the insulin-sensitive groupings. 47

Insulin resistance is linked to musculoskeletal com- plaints both through chronic inflammation and the effects of AGEs. Advanced glycation end-products have been shown to extensively accumulate in osteoarthritic cartilage and treatment of human chondrocytes with AGEs increased their catabolic activity. 51 Advanced glycation end-products increase collagen stiffness via cross-linking and likely contribute to reduced joint mobility seen in elderly patients with T2DM.52 Com- pared to non-diabetics, type II diabetic patients are known to have altered proteoglycan metabolism in their intervertebral discs. This altered metabolism may pro- mote weakening of the annular fibers and subsequently, disc herniation.53 The presence of T2DM increases a person’s risk of expressing disc herniation in both the cervical and lumbar spines.17,54 Patients with T2DM are also more likely to develop lumbar stenosis compared with non-diabetics, and this has been documented as a plausible relationship between MetS risk factors and physician-diagnosed lumbar disc herniation. 55�57

There are no specific symptoms that denote early skeletal muscle structural changes. Fatty infiltration and decreased muscle mitochondria content are observed within age-related sarcopenia 58 ; however, it is still being argued whether fatty infiltration is a risk factor for low back pain. 59,60

Clinical management of MetS should be geared toward improving insulin sensitivity and reducing chronic low-grade inflammation. 1 Regular exercise without weight loss is associated with reduced insulin resistance, and at least 30 minutes of aerobic activity and resistance training is recommended daily. 61,62 Although frequently considered preventative, exercise, dietary, and weight loss interventions should be considered alongside pharmacological management in those with MetS. 1

Data regarding the exact amount of weight loss needed to improve chronic inflammation are inconclusive. In overweight individuals without diagnosed MetS, a very-low-carbohydrate diet (b 10% calories from carbohydrate) has significantly reduced plasma inflammatory markers (TNF-?, hsCRP, and IL-6) with�as little as 6% reduction in body weight.63,64 Individuals who meet MetS criteria may require 10% to 20% body weight loss to reduce inflammatory markers. 65 Interestingly, the Mediterranean Diet has been shown to reduce markers of systemic inflammation independent of weight loss65 and was recommended in the American College of Cardiology and American Heart Association Adult Treatment Panel 4 guidelines.66

A growing body of research has examined the effects of the Spanish ketogenic Mediterranean diet, including olive oil, green vegetables and salads, fish as the primary protein, and moderate red wine consumption. In a sample of 22 patients, adoption of the Spanish ketogenic Mediterranean diet with 9 g of supplemental salmon oil on days when fish was not consumed has led to complete resolution of MetS.67 Significant reductions in markers of chronic systemic inflammation were seen in 31 patients following this diet for 12 weeks.68

A Paleolithic diet based on lean meat, fish, fruits, vegetables, root vegetables, eggs, and nuts has been described as more satiating per calorie than a diabetes diet in patients with T2DM.69 In a randomized crossover study, a Paleolithic diet resulted in lower mean HbA1c values, triglycerides, diastolic blood pressure, waist circumference, improved glucose tolerance, and higher high-density lipoprotein (HDL) values compared to a diabetes diet.70 Within the context of these changes, a referral for medication management may be advisable.

Irrespective of name, a low-glycemic diet that focuses on vegetables, fruits, lean meats, omega-3 fish, nuts, and tubers can be considered anti-inflammatory and has been shown to ameliorate insulin resistance. 49,71�73 Inflammatory markers and insulin resistance further improve when weight loss coincides with adherence to an anti-inflammatory diet.70 A growing body of evidence suggests that specific supplemental nutrients also reduce insulin resistance and improve chronic low-grade inflammation.

Key Nutrients That Promote Insulin Sensitivity

metabolic nutrients Research has identified nutrients that play key roles in promoting proper insulin sensitivity, including vitamin D, magnesium, omega-3 (n-3) fatty acids, curcumin, gymnema, vanadium, chromium, and ?-lipoic acid. It is possible to get adequate vitamin D from sun exposure and adequate amounts of magnesium and omega-3 fatty acids from food. Contrastingly, the therapeutic levels of chromium and ?-lipoic acid that affect insulin sensitivity and reduce�insulin resistance cannot be obtained in food and must be supplemented.

Vitamin D, Magnesium, Omega-3 Fatty Acids, & Curcumin

metabolic Vitamin D, Magnesium, Omega-3 Fatty Acids, Curcumin Vitamin D, magnesium, and n-3 fatty acids have multiple functions, and generalized inflammation reduction is a common mechanism of action.74�80 Their supplemental use should be considered in the context of low-grade inflammation reduction and health promotion, rather than as a specific treatment for MetS or T2DM.

Evidence pertaining to the precise role of vitamin D in MetS and insulin resistance is inconclusive. Increas- ing dietary and supplemental vitamin D intake in young men and women may lower the risk of MetS and T2DM development,81 and a low serum vitamin D level has been associated with insulin resistance and T2DM expression. 82 Supplementation to improve low serum vitamin D (reference range, 32-100 ng/mL) is effective, but its impact on improving central glycemia and insulin sensitivity is conflicting. 83 Treating insulin resistance and MetS with vitamin D as a monotherapy appears to be unsuccessful. 82,83 Achieving normal vitamin D blood levels through adequate sun exposure and/or supplementation is advised for general health. 84�86

The average American diet commonly contains a low magnesium intake.80 Recent studies suggest that supple- mental magnesium can improve insulin sensitivity. 81,82 Taking 365 mg/d may be effective in reducing fasting glucose and raising HDL cholesterol in T2DM,83 as well as normomagnesemic, overweight, nondiabetics. 84

Diets high in the omega-6 fat linoleic acid have been associated with insulin resistance85 and higher levels of serum pro-inflammatory mediator markers including IL-6, IL-1?, TNF-?, and hsCRP.87 Supplementation to increase dietary omega-3 fatty acids at the expense of omega-6 fatty acids has been shown to improve insulin sensitivity. 88�90 Six months of omega-3 supplementation at 3 g/d with meals has been shown to reduce MetS markers including fasting triglycerides, HDL cholesterol, and an increase in anti-inflammatory adiponectin. 91

Curcumin is responsible for the yellow pigmentation of the spice turmeric. Its biological effects can be characterized as antidiabetic and antiobesity via down- regulating TNF-?, suppressing nuclear factor ?B activation, adipocytokine expression, and leptin level modulation,. 92�95 Curcumin has been reported to activate peroxisome proliferator-activated receptor-?, the nuclear target of the thiazolidinedione class of antidiabetic drugs,93 and it also protects hepatic and pancreatic cells. 92,93 Numerous studies have reported�weight loss, hsCRP reduction, and improved insulin sensitivity after curcumin supplementation.92�95

There is no established upper limit for curcumin, and doses of up to 12 g/d are safe and tolerable in humans. 96 A randomized, double-blinded, placebo- controlled trial (N = 240) showed a reduced progression of prediabetes to T2DM after 9 months of 1500 mg/d curcumin supplementation.97

Curcumin, 98 vitamin D, 84 magnesium, 91 and omega-3 fatty acids80 are advocated as daily supplements to promote general health. A growing body of evidence supports the views of Gymnema sylvestre, vanadium, chromium, and ?-lipoic acid should as therapeutic supplements to assist in glucose homeostasis.

G Sylvestre

metabolic Gymnema sylvestre medicinal herb Gymnemic acids are the active component of the G sylvestre plant leaves. Gymnemic acids are the active component of the G sylvestre plant leaves. Studies evaluating G sylvestre’s effects on diabetes in humans have generally been of poor methodological quality. Experimental animal studies have found that gymnemic acids may decrease glucose uptake in the small intestine, inhibit gluconeogenesis, and reduce hepatic and skeletal muscle insulin resistance.99 Other animal studies suggest that gymnemic acids may have comparable efficacy in reducing blood sugar levels to the first-generation sulfonylurea, tolbutamide.100

Evidence from open-label trials suggests its use as a supplement to oral antidiabetic hypoglycemic agents. 96 One quarter of patients were able to discontinue their drug and maintain normal glucose levels on an ethanolic gymnema extract alone. Although the evidence to date suggests its use in humans and animals is safe and well tolerated, higher quality human studies are warranted.

Vanadyl Sulfate

metabolic Vanadyl Sulfate Vanadyl sulfate has been reported to prolong the events of insulin signaling and may actually improve insulin sensitivity.101 Limited data suggest that it inhibits gluconeogenesis, possibly ameliorating hepatic insulin resistance. 100,101 Uncontrolled clinical trials have reported improvements in insulin sensitivity using 50 to 300 mg daily for periods ranging from 3 to 6 weeks. 101�103 Contrastingly, a recent randomized, double-blind, placebo-controlled trial found that 50 mg of vanadyl sulfate twice daily for 4 weeks had no effect in individuals with impaired glucose tolerance. 104 Limited clinical and experimental data exist supporting the use of vanadyl sulfate to improve insulin resistance,�and further research is warranted regarding its safety and efficacy.

Chromium

metabolic Chromium Diets high in refined sugar and flour are deficient in chromium (Cr) and lead to an increased urinary excretion of chromium. 105,106 The progression of MetS is not likely caused by a chromium deficiency, 107 and dosages that benefit glycemic regulation are not achievable through food. 106,108,109

A recent randomize, double-blind trial demonstrated that 1000 ?g Cr per day for 8 months improved insulin sensitivity by 10% in subjects with T2DM.110 Cefalu et al110 further suggested that these improvements might be more applicable to patients with a greater degree of insulin resistance, impaired fasting plasma glucose, and higher HbA1c values. Chromium’s mechanism of action for improving insulin sensitivity is through increased Glut4 translocation via prolonging insulin receptor signaling.109 Chromium has been well tolerated at 1000 ?g/d,105 and animal models using significantly more than 1000 ? Cr per day were not associated with toxicological consequences.109

?-Lipoic Acid

metabolic alpha-lipoic-acid Humans derive ?-lipoic acid through dietary means and from endogenous synthesis. 111 The foods richest in ?-lipoic acid are animal tissues with extensive metabolic activity such as animal heart, liver, and kidney, which are not consumed in large amounts in the typical American diet. 111 Supplemental amounts of ?-lipoic acid used in the treatment of T2DM (300-600 mg) are likely to be as much as 1000 times greater than the amounts that could be obtained from the diet.112

Lipoic acid synthase (LASY) appears to be the key enzyme involved in the generation of endogenous lipoic acid, and obese mice with diabetes have reduced LASY expression when compared with age-and sex- matched controls.111 In vitro studies to identify potential inhibitors of lipoic acid synthesis suggest a role for diet-induced hyperglycemia and the PIC TNF- ? in the down-regulation of LASY.113 The inflammatory basis of insulin resistance may therefore drive lowered levels of endogenous lipoic acid via reducing the activity of LASY.

?-Lipoic acid has been found to act as insulin mimetic via stimulating Glut4-mediated glucose trans- port in muscle cells. 110,114?-Lipoic acid is a lipophilic free radical scavenger and may affect glucose homeostasis through protecting the insulin receptor from damage114 and indirectly via decreasing nuclear factor ?B�mediated TNF-? and IL-1 production. 110 In�postmenopausal women with MetS (presence of at least 3 ATPIII clinical criteria) 4 g/d of a combined inositol and ?-lipoic acid supplement for 6 months significantly improved OGTT scores by 20% in two thirds of the subjects. 114 A recent randomized double-blinded placebo-controlled study showed that 300 mg/d ?- lipoic acid for 90 days significantly decreased HbA1c values in subjects with T2DM.115

Side effects to ?-lipoic acid supplementation as high as 1800 mg/d have largely been limited to nausea. 116 It may be best to take supplemental ?-lipoic acid on an empty stomach (1 hour before or 2 hours after eating) because food intake reportedly reduces its bioavailability.117 Clinicians should be aware that ?-lipoic acid supplementation might increase the risk of hypoglycemia in diabetic patients using insulin or oral antidiabetic agents.117

Limitations

metabolic limitations sign This is a narrative overview of the topic of MetS. A systematic review was not performed; therefore, there may be relevant information missing from this review. The contents of this overview focuses on the opinions of the authors, and therefore, others may disagree with our opinions or approaches to management. This overview is limited by the studies that have been published. To date, no studies have been published that identify the effectiveness of a combination of a dietary intervention, such as the Spanish ketogenic diet, and nutritional supplementation on the expression of the MetS. Similarly, this approach has not been studied in patients with musculoskeletal pain who also have the MetS. Consequently, the information presented in this article is speculative. Longitudinal studies are needed before any specific recommendations can be made for patients with musculoskeletal that may be influenced by the MetS.

Conclusion: Metabolic Syndrome

This overview suggests that MetS and type 2 diabetes are complex conditions, and their prevalence is expected to increase substantially in the coming years. Thus, it is important to identify if the MetS may be present in patients who are nonresponsive to manual care and to help predict who may not respond adequately.

We suggest that diet and exercise are essential to managing these conditions, which can be supported with key nutrients, such as vitamin D, magnesium, and�omega-3 fatty acids. We also suggest that curcumin, G sylvestre, vanadyl sulfate chromium, and ?-lipoic acid could be viewed as specific nutrients that may be taken during the process of restoring appropriate insulin sensitivity and signaling.

Chiropractic Care

David R. Seaman DC, MS,?, Adam D. Palombo DC

Professor, Department of Clinical Sciences, National University of Health Sciences, Pinellas Park, FL Private Chiropractic Practice, Newburyport, MA

Funding Sources and Conflicts of Interest

No funding sources were reported for this study. David Seaman is a paid consultant for Anabolic Laboratories, a manufacturer of nutritional products for health care professionals. Adam Palombo was sponsored and remunerated by Anabolic laboratories to speak at chiropractic conventions/meetings.

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Astaxanthin and Its Benefits

Do you feel:

Astaxanthin

A Powerful Antioxidant

Boosts the Immune System

Controls Glucose and Lipids

Exercise Enhancement

Conclusion

References:

Modern Integrative Wellness- Esse Quam Videri

Ketogenic Diet for Metabolic Syndrome

What is the Ketogenic Diet?

How the Keto Diet Helps Improve Metabolic Syndrome

Type 2 Diabetes

Obesity

Metabolic Syndrome

Dr. Alex Jimenez Podcast: Metabolic Syndrome

Neural Zoomer Plus for Neurological Disease

Food Sensitivity for the IgG & IgA Immune Response

Gut Zoomer for Small Intestinal Bacterial Overgrowth (SIBO)

Formulas for Methylation Support

Modern Integrated Medicine

Berberine and Metabolic Syndrome

Do you feel:

What Is Berberine?

The Health Benefits from Berberine

Bacterial Infections

Regulates Blood Glucose

Help Losing Weight

Conclusion

References:

Modern Integrative Wellness- Esse Quam Videri

What Is Metabolic Syndrome?

References:

Mayo Clinic Staff. �Metabolic Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 14 Mar. 2019, www.mayoclinic.org/diseases-conditions/metabolic-syndrome/symptoms-causes/syc-20351916.

Sherling, Dawn Harris, et al. �Metabolic Syndrome.� Journal of Cardiovascular Pharmacology and Therapeutics, vol. 22, no. 4, 2017, pp. 365�367., doi:10.1177/1074248416686187.

Three Metabolic Energy Systems

Personal Training 101

How You Get Energy & How You Use It

ATP Re-Synthesis

1. Phosphagen System

2. Glycolysis

3. Aerobic System

Energy System Characteristics

Energy System Workouts

References:

Dietary Strategies: Treatment Of Metabolic Syndrome

1. Metabolic Syndrome

2. Dietary Patterns

2.1. Energy-Restricted Diet Strategies

2.2. Diets Rich in Omega-3 Fatty Acids

2.3. Diets Based on Low Glycemic Index/Load

2.4. Diets with High Total Antioxidant Capacity

2.5. Moderate-High Protein Diets

2.6. High Meal Frequency Pattern

2.7. The Mediterranean Diet

3. Dietary: Single Nutrients and Bioactive Compounds

3.1. Ascorbate

3.2. Hydroxytyrosol

3.3. Quercetin

3.4. Resveratrol

3.5. Tocopherol

3.6. Anthocyanins

3.7. Catechins

4. Conclusions

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References:

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Metabolic Syndrome And Chiropractic

Introduction: Metabolic Syndrome

Methods

Discussion

Insulin Resistance Overview

Visceral Adiposity And Insulin Resistance

Hypothalamic Inflammation And Insulin Resistance

Clinical Correlates Diet-Induced Inflammation & Insulin Resistance

MetS And Disease Expression