Back Clinic Functional Medicine Team. Functional medicine is an evolution in the practice of medicine that better addresses the healthcare needs of the 21st century. By shifting the traditional disease-centered focus of medical practice to a more patient-centered approach, functional medicine addresses the whole person, not just an isolated set of symptoms.
Practitioners spend time with their patients, listening to their histories and looking at the interactions among genetic, environmental, and lifestyle factors that can influence long-term health and complex, chronic disease. In this way, functional medicine supports the unique expression of health and vitality for each individual.
By changing the disease-centered focus of medical practice to this patient-centered approach, our physicians are able to support the healing process by viewing health and illness as part of a cycle in which all components of the human biological system interact dynamically with the environment. This process helps to seek and identify genetic, lifestyle, and environmental factors that may shift a person’s health from illness to well-being.
A butterfly-shaped gland found at the front of the neck, the thyroid gland, may not look like much, but it can wreak havoc on your health, when it isn’t functioning properly. The thyroid gland produces thyroxin (T4) and triiodothyronine (T3), hormones which control the metabolism, respiration, temperature and other essential functions of the human body. Too much or too little of these hormones can lead to thyroid disease, such as hypothyroidism and hyperthyroidism.
What can you do to treat thyroid disorders?
To treat thyroid disorders, drugs and medications are often prescribed. The most commonly prescribed medication for treating hypothyroidism is levothyroxine, while treatment for hyperthyroidism includes anti-thyroid medicines, such as propylthiouracil or methimazole, radioactive iodine which may destroy the thyroid gland and stop the excess production of thyroid hormones, even surgery to remove the thyroid gland altogether.
A dissatisfaction with normal care, however, has resulted in an increasing interest in a more holistic approach to thyroid disease treatment, one which prefers natural, lifestyle changes, not drugs or medications. Jen Wittman, CHHC, AADP, creator of Thyroid Loving Care and a certified holistic health expert, chef and writer, is an advocate of this strategy. Wittman was diagnosed with Hashimoto’s thyroid disease, an autoimmune disorder which attacks the thyroid gland itself, but was able to undo the illness without the use of medicines.
“In my experience, changing diet, improving gut health, managing stress and maintaining overall health and wellness helps support the body so that medicine is unnecessary, or at minimum, may work more effectively,” Wittman said.
Adopting a Healthy Diet
Wittman recommends eliminating gluten, caffeine and soy, in addition to reducing sugar for all thyroid diseases, however, she says that diets are contingent on the individual.
She clarified that some folks gain from a Paleo or Autoimmune Paleo protocol, while others will need to avoid foods like nightshades such as paprika, cayenne, tomatoes, bell peppers, eggplant and potatoes or polyunsaturated fatty acids such as peppermint and vegetable oils. Others also find cutting out milk or alcohol from their diet helps.
“There is not any effective one-size fits all approach when it comes to reversing autoimmune and thyroid conditions”.
According to Charlie Seltzer, MD, owner of Lean4Life Weight Loss & Fitness Solutions, another change some healthcare professionals suggest for individuals suffering from thyroid disease is to avoid eating raw goitrogenic foods like cruciferous vegetables, such as broccoli and kale, that interfere with the function of the thyroid gland.
But comments on diet’s influence on thyroid function have a tendency to vary. Jabbour, for example, doesn’t believe that exercise and diet can cure thyroid disorder. But one thing they could all agree on though is that eating healthier can fight weight gain and reduce a few of the symptoms like fatigue and depression, especially in the first six months of hormonal therapy when a balance of hormones has not yet been attained.
To Supplement or Not?
Too much or too little of certain nutrients can greatly impact thyroid function. Stella Lucia Volpe, PhD, RD, LDN, FACSM, professor and chair of the department of nutrition sciences at Drexel University at the College of Nursing & Health Professions, clarified that some thyroid diseases could be, but not necessarily is, a consequence of iodine deficiency. Iron or Zinc deficiencies can be variables as well. For instance, the thyroid converts iodine into thyroxin (T4) and triiodothyronine (T3) so a deficiency of iodine in your diet can interfere with hormone production.
But iodine deficiency is uncommon in the USA, Jabbour cautioned. Therefore supplementation could be harmful if no authentic deficiency is present, leading to the specific opposite problem. Too much iodine in your diet can also be an issue if you’re at risk for thyroid disease. Mario Skugor, MD, advises his patients with Graves’ disease, another autoimmune thyroid disease, because their thyroid is secreting a surplus of both T4 and T3 to prevent foods.
Wittman considers that most people with thyroid disorder need supplements at least short-term, but that they often can be weaned off them. “There is just not one simple way to reverse these conditions in everybody,” Wittman said. “Rather there are several unique supplements, lifestyle changes, healing modalities and dietary alterations which can be used to reverse the conditions and eliminate symptoms.” Seltzer cautioned against supplementing on your own. See your doctor and get appropriate testing first to make sure it’s necessary in the first location.
Exercise & Your Thyroid
Opinions on exercise also differ. Seltzer does not see it playing an important role in proper thyroid function while exercise in general is good for everybody. “The best exercise routine is the one that a individual is most likely to stay with,” Seltzer said. “I enjoy resistance training supplemented with cardiovascular exercise, with a focus on interval training, but if someone hates lifting weights, then anything is better than nothing.”
Wittman advises her clients to choose exercises which don’t tax the adrenal gland like gentle yoga, walking or Tai Chi. Jabbour and Skugor say patients with hyperthyroidism must watch the intensity and duration of the workouts because exercise may exacerbate an already rapid heart rate along with other symptoms.
What is the Best Strategy?
The absence of consensus on holistic approaches will likely cause your head to spin, right? Can you choose alternative remedies or would you rather stick with normal care for treating thyroid disease? The American Thyroid Association recommends that you work with your healthcare professional about the best strategies to include alternative or complementary medicine and always keep the lines of communication open if your doctor doesn’t approve of these practices. Your well-being is the priority, and a few inappropriate options, could interfere with your treatment.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Any doctor can tell you that to handle thyroid disease, you need a suitable dose of thyroid hormone to replace what your body isn’t currently making on its own, or that you may need other forms of medications to control the excess. However, it may also be worthwhile to consider that making lifestyle changes can be just as significant as these.
How can lifestyle changes help with thyroid disease?
‘If you’re not feeling well, there is much to be gained from focusing on a wholesome diet, regular exercise, stress control, and more to help you feel your best with thyroid disease”, states David Borenstein, MD, an integrative medicine physician in New York City. “It is extremely important to have a lifestyle which controls stress and provides appropriate nutrition and fitness,” he added.
You might start by analyzing your daily diet to see whether any changes or swaps could be made.�More exercise is just another lifestyle change that could make a large difference in the way you feel. As with a change in your diet, ask your doctor and start exercise routines.�Yoga classes, along with tai committed or chi meditation, can decrease tension or anxiety, which can be important when you live with hypothyroidism.
If you’re not feeling well despite following your thyroid disease treatment regimen as recommended by a healthcare professional, try these lifestyle hints from experts and people living with thyroid disease.
Be Vigilant About Eating Vegetables
Vegetables are a necessary part of a healthy diet, but people with hypothyroidism, or any other thyroid disease at that, might want to avoid cruciferous vegetables, like turnips and cabbage, as they can block thyroid hormone generation.
However, Benjamin Snider, ND, a naturopathic doctor at Authentic Wellness Integrative Health Centre at Kitchener, Ontario, says that cruciferous vegetables offer you many health benefits, and you should just limit them in case you’ve got a serious iodine deficiency, as that is when they are most likely to influence thyroid function. Dr. Snider recommends steaming cruciferous vegetables, which may limit their harmful tendencies.
Eat a Clean, Balanced Diet Daily
Lorraine Williams, a volunteer for the British Thyroid Foundation and a blogger in Thyroid Hope, demands people to avoid eating any highly processed foods. “Learn to listen to your body and eat for good health,” she says. Janelle Flores, a hypothyroidism blogger in Adventures of a Thyroidless Girl, is also an advocate for “clean” eating (she’s also gluten-free). “I’ve discovered that eating healthy provides me the most energy and the best outcome,” she states.
Exercise Often but With Certain Limits
Flores emphasizes the value of daily exercise while also listening to your own body. “If I’m having a bad day, I give myself a rest,” she states. “However, I feel that I don’t have as many bad times when I focus on eating correctly.” With the appropriate dose of medication and routine exercise, my energy level is a lot higher, ” she says.
“Moderate exercise is quite good for you. Just don’t overdo it,” Borenstein illustrated. Overexertion can affect the body’s ability to convert inactive thyroid hormone (T4) to the active form (T3) by eliminating an iodine molecule,” he explains, and “when that procedure does not happen properly, it can cause thyroid disease symptoms.”
Be Careful With Supplements
“Use caution when considering nutritional supplements that claim to boost thyroid function. These nutritional supplements aren’t proven effective”, says Anne R. Cappola, MD, an associate professor at the Perelman School of Medicine at the University of Pennsylvania at Philadelphia. Some contain unregulated amounts of thyroid hormones, leading to unregulated levels of the thyroid hormones.
In addition, a few alternative medicine practitioners may recommend iodine nutritional supplements for thyroid disease, but the majority of people in the United States actually have adequate iodine levels (although pregnant women can be an exception). “Substantial amounts of iodine in nutritional supplements can cause a faster drop in thyroid function in people predisposed to thyroid insufficiency,” Dr. Cappola states. “These supplements should be avoided.”
Maintain a Healthy Body Weight
Carrying too many pounds may lead to insulin resistance, which affects hormone levels, according to Borenstein. Plus, people that are overweight need more thyroid gland hormones. Individuals with borderline thyroid function might observe improvements in thyroid function when they maintain a healthy weight or lose weight.
Another weight reduction benefit includes the reduced risk of thyroid cancer. According to the University of Maryland Medical Center, the most common form of hypothyroidism, Hashimoto’s thyroiditis, raises the danger of a sort of thyroid cancer called thyroid lymphoma. And a study published online at Medical Science Monitor in January 2015 found that the risk for thyroid cancer also increases among overweight and obese individuals.
Manage Stress With Yoga or Meditation
“Introducing stress management and mindfulness techniques ought to be a component of any hypothyroid application,” Snider says. “That’s because stress weakens the immune system and also can raise the resistance of thyroid gland cells”, he says. Flores exercises to be physically fit, but also to lower stress. “I especially find jogging or running curative,” she states. However, when she is not feeling good, she allows herself to relax and indulge in a day. Borenstein recommends yoga, tai chi, and meditation to help alleviate stress.
Practice Restorative Sleep Habits Every Night
“Good sleep is a no-brainer,” Borenstein says. To repair tissues you will need sleep to help your body heal. “Sleep is critical in optimizing thyroid function because it helps to modulate the stress hormone cortisol,” Snider says. Stress management and exercise can enhance sleep quality, as can a normal sleep schedule and avoiding late-day caffeine, according to the National Sleep Foundation. Additionally, it is important to achieve a wholesome sleep environment.
Learn to Listen to Signals From Your Body
Thyroid disease is different for everybody, and everyone responds differently to treatment. “I have discovered my own body well enough to understand when I am feeling like when I need a drug dose shift,” Flores says. “Overall, medication is helpful because I need it to work effectively, but for me personally, I don’t think medication alone is the answer.”
Lee Parks, MD, an endocrinologist and also the clinical director of the Vanderbilt Thyroid Center at Vanderbilt University Medical Center in Nashville, Tennessee, says suitably treated hypothyroidism and other thyroid diseases shouldn’t result in weight gain, fatigue, or other common thyroid dysfunction symptoms. But lifestyle changes are just for fundamental good health, not a replacement for treatment, Dr. Parks concludes.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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
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
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
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
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
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
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
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
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, 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
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
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
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
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
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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References:
1. Kaur J. A comprehensive review on metabolic syndrome.<br />
Cardiol Res Pract 2014:943162, http://dx.doi.org/10.1155/<br />
2014/943162.<br />
2. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic<br />
syndrome among US adults. Findings from the Third National<br />
Health and Nutrition Examination Survey. J Am Med Assoc<br />
2006;287:356�9.<br />
3. Boyle JP, Thompson TJ, Gregg EW, Barker LE, Williamson<br />
DF. Projection of the year 2050 burden of diabetes in the US<br />
adult population: dynamic modeling of incidence, mortality,<br />
and prediabetes prevalence. Popul Health Metr 2010;8:29,<br />
http://dx.doi.org/10.1186/1478-7954-8-29.<br />
4. [Internet]Centers for Disease Control and Prevention.<br />
Adult Obesity Facts. Atlanta: CDC; 2014. [Available from<br />http://www.cdc.gov/obesity/data/adult.html].<br />
5. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of<br />
childhood and adult obesity in the United States, 2011�2012.<br />
JAMA 2014;311(8):806�14.<br />
6. Riksman JS, Williamson OD, Walker BF. Delineating<br />
inflammatory and mechanical sub-types of low back pain: a<br />
pilot survey of fifty low back pain patients in a chiropractic<br />
setting. Chiropr Man Therap 2011;19(1):5, http://dx.doi.org/<br />
10.1186/2045-709X-19-5.<br />
7. Dobretsov M, Ghaleb AH, Romanovsky D, Pablo CS, Stimers<br />
JR. Impaired insulin signaling as a potential trigger of<br />
pain in diabetes and prediabetes. Int Anesthesiol Clin<br />
2007;45(2):95�105.<br />
8. Mantyselka P, Miettola J, Niskanen L, Kumpusalo E. Glucose<br />
regulation and chronic pain at multiple sites. Rheumatology<br />
2008;47(8):1235�8.<br />
9. M�ntyselk� P, Miettola J, Niskanen L, Kumpusalo E.<br />
Persistent pain at multiple sites�connection to glucose<br />
derangement. Diabetes Res Clin Pract 2009;84(2):e30�2.<br />
10. Mantyselka P, Kautianen H, Vanhala M. Prevalence of neck<br />
pain in subjects with metabolic syndrome�a cross-sectional<br />
population-based study. BMC Musculoskelet Disord 2010;11:<br />
171, http://dx.doi.org/10.1186/1471-2474-11-171.<br />
11. Rechardt M, Shiri R, Karppinen J, Jula A, Heli�vaara M,<br />
Viikari-Juntura E. Lifestyle and metabolic factors in relation<br />
to shoulder pain and rotator cuff tendinitis: a population-based<br />
study. BMC Musculoskelet Disord 2010;11:165.<br />
12. Gaida JE, Alfredson L, Kiss ZS, Wilson AM, Alfredson H,<br />
Cook JL. Dyslipidemia in Achilles tendinopathy is<br />
characteristic of insulin resistance. Med Sci Sports Exerc<br />
2009;41:1194�7.<br />
13. Malliaras P, Cook JL, Kent PM. Anthropometric risk factors<br />
for patellar tendon injury among volleyball players. Br J<br />
Sports Med 2007;41:259�63.<br />
14. Skrzynski S. DSC study of collagen in disc disease. J Biophys<br />
2009;2009:819635, http://dx.doi.org/10.1155/2009/819635.<br />
15. Luevano-Contreras C, Chapman-Novakofski K. Dietary<br />
advanced glycation end products and aging. Nutrients<br />
2010;2(12):1247�65 [2009;2009:819635].<br />
16. Abate M, Schiavone C, Pelotti P, Salini V. Limited joint<br />
mobility (LJM) in elderly subjects with type II diabetes<br />
mellitus. Arch Gerontol Geriatrics 2011;53:135�40.<br />
17. Sakellaridis N. The influence of diabetes mellitus on lumbar<br />
intervertebral disk herniation. Surg Neurol 2006;66:152�4.<br />
18. Shepherd PR, Kahn BB. Glucose transporters and insulin<br />
action: implications for insulin resistance and diabetes<br />
mellitus. New Eng J Med 1999;341(4):248�57.<br />
19. Abdul-Ghani MA, DeFronzo RA. Pathogenesis of insulin<br />
resistance in skeletal muscle. J Biomed Biotechnol 2010:19,<br />
http://dx.doi.org/10.1155/2010/476279 [Article ID 476279].<br />
20. [Internet]American Heart Association. About metabolic<br />
syndrome. Dallas: The Association; 2014. [Available from<br />http://www.heart.org/HEARTORG/Conditions/More/<br />MetabolicSyndrome/About-Metabolic-Syndrome_UCM_<br />301920_Article.jsp].<br />
21. Hotamisligil GS. Inflammation and metabolic disorders.<br />
Nature 2006;444:860�7.<br />
22. Glass CK, Olefsky JM. Inflammation and lipid signaling in the<br />
etiology of insulin resistance. Cell Metab 2012;15(5):635�45.<br />
23. Reaven GM. All obese individuals are not created equal:<br />
insulin resistance is the major determinant of cardiovascular<br />
disease in overweight/obese individuals. Diabetes Vasc Dis<br />
Res 2005;2:105�12.<br />
24. Ritov VB, Menshikova EV, He J, Ferrell RE, Goodpaster<br />
BH, Kelley DE. Deficiency of subsarcolemmal mitochondria<br />
in obesity and type 2 diabetes. Diabetes 2005;54:8�14.<br />
25. Corcoran MP, Lamon-Fava S, Fielding RA. Trans fats and<br />
insulin resistance: skeletal muscle lipid deposition and insulin<br />
resistance: effect of dietary fatty acids and exercise. Am J Clin<br />
Nutr 2007;85:662�77.<br />
26. Schipper HS, Prakken B, Kalkhoven E, Boes M. Adipose<br />
tissue-resident immune cells: key players in immunometabolism.<br />
Trends Endocrinol Metab 2012;23:407�15.<br />
27. Antuna-Puente B, Feve B, Fellahi S, Bastard JP. Adipokines:<br />
the missing link between insulin resistance and obesity.<br />
Diabetes Metab 2008;34:2�11.<br />
28. Grimble RF. Inflammatory status and insulin resistance. Curr<br />
Opin Clin Nutr Metab Care 2003;5:551�9.<br />
29. Tilg H, Moschen AR. Inflammatory mechanisms in<br />
the regulation of insulin resistance. Mol Med 2008;3�4:222�31.<br />
30. Johnson DR, O’Conner JC, Satpathy A, Freund GG.<br />
Cytokines in type 2 diabetes. Vitam Horm 2006;74:405�41.<br />
31. Ridker PM, Wilson PW, Grundy SM. Should C-reactive<br />
protein be added to the metabolic syndrome and to<br />
assessment of global cardiovascular risk? Circulation 2004;<br />
109:2818�25.<br />
32. Gelaye B, Revilla L, Lopez T, et al. Association between<br />
insulin resistance and c-reactive protein among Peruvian<br />
adults. Diabetol Metab Syn 2010;2:30.<br />
33. Singh VP, Bali A, Singh N, et al. Advanced glycation end<br />
products and diabetic complications. Korean J Physiol<br />
Pharmacol 2014;18(1):1�14.<br />
34. Baker RG, Hayden MS. NF-kB, inflammation and metabolic<br />
disease. Cell Metab 2011;13(1):11�22.<br />
35. Purkayastha S, Cair D. Neuroinflammatory basis of metabolic<br />
syndrome. Mol Metab Nov 2013;2(4):356�63.<br />
36. Ehse JA, Boni-Schnetzler M, Faulenbach M, Donath MY.<br />
Macrophages, cytokines and beta-cell death in type 2 diabetes.<br />
Biochem Soc Trans 2008;36(3):340�2.<br />
37. Boni-Schnetzler M, Ehses JA, Faulenbach M, Donath MY.<br />
Insulitis in type 2 diabetes. Diabetes Obes Metab 2008;10<br />
(Suppl 4):201�4.<br />
38. Donath MY, Schumann DM, Faulenbach M, Ellingsgaard H,<br />
Perren A, Ehses JA. Islet inflammation in type 2<br />
diabetes: from metabolic stress to therapy. Diabetes Care<br />
2008;31(Suppl 2):S161�4.<br />
39. Donath MY, Boni-Schnetzler M, Ellingsgaard H, Ehses JA.<br />
Islet inflammation impairs the pancreatic beta-cell in type 2<br />
diabetes. Physiology 2009;24:325�31.<br />
40. Harford KA, Reynolds CM, McGillicuddy FC, Roche HM.<br />
Fats, inflammation and insulin resistance: insights to the role<br />
of macrophage and T-cell accumulation in adipose tissue.<br />
Proc Nutr Soc 2011;70:408�17.<br />
41. Munoz A, Costa M. Nutritionally mediated oxidative stress and<br />
inflammation. Oxid Med Cell Longev 2013;2013:610950, http://<br />
dx.doi.org/10.1155/2013/610950.<br />
42. Wisse BE, Schwartz MW. Does hypothalamic inflammation<br />
cause obesity? Cell Metab 2009;10(4):241�2.<br />
43. Purkayastha S, Cair D. Neuroinflammatory basis of metabolic<br />
syndrome. Mol Metab Nov 2013;2(4):356�63.<br />
44. Calegari VC, Torsoni AS, Vanzela EC, Ara�jo EP, Morari<br />
J, Zoppi CC, et al. Inflammation of the hypothalamus leads<br />
to defective pancreatic islet function. J Biol Chem 2011;<br />
286(15):12870�80.<br />
45. Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution<br />
of the Western diet: health implications for the 21st century.<br />
Am J Clin Nutr 2005;81:341�54.<br />
46. Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic<br />
index, glycemic load, and chronic disease risk�a metaanalysis<br />
of observational studies. Am J Clin Nutr<br />
2008;87:627�37.<br />
47. Facchini FS, Hua N, Abbasi F, Reaven GM. Insulin resistance<br />
as a predictor of age-related disease. J Clin Endocrinol Metab<br />
2001;86:3574�8.<br />
48. Lin H, Lee B, Ho Y, et al. Postprandial glucose improves the<br />
risk prediction of cardiovascular death beyond the metabolic<br />
syndrome in the nondiabetic population. Diabetes Care Sep<br />
2009;32(9):1721�6.<br />
49. O’Keefe JH, Bell DS. Postprandial hyperglycemia/<br />
hyperlipidemia (postprandial dysmetabolism) is a cardiovascular<br />
risk factor. Am J Cardiol 2007;100:899�904.<br />
50. Cao H. Adipocytokines in obesity and metabolic disease.<br />
J Endocrinol 2014;220(2):T47�59.<br />
51. Nah SS, Choi IY, Lee CK, et al. Effects of advanced glycation<br />
end products on the expression of COX2, PGE2 and NO in human osteoarthritic chondrocytes. Rheumatology (Oxford)<br />
2008;47(4):425�31.<br />
52. Abate M, Schiavone C, Pelotti P, Salini V. Limited joint<br />
mobility (LJM) in elderly subjects with type II diabetes<br />
mellitus. Arch Gerontol Geriatr 2011;53:135�40.<br />
53. Robinson D, Mirovsky Y, Halperin N, Evron Z, Nevo Z.<br />
Changes in proteoglycans of intervertebral disc in diabetic<br />
patients: a possible cause of increased back pain. Spine<br />
1998;23:849�56.<br />
54. Sakellaridis N, Androulis A. Influence of diabetes mellitus on<br />
cervical intervertebral disc herniation. Clin Neurol Neurosurg<br />
2008;110:810�2.<br />
55. Jhawar BS, Fuchs CS, Colditz GA, Stampfer MJ. Cardiovascular<br />
risk factors for physician-diagnosed lumbar disc<br />
herniation. Spine J 2006;6:684�91.<br />
56. Lotan R, Oron A, Anekstein Y, Shalmon E, Mirovsky Y.<br />
Lumbar stenosis and systemic diseases: is there any relevance.<br />
J Spinal Disord Tech 2008;21:247�51.<br />
57. Anekstein Y, Smorgick Y, Lotan R, et al. Diabetes mellitus as<br />
a risk factor for the development of lumbar spinal stenosis. Isr<br />
Med Assoc J 2010;12:16�20.<br />
58. Choi KM. Sarcopenia and sarcopenic obesity. Endocrinol<br />
Metab (Seoul) 2013;28(2):86�9.<br />
59. D’hooge R, Cagnie B, Crombez G, et al. Increased<br />
intramuscular fatty infiltration without differences in lumbar<br />
muscle cross-sectional area during remission of unilateral<br />
recurrent low back pain. Man Ther 2012 Dec;17(6):5584�8.<br />
60. Chen YY, Pao JL, Liaw CK, et al. Image changes of paraspinal<br />
muscles and clinical correlations in patients with unilateral<br />
lumbar spinal stenosis. Eur Spine J 2014;23(5):999�1006.<br />
61. Kim Y, Park H. Does regular exercise without weight loss<br />
reduce insulin resistance in children and adolescents? In J<br />
Endocrinol 2013:402592, http://dx.doi.org/10.1155/2013/<br />
402592 [Epub 2013 Dec 12].<br />
62. Strasser B, Siebert U, Schobersberger W. Resistance training<br />
in the treatment of the metabolic syndrome: a systematic<br />
review and meta-analysis of the effect of resistance training on<br />
metabolic clustering in patients with abnormal glucose<br />
metabolism. Sports Med 2010;40:397�415.<br />
63. Sharman MJ, Volek JS. Weight loss leads to reductions in<br />
inflammatory biomarkers after a very-low-carbohydrate diet<br />
and a low-fat diet in overweight men. Clin Sci (Lond)<br />
2004;13:365�9.<br />
64. Teng KT, Chang CY, Chang LF, et al. Modulation of obesityinduced<br />
inflammation by dietary fats: mechanisms and<br />
clinical evidence. Nutr J 2014;13:12, http://dx.doi.org/<br />
10.1186/1475-2891-13-12.<br />
65. Tzotzas T, Evangelou P, Kiortsis DN. Obesity, weight loss<br />
and conditional cardiovascular risk factors. Obes Rev 2011;12<br />
(5):e282�9.<br />
66. Stone N, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA<br />
Guideline on the Treatment of Blood Cholesterol to Reduce<br />
Atherosclerotic Cardiovascular Risk in Adults: A report of<br />
the American College of Cardiology/American Heart<br />
Association Task Force on practice guidelines. Circulation<br />
2014;129(25 Suppl 2):S1�S45.<br />
67. P�rez-Guisado J, Mu�oz-Serrano A. A pilot study of the<br />
Spanish ketogenic Mediterranean diet: an effective therapy for<br />
the metabolic syndrome. J Med Food 2011;14(7�8):681�7.<br />
68. P�rez-Guisado J, Mu�oz-Serrano A, Alonso-Moraga A.<br />
Spanish ketogenic Mediterranean diet: a healthy cardiovascular<br />
diet for weight loss. Nutr J 2008;7:30, http://dx.doi.org/<br />
10.1186/1475-2891-7-30.<br />
69. Jonsson T, Granfeldt Y, Lindeberg S, et al. Subjective satiety<br />
and other experiences of a Paleolithic diet compared to a<br />
diabetes diet in patients with T2DM. Nutr J 2013;12:105,<br />
http://dx.doi.org/10.1186/1475-2891-12-105.<br />
70. Jonsson T, Granfeldt Y, Ahren B, et al. Beneficial effects of a<br />
Paleolithic diet on cardiovascular risk factors in T2DM: a<br />
randomized cross-over pilot study. Cardiovasc Diabetol<br />
2009;8:35, http://dx.doi.org/10.1186/1475-2840-8-35.<br />
71. Nicklas BJ, You T, Pahor M. Behavioural treatments<br />
for chronic system inflammation: effects of dietary<br />
weight loss and exercise training. Can Med Assoc J<br />
2005;172(9):1199�209.<br />
72. O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary<br />
strategies for improving post-prandial glucose, lipids, inflammation,<br />
and cardiovascular health. J Am Coll Cardiol<br />
2008;51:249�55.<br />
73. O’Keefe Jr JH, Cordain L. Cardiovascular disease resulting<br />
from a diet and lifestyle at odds with our Paleolithic genome:<br />
how to become a 21st-century hunter�gatherer. Mayo Clin<br />
Proc 2004;79(1):101�8.<br />
74. Ames BN. Low micronutrient intake may accelerate the<br />
degenerative diseases of aging through allocation of scarce<br />
micronutrients by triage. Proc Natl Acad Sci U S A 2006;103<br />
(47):17589�94.<br />
75. Holick MF, Chen TC. Vitamin D deficiency: a worldwide<br />
problem with health consequences. Am J Clin Nutr<br />
2008;87:1080S�6S [Suppl.].<br />
76. Toubi E, Shoenfeld Y. The role of vitamin D in regulating<br />
immune responses. Isr Med Assoc J 2010;12(3):174�5.<br />
77. King DE, Mainous AG, Geesey ME, Egan BM, Rehman S.<br />
Magnesium supplement intake and C-reactive protein levels<br />
in adults. Nutr Res 2006;26:193�6.<br />
78. Rosanoff A, Weaver CM, Rude RK. Suboptimal magnesium<br />
status in the United States: are the health consequences<br />
underestimated? Nutr Rev 2012;70(3):153�64.<br />
79. Simopoulos AP. Omega-3 fatty acids in inflammation and<br />
autoimmune diseases. J Am Coll Nutr 2002;21(6):495�505.<br />
80. Simopoulos AP. The importance of the omega-6/omega-3<br />
fatty acid ratio in cardiovascular disease and other chronic<br />
diseases. Exp Biol Med 2008;233:674�88.<br />
81. Fung GJ, Steffen LM, Zhou X, et al. Vitamin D intake is<br />
inversely related to risk of developing metabolic syndrome<br />
in African American and white men and women over 20 y:<br />
the Coronary Artery Risk Development in Young Adults<br />
study. Am J Clin Nutr 2012;96(1):24�9 [Published online<br />2012 May 30].<br />
82. Palomer X, Gonzalez-Clemente JM, Blanco-Vaca F, Mauricio<br />
D. Role of vitamin D in the pathogenesis of type 2 diabetes<br />
mellitus. Diabetes Obes Metab 2008;10:185�97.<br />
83. Guadarrama-Lopez AL, Valdes-Ramos R, Martinex-Carrillo<br />
BE. T2DM, PUFAs, and vitamin D: their relation to<br />
inflammation. J Immunol Res 2014;2014:860703, http://dx.<br />
doi.org/10.1155/2014/860703.<br />
84. Cannell JJ, Hollis BW. Use of vitamin D in clinical practice.<br />
Altern Med Rev 2008;13(1):6�20.<br />
85. Davidson MB, Duran P, Lee ML, Friedman TC. High-dose<br />
vitamin D supplementation in people with prediabetes and<br />
hypovitaminosis D. Diabetes Care 2013;36(2):260�6, http://<br />
dx.doi.org/10.2337/dc12-1204.<br />
86. Schwalfenberg G. Vitamin D, and diabetes: improvement of<br />
glycemic control with vitamin D3 repletion. Can Fam<br />
Physician 2008;54:864�6.<br />
87. Kim DJ, Xun P, Liu K, et al. Magnesium intake in relation to<br />
systemic inflammation, insulin resistance, and the incidence<br />
of diabetes. Diabetes Care 2010;33(12):2604�10, http://dx.<br />
doi.org/10.2337/dc10-0994.<br />
88. Guerrero-Romero F, Tamez-Perez HE, Gonz�lez-Gonz�lez G,<br />
et al. Oral magnesium supplementation improves insulin<br />
sensitivity in non-diabetic subjects with insulin resistance. A<br />
double-blind placebo-controlled randomized trial. Diabetes<br />
Metab 2004;30(3):253�8.<br />
89. Rodr�guez-Mor�n M, Guerrero-Romero F. Oral magnesium<br />
supplementation improves insulin sensitivity and metabolic<br />
control in type 2 diabetic subjects: a randomized double-blind<br />
controlled trial. Diabetes Care 2003;26(4):1147�52.<br />
90. Song Y, He K, Levitan EB, Manson JE, Liu S. Effects of oral<br />
magnesium supplementation on glycaemic control in type 2<br />
diabetes: a meta-analysis of randomized double-blind controlled<br />
trials. Diabet Med 2006;23(10):1050�6.<br />
91. Mooren FC, Kr�ger K, V�lker K, Golf SW,Wadepuhl M, Kraus<br />
A. Oral magnesium supplementation reduces insulin resistance<br />
in non-diabetic subjects�a double-blind, placebo-controlled,<br />
randomized trial. Diabetes Obes Metab 2011;13(3):281�4.<br />
92. Aggarwal BB. Targeting inflammation induced obesity and<br />
metabolic diseases by curcumin and other nutraceuticals.<br />
Annu Rev Nutr 2010;30:173�9.<br />
93. Alappat L, Awad AB. Curcumin and obesity: evidence and<br />
mechanisms. Nutr Rev 2010;68(12):729�38.<br />
94. Gonzales AM, Orlando RA. Curcumin and resveratrol inhibit<br />
nuclear factor-kappaB-mediated cytokine expression in adipocytes.<br />
Nutr Metab 2008;5:17, http://dx.doi.org/10.1186/<br />
1743-7075-5-17.<br />
95. Sahebkar A. Why it is necessary to translate curcumin into<br />
clinical practice for the prevention and treatment of metabolic<br />
syndrome? Biofactors 2012, http://dx.doi.org/10.1002/<br />
biof.1062 [Epub ahead of print].<br />
96. Hsu CH, Cheng AL. Clinical studies with curcumin. Adv Exp<br />
Med Biol 2007;595:471�80.<br />
97. Chuengsamarn S, Rattanamongkolgul S, Luechapudiporn R,<br />
Phisalaphong C, Jirawatnotai S. Curcumin extract for prevention<br />
of type 2 diabetes. Diabetes Care 2012;35(11):2121�7.<br />
98. Jurenka JS. Anti-inflammatory properties of curcumin, a<br />
major constituent of curcuma longa: a review of preclinical<br />
and clinical research. Altern Med Rev 2009;14(2):141�53.<br />
99. Leach M. Gymnema sylvestre for diabetes mellitus: a systematic<br />
review. J Altern Complement Med 2007;13(9):977�83.<br />
100. Chattopadhyay R. A comparative evaluation of some blood<br />
sugar lowering agents of plant origin. J Ethnopharmacol<br />
1999;67:367�72.<br />
101. Nahas R, Moher M. Complementary and alternative medicine<br />
for the treatment of type 2 diabetes. Can Fam Physician<br />
2009;55:591�6.<br />
102. Vanadium/Vanadyl sulfate: monograph. Altern Med Rev<br />
2009;14:17�80.<br />
103. Boden G, Chen X, Ruiz J, et al. Effects of vanadyl sulfate<br />
on carbohydrate and lipid metabolism in patients with noninsulin-dependent<br />
diabetes mellitus. Metabolism 1996;45:<br />
1130�5.<br />
104. Jacques-Camarena O, Gonz�lez-Ortiz M, Mart�nez-Abundis E,<br />
et al. Effect of vanadium on insulin sensitivity in patients with<br />
impaired glucose tolerance. Ann Nutr Metab 2008;53:195�8.<br />
105. Vincent JB. The biochemisty of chromium. J Nutr<br />
2000;130:715�8.<br />
106. Anderson RA. Chromium and insulin resistance. Nutr Res<br />
Rev 2003;16:267�75.<br />
107. Vincent JB. Chromium: celebrating 50 years as an essential<br />
element? Dalton Trans 2010;39:3787�94.<br />
108. Office of Dietary Supplements. [Internet]. Dietary supplement<br />
fact sheet: Chromium. Washington, DC: United States<br />
Department of Health and Human Services. http://ods.od.nih.<br />
gov/factsheets/chromium/. Reviewed November 4, 2013.<br />
109. Anderson RA. Chromium, glucose intolerance and diabetes.<br />
J Am Coll Nutr 1998;17(6):548�55.<br />
110. Cefalu WT, Rood J, Patricia Pinsonat P, et al. Characterization<br />
of the metabolic and physiologic response to chromium<br />
supplementation in subjects with type 2 diabetes mellitus.<br />
Metab Clin Exp 2010;59:755�62.<br />
111. Heimbach JT, Anderson RA. Chromium: recent studies regarding<br />
nutritional roles and safety. Nutr Today 2005;40(4):180�95.<br />
112. Shay KP, Moreau RF, Smith EJ, Smith AR, Hagen TM.<br />
Alpha-lipoic acid as a dietary supplement: molecular<br />
mechanisms and therapeutic potential. Biochim Biophys<br />
Acta 2009;1790:1149�60.<br />
113. Morikawa T, Yasuno R, Wada H. Do mammalian cells<br />
synthesize lipoic acid? Identification of a mouse cDNA<br />
encoding a lipoic acid synthase located in mitochondria.<br />
FEBS Lett 2001;498:16�21.<br />
114. Singh U, Jialal I. Alpha-lipoic acid supplementation and<br />
diabetes. Nutr Rev 2008;66(11):646�57.<br />
115. Padmalayam I, Hasham S, Saxena U, Pillarisetti S. Lipoic acid<br />
synthase (LASY): a novel role in inflammation, mitochondrial<br />
function, and insulin resistance. Diabetes 2009;58:600�8.<br />
116. Capasso I, Esposito E, Maurea N, et al. Combination of<br />
inositol and alpha lipoic acid in metabolic syndrome-affected<br />
women: a randomized placebo-controlled trial. Trial<br />
2013;14:273, http://dx.doi.org/10.1186/1745-6215-14-273.<br />
117. Udupa A, Nahar P, Shah S, et al. A comparative study of<br />
effects of omega-3 fatty acids, alpha lipoic acid and vitamin E<br />
in T2DM. Ann Med Health Sci Res 2013;3(3):442�6.
The thyroid gland may be small but it plays a big role in how well your body functions. That is because the thyroid produces a hormone that regulates your metabolism, the process which converts everything you drink and eat into energy. However, when your metabolism slows, causing you to lose weight and feel sluggish and fatigued, you may have an underactive thyroid, medically referred to as hypothyroidism.
How can hypothyroidism affect your body?
Decreased levels of the thyroid hormone can lead to an increase in LDL cholesterol, or fat, in your blood. The thyroid hormone helps the liver break down the cholesterol circulating in your blood and stimulates. Triglycerides and your LDL cholesterol may substantially increase whenever you don’t have enough of the thyroid hormone. What’s more, hypothyroidism may also negatively affect your mood. The thyroid gland helps regulate the chemical messengers, or neurotransmitters, which your brain utilizes to communicate with your own nerves. These messengers can go haywire, causing one to feel anxious and depressed when your thyroid doesn’t function properly.
“The most important thing that you can do for hypothyroidism is to see your doctor and get on the right dose of thyroid hormone,” says R. Mack Harrell, MD, president-elect of the American Association of Clinical Endocrinologists and an endocrinologist at Memorial Regional Hospital in Hollywood, Fla..
Visiting your local healthcare professional’s office is a fundamental first step towards diagnosing and treating an underactive thyroid, or hypothyroidism, but what can you do to help yourself? Add exercise on your list. Regular exercise is an important part of your overall strategy to manage hypothyroidism symptoms. Exercise can offset the effects of your sluggish metabolism and burns calories to prevent weight gain. A good fitness routine may be a mood-booster as well because while you exercise, your body releases endorphins and other substances.
The Hypothyroidism-Exercise Link
What is the best type of exercise for hypothyroidism? A program of high heeled aerobic exercises and strength training is recommended by Yaroslav Gofnung, MD, an endocrinologist at Los Robles Hospital in Thousand Oaks, Calif.. Low-impact aerobics get your heart rate up and your lungs moving without putting too much strain on your joints, which can be vital because joint pain is another common hypothyroidism symptom, Dr. Gofnung says.
A stationary reclining or recumbent bicycle and a low-impact elliptical machine are exceptional machine choices for cardio exercise. “Walking is a fantastic exercise too, as long as you don’t have swelling in your knees or ankles,” Gofnung adds. Additionally, Pilates or gentle yoga may improve core muscles and alleviate the spine and hip pain which could be associated with hypothyroidism.
Individuals with hypothyroidism can also benefit from strength training exercises, such as lunges, leg lifts, and push-ups while other people may benefit from other strength training exercises involving weight-training machines. Strength training builds muscle mass, and muscle burns more calories even when you’re at rest. Building muscle can help prevent potential weight gain from an underactive thyroid gland.
The Best Exercises for Hypothyroidism
For people with hypothyroidism, Igor Klibanov, a personal coach in Toronto, founder of Fitness Solutions Plus, and also writer of “Unlimited Progress: The Way To Unlock Your Body’s Potential,” recommends cardio along with a strength-training routine that incorporates these six exercises:
One-legged dead lift: Stand on one leg while holding onto something for balance (not for support). Keep one hand relaxed in front of your thighs. Push on your hips up as far as you can, until your hand touches the ground. Come back up. This ought to be felt at the buttocks muscles. The back shouldn’t curve; but does not have to be upright.
Squats: Stand up straight and then bend at your knees and hips till you are at a sitting position. Go all of the way down. (Klibanov says it’s a myth that this may damage your knees if you have healthy knees to start with.) .
Overhead press or comparable vertical push movement. Boost a set of dumbbells to shoulder height. So they are facing forward switch your arms. Lift up the dumbbells until your elbows are right. Then lower them back down.
Lat pull-down or similar vertical pull move. Catch a pull-down bar with an overhand grip (palms facing away), and pull it down into your collar bone. Make certain that that the bar travels near to your face as you can.
Push-up or comparable horizontal push movement. Place both hands on the floor, shoulder width apart. Feet must be extended out and together. Till you are close to the ground, Bend your elbows and shoulders. In case a push is too hard, do the same thing either together with your hands on a table (while feet stay on the ground) or a wall socket.
Rowing or similar horizontal pull move. Sit with your hands holding the grip that’s connected to the cable. Keep your back straight, and lean back about 10 to15 degrees. Pull on back the cable until your mid-stomach touches. Then release under control.
Start with 15 repetitions of each exercise and work up to around 20. “Most people with joint issues find these to be easy on the joints,” Klibanov says. When you’re starting out, it might take you 15 to 20 minutes to finish your routine. A eventual aim: Work up which should take about 40 to 45 minutes, he adds. Schedule aerobic exercise a few times a week and participate in strength training routines with these motions two to three days weekly, Klibanov recommends. Doing this can get you on the ideal track to feeling better and losing weight.
Ease Into Exercise
Start slowly and build up. “If you go too quickly, it is possible to injure yourself and set yourself back,” Gofnung warns. Choose exercises that you enjoy and that your body is able to tolerate to increase the probability of your sticking to your regular, ” he advises.
Adjust the number of repetitions as you progress. “In just two weeks, you’ll have another body and you should have a different pattern,” Klibanov states. And do not be timid about progressing, he adds, “The further out of shape you are, the faster progress will come.”
If something hurts, you may have to make a small change like the angle or position of an exercise or motion. If it hurts, stop and find another exercise that does not cause discomfort. If you’re having difficulty by yourself, invest with a trainer that will make recommendations in time and explain to you how you can lose weight through the exercises you select.
Always talk with your doctor before beginning any exercise regimen. And never make exercise a substitute for thyroid drugs. With the right medication, you should feel better within a few weeks and have the motivation to get back to (or get into) a regular exercise regimen, Dr. Harrell says.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
Hypothyroidism can be a tricky condition to handle, and what you eat could interfere with your treatment. Some nutrients influence the function of the thyroid gland, and certain foods can inhibit your body’s ability to absorb them.
What foods can affect thyroid disease?
Having a thyroid condition is often difficult, but you are not alone with this particular health issue. According to the American Thyroid Association, more than 12 percent of the populace may wind up coping with a thyroid disease.
As with many health conditions, some factors are out of your control, such as your family history and the environment around you. But nutrition and diet also plays a role in thyroid health and since you’re the one in control of your plate, then you can decide which thyroid-friendly foods to pick as you handle hypothyroidism and its symptoms.
Foods with Soy (Edamame, Tofu, and Miso)
There’s long been concern over the potential negative effects that certain compounds in soy, called isoflavones, may have on the thyroid gland. Some researchers think that a person’s risk for hypothyroidism can increase. However others theorize that those with both hypothyroidism and an iodine deficiency should observe their intake.
So there are no specific nutritional guidelines regarding the consumption of soy, but some studies do indicate that the ingestion of soy may interfere with the ability to intake thyroid drugs and medications. Because of this, you may want to wait four hours before taking your dose, after eating these foods. Check with your doctor.
Cruciferous Vegetables (Broccoli and Cauliflower)
Cruciferous vegetables, such as broccoli and cabbage, are full of fiber and other nutrients, but they could interfere with the production of thyroid gland when you experience an iodine deficiency. Therefore, in case you do, it is a great idea to restrict your intake of Brussels sprouts, cabbage, cauliflower, kale, turnips, and bok choy, since research indicates digesting these veggies may block the thyroid’s ability to utilize iodine, which is vital for normal thyroid function.
If you have been diagnosed with both hypothyroidism and iodine deficiency, there are a number of things you can do to make these vegetables less dangerous. Cooking them can reduce the impact that cruciferous vegetables have on the thyroid gland, and limiting your intake of these (cooked) vegetables to 5 ounces a day can help too, because that amount appears to have no negative impact on thyroid functioning.
Gluten (Bread, Pasta, and Rice)
People who have migraines might wish to look at decreasing their intake of gluten, a protein found in foods processed from barley, wheat, rye, and other grains, ” says Ruth Frechman, RDN, a dietitian in the Los Angeles area and a spokesperson for the Academy of Nutrition and Dietetics. And in case you’re diagnosed with celiac disease, gluten may hamper absorption of thyroid hormone replacement medication, and can irritate the small intestine.
An article published in May 2017 in the journal “Endocrine Connections” noted that celiac and rheumatoid disease tend to be present together, and while no research has demonstrated that a gluten-free diet can treat thyroid problems, you might want to speak to a healthcare professional about whether it might be well worth eliminating gluten, or becoming tested for celiac disease. If you do decide to eat gluten, make sure to choose whole-grains varieties of bread, pasta, and rice, that are high in fiber and other nutrients and can help improve bowel irregularity, a symptom of hypothyroidism.
Fatty Foods (Butter, Meat, and Fried Foods)
Fats have been found to disrupt the human body’s ability to absorb thyroid hormone replacement medicines, says Stephanie Lee, MD, PhD, associate chief of endocrinology, nutrition, and diabetes in Boston Medical Center and an associate professor in the Boston University School of Medicine in Massachusetts.
Fats may also interfere with the thyroid’s ability to produce hormone as well. Some healthcare professionals recommend that you just cut out on foods that are fried and lower your intake of fats from resources such as butter, mayonnaise, margarine, and fatty cuts of beef.
Sugary Foods (Chocolate and Desserts)
Hypothyroidism may cause the body’s metabolism to slow down, Frechman states. That means it’s simple to put on pounds if you aren’t careful. “You would like to avoid foods with excess amounts of sugar because it’s a lot of calories without the nourishment,” she states. Attempt to eliminate it completely or it is best to decrease.
Processed Foods in Packages
“Processed foods generally get lots of sodium, and individuals with hypothyroidism should avoid sodium,” Frechman states. Having an underactive thyroid increases a individual’s risk for high blood pressure, and sodium that is an excessive amount of increases this risk.
Read the “Nutrition Facts” label on the packaging of processed foods to seek out options lowest in sodium. Individuals with an increased risk for hypertension should restrict their sodium intake according to the American Heart Association.
Excessive Fiber (Beans, Legumes, and Vegetables)
Getting enough fiber is good for you, but also much may complicate your hypothyroidism therapy. The government Strategies for Americans recommends that adults choose in 20 to 35 g of fiber a day. Amounts of fiber from fruits, vegetables, whole grains, beans, and legumes which go above that amount affect your digestive tract and may interfere with absorption of thyroid hormone replacement drugs.
If you’re on a high-fiber diet, ask your physician if you will need a higher dose of thyroid medicine. If you aren’t absorbing enough medication your maintenance dose may have to be increased.
Coffee (Time your First Cup Carefully)
Caffeine has been shown to block absorption of thyroid hormone replacement, says Dr. Lee. “People who had been taking their thyroid medication with their morning coffee had uncontrollable thyroid levels, and we couldn’t figure it out,” she states. “I now must be very careful to tell people, ‘Simply take your medicine with water.'” You should wait at least 30 minutes before having a cup of coffee after taking your medication.
Alcohol and Thyroid Health
Alcohol consumption can cause a mess on both thyroid hormone levels in the body and the ability of the thyroid gland to produce these hormones. Alcohol appears to have a toxic effect in the thyroid gland and it also suppresses the ability of the body to utilize thyroid gland hormones. Ideally, individuals with migraines should cut out alcohol completely..
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
The thyroid gland is a butterfly-shaped gland in your neck. Among its primary functions is to pump out a hormone called thyroxine. It is that hormone which sets the rate of the human body. It’s what regulates energy generation. Some of thyroid hormone’s imbalances common indicators include tiredness, bloating, hair loss, dry skin, joint pain, muscle stiffness, elevated cholesterol, sleep disturbance, infertility, melancholy, cold hands and feet, along with weight gain.
How do you recognize thyroid gland imbalances?
Patients eliminate weight with hypothyroidism while gaining weight is a textbook symptom of hypothyroidism. In some cases a part of their disease is that their gut is so broken down that their thyroid is malfunctioning however they’re currently slimming down and that they’re malabsorbing nourishment. If we fall into those health care conceptions with by each person who has hypothyroidism then we are likely to miss a great deal of individuals.
Identifying Thyroid Disease
Traditional diagnosis is made depending on the lab test TSH (thyroid stimulating hormone) normally ordered by a general physician, internist, or endocrinologist. One of the many problems with this strategy is that it isn’t comprehensive. If your TSH comes back high, the physician tends to diagnose you. This approach often times contributes to treatment with thyroid hormone replacement medication without further investigation. Keep in mind one fundamental point, taking thyroid medication and using a minimal thyroid diagnosis doesn’t fix the problem.
Ultimately, the objective of the healthcare professional and patient should be to recognize why the thyroid levels are abnormal. And that requires a basic knowledge of biochemistry and nutrition. Let us take a deeper look at a few of the common items, in the diet and nutrition standpoint, that can contribute to low thyroid hormone production:
Gluten
Sugar
Goitrogenic foods
Dairy
Nutritional deficiencies
Gluten and your Thyroid Gland
Gluten sensitivity contributes to thyroid disease in many of different ways. Gluten induced gastrointestinal harm is one of the mechanisms of action. It is this mechanism that leads to a domino-like effect. The very first step in this process is the invention of intestinal hyper-permeability, or Leaky Gut. When the barrier is compromised, a cascade of inflammation, immune over-stimulation, and mimicry may ensue. Over time these procedures can result in an autoimmune thyroid response leading to Hashimoto’s thyroid disease or Graves’ disease.
Gluten induced gastrointestinal damage may contribute to inadequate digestion and absorption of thyroid crucial nutrients. Gluten can alter gut bacteria that are ordinary. These bacteria play a important role in thyroid gland conversion. Physicians will assert that no study exists between thyroid free and gluten disorder. They are incorrect.
Where do we find gluten? Folks will say that barley, wheat and rye are the grains that contain gluten. In reality there are distinct sorts of gluten and they’re observed in all the different forms of grain.
Sugar
This refers specifically to processed sugar like dextrose, glucose, fructose, maltodextrin, all the different kinds of sugar that is processed, even organic processed sugars. Many of the food manufacturers have gotten wise about people wanting to prevent sugar so they’ve started saying it. For example sucanat is processed sugar. Avoidance of processed sugar must be a priority to prevent imbalances with the thyroid gland and thyroid disease.
Goitrogens
There are numerous foods that can suppress thyroid hormone production and bring about goiter (thyroid enlargement). Listed below are several foods which can cause this. You can get in trouble if you consume excessive quantities of these foods, for example if you are doing a great deal of juicing and using a pound of each time or if it’s raw and it hasn’t been cooked. If you also have a thyroid condition and if you’re eating cruciferous vegetables, its advice not to stop eating them just cook them and do not make them the key foods in your diet plan.
Soy (prevent soy, particularly GMO soy)
Brussels Sprouts
Bok choy
Cabbage
Cauliflower
Collards
Cassava
Broccoli
Kale
Bamboo shoots
Spinach
Radishes
Rutabaga
Turnips
Watercress
Kohlrabi
Mustard greens
Flax
Pine nuts
Peanuts
The protein casein in milk can mimic glutenfree. Therefore it may be the dairy in their diet that mimics gluten. Gluten, sugar, goitrogenic foods, and dairy are the most usual food-based causes for thyroid hormone disturbance.
Nutrition is Vital for a Healthy Thyroid
Now let’s discuss a food component that is going to be helpful for the thyroid gland to function. There are a number of nutrients necessary for thyroid function. Vitamins and minerals help drive the chemistry behind the production of the thyroid hormones. Additionally they help these hormones and other organs and both the DNA communicate to improve and regulate metabolism.
As mentioned before, often times healthcare professionals will only conduct one laboratory test known as TSH (thyroid stimulating hormone) for the identification and treatment of thyroid disease. If TSH is above normal, you’re diagnosed “hypothyroid”. If TSH is below normal, you’re diagnosed “hyperthyroid”. Simple, right? No, far from it.
TSH is a regulatory hormone produced in the brain from the pituitary gland. TSH then travels to the thyroid gland in your neck out of the brain and tells it to produce the thyroid hormone T4. TSH needs to be made first. What ingredients does your body need to generate TSH? The number one ingredient is protein. How much is enough protein? To get a mean calculation, take your body weight in kilograms (whatever you weigh in pounds split that by 2.2 to give you your weight in kilograms) and multiply that by 0.8 and that’s how many grams of protein you need daily. Another way to calculate this amount is to multiply the amount 0.36 by your weight in lbs. As an instance, for a woman, that could be 54 g of protein. This number is individual for each individual and varies by the individual’s level of physical activity. Speak with your doctor if you suffer from kidney dysfunction. What else does our body need to generate TSH? Magnesium, Vitamin B12, and zinc. Without adequate levels of these ingredients your body cannot produce TSH and you will have low thyroid function from the start.
Now lets discuss thyroxine, T4. Thyroid hormone is potassium and protein. Protein is crucial to form the thyroid hormone (particularly the amino acid in protein called tyrosine). The “4” in T4 signifies the number of molecules of iodine are present. You need iodine for that sport car to run smoothly. Where do we get iodine? Iodine is got by us from things found not in lakes, not from rivers. Seafood, kelp, and seaweed are great sources of iodine. Consider the thyroid gland as a car factory. Internally on your thyroid gland, your thyroid uses a ton of vitamin C. Vitamin C is very important to add those iodine tires to that thyroid gland. You also need vitamin B2. There is something in your thyroid gland known as. It when you consume the iodine and iodine-rich foods is absorbed into the bloodstream. The symporter necessitates B2 to function. Is vitamin B3. To make thyroid hormone T4, you need Vitamin B3, Vitamin B2, Vitamin C, C, and vitamin.
T4 is inactive thyroid hormone. Protein is responsible for carrying T4 to your own tissues including muscle and your liver in which it has converted to T3 thyroid gland through the blood stream. Think of the proteins into your bloodstream that take the T4 thyroid hormone. The inactive T4 thyroid hormone is being hauled to the liver, muscle, and other tissues in which they are converted to the active T3 hormone. There is a process called deiodinization, where the body takes that T4 thyroid gland and eliminates one molecule of iodine to convert it. A whole lot of the conversion of T4 to T3 happens in the liver and that is because their liver is not good at converting T4 to T3, the reason why a person who has liver problems can also have thyroid problems. This conversion takes place in the muscle which is the reason why people with muscle inflammation frequently have thyroid issues. Which nutrient is required for this conversion? Selenium. You require selenium to eliminate that one molecule of iodine to convert T4 into T3 thyroid gland. You need iron to the conversion of T4 into T3.
It’s T3 we consider the active thyroid hormone. Each cell of the body has. There are receptors that act like a gap. T3 is your key that activates the enzymes that ramp up your metabolism and binds to all those receptors around the nucleus. You need Vitamin vitamin D to bind to a T3 to make a super key that unlocks your DNA and fits the nuclear receptors.
In the conclusion, you need Omega-3 fatty acids around the membrane of these cells for the hormone to be received appropriately. If you’re missing even one of those nutrients, you will have some kind of biochemical thyroid suppression.
This seems different for different people. For instance, some people have severe selenium deficiency in which they are currently converting T4 thyroid hormone that is hardly any inactive . Their physician is prescribing a sort of synthetic thyroxine T4 thyroid hormone (levothyroxine, Synthroid, etc.), however they can not convert the T4 in thyroxine into the active T3. They believe much worse being on the medication. I see other people with a genetic susceptibility for Vitamin B2 deficiency who can’t get iodine. You can fix them with foods rich in the nutrients and/or with supplements, if you have one of those nutrient deficiencies. The first step is deciding whether or not you have one or more of these deficiencies.
The following is a summary of nutrition your doctor should measure when evaluating your thyroid:
Protein
Magnesium
Zinc
Selenium
Iodine
Iron
Vitamin C
Vitamin B2
Vitamin B3
Vitamin D
Vitamin A
Vitamin B12
Omega-3
If you don’t have your healthcare professional test for these nutrient deficiencies, then you’ll never know why you’ve got a thyroid problem. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
The thyroid gland is a 2-inch butterfly-shaped organ located in the front part of the neck. Although small, the thyroid glans is a major gland in the endocrine system and affects virtually every organ in the body.
What is the function of the thyroid gland?
The thyroid gland regulates fat and carbohydrate metabolism, respiration, body temperature, brain growth, cholesterol levels, the heart and nervous system, blood glucose levels cycle, skin integrity, and more.
Thyroid Diseases Explained
Thyroid disease generally involves an underactive thyroid gland, also known as hypothyroidism. In the USA, an autoimmune reaction called autoimmune thyroiditis or Hashimoto’s disease usually causes hypothyroidism. As with all autoimmune disorders, the body identifies its own tissues as an invader and strikes until the organ is destroyed. This chronic attack will finally prevent the thyroid gland from producing thyroid hormones. The lack of these hormones may slow down metabolism and also cause weight gain, fatigue, dry skin and hair loss as well as lead to difficulty concentrating. Hashimoto’s thyroid disease affects approximately 5 percent of the US population, is seven times more prevalent in women than men, and generally occurs during middle age.
Hyperthyroidism, or an overactive thyroid gland, is another frequent thyroid disease. The form is Graves’ disease in which the body’s autoimmune reaction causes the thyroid gland to make too much T3 and T4. Symptoms of hyperthyroidism may include weight loss, high blood pressure, nausea, and a rapid heartbeat. The disease also disproportionately affects women and presents until the age of 40.
Hashimoto’s thyroid disease is more common than Graves’ disease, but both are known as autoimmune thyroid disease (ATD), which has a strong genetic link and is associated with other autoimmune disorders, such as type 1 diabetes, rheumatoid arthritis, lupus, and celiac disease. A goiter, or enlargement of the thyroid gland, may be caused by hypothyroidism, hyperthyroidism, excessive or insufficient consumption of iodine from the diet, or thyroid gland, the most frequent endocrine cancer whose prevalence studies imply is increasing.
Key Nutrients for Thyroid Disease
Many dietary factors play a role in optimizing thyroid function. But, excesses and both nutrient deficiencies could cause or exacerbate symptoms. Working in collaboration with a doctor is ideal to determine status for optimal thyroid health. Many functional medicine practitioners specialize in functional nutrition, which can help with thyroid disease.
Iodine
Iodine is a vital nutrient in the human body and essential to thyroid function; thyroid hormones have been constituted of iodine. Iodine deficiency is the cause while disorder is the primary cause of thyroid dysfunction in the United States
Iodine deficiency has been considered uncommon in america since the 1920s, largely as a result of widespread utilization of iodized salt. This, along with poultry, milk, and grains, is a major source of iodine in the conventional American diet.
However, iodine intake has decreased during the last few decades. Americans get approximately 70 percent of their salt intake from foods which, in the USA and Canada, don’t contain iodine. A 2012 Centers for Disease Control and Prevention report indicates that, on average, Americans are receiving sufficient amounts of iodine, together with the potential exclusion of women of childbearing age.
Both iodine deficiency and surplus have significant dangers; thus, supplementation ought to be approached with care. Supplemental iodine might lead to symptom flare-ups in individuals with Hashimoto’s thyroid disease because it stimulates antibodies.
Iodine intake often is not easily apparent on a dietary recall because the quantity in foods is largely determined by levels from the soil and extra salt. But, experts state that, “Clients carrying iodine tablets are a red flag. Frequent intake of foods such as seaweed or an avoidance of all iodized salt may serve as signals that further exploration is required.”
Vitamin D
Vitamin D deficiency is connected to Hashimoto’s, according to one study showing that over 90 percent of patients studied were deficient. It’s uncertain whether the low vitamin D levels were the direct cause of Hashimoto’s or the result of the disease process itself.
Hyperthyroidism, especially Graves’ disease, is known to cause bone loss, which can be compounded by the vitamin D deficiency commonly seen in people with hyperthyroidism. This bone mass could be recovered with therapy for hyperthyroidism, and specialists indicate that sufficient nourishment, such as vitamin D, which are particularly important during and following
Foods which contain some vitamin D include fatty fish, milk, legumes, eggs, and mushrooms. Sunlight also is a source, but the sum of vitamin production depends upon the season and latitude. Supplemental D3 could be necessary, if clients have low vitamin D levels, along with the customer’s doctor should monitor progress to ensure the individual’s levels stay within a suitable range.
Selenium
The maximum concentration of selenium is found in the thyroid gland, and it has been demonstrated to be a necessary element of enzymes integral to thyroid function. Selenium is a vital trace mineral and was shown to have a deep effect in the immune system, cognitive function, fertility in both women and men, and mortality rate.
A meta-analysis of randomized, placebo-controlled studies has shown advantages of selenium on both the thyroid antibody titers and mood in patients with Hashimoto’s, but this impact appears more pronounced in people who have a selenium deficiency or insufficiency in the outset. Conversely, an excessive intake of selenium can lead to gastrointestinal distress or perhaps raise the risk of type 2 diabetes and cancer. So clients will benefit from getting their selenium levels tested and integrating healthful foods into their diets, including Brazil nuts, tuna, crab, and lobster.
Vitamin B12
Studies show that about 30 percent of people with ATD experience a vitamin B12 deficiency. Food sources of B12 include salmon, sardines, mollusks, organ meats such as liver, muscle meat, and dairy. Vegan sources include fortified cereals and yeast. Severe B12 deficiency may be irreversible, therefore it is important for dietitians to suggest clients have their levels analyzed.
Goitrogens
Cruciferous vegetables like broccoli, cauliflower, and cabbage naturally discharge a chemical known as goitrin when they are hydrolyzed, or broken down. Goitrin can interfere with the synthesis of thyroid hormones. Nonetheless, this is usually a concern only when combined with an iodine deficiency. Heating cruciferous vegetables denatures much or all of this possible goitrogenic effect.
Soy is another possible goitrogen. The isoflavones in soy may lower thyroid hormone synthesis, but many studies have discovered that consuming soy does not result in hypothyroidism in individuals with adequate iodine stores. But Dean cautions clients to consume soy in moderation.
The potential exclusion is millet, a nutritious gluten-free grain, which might suppress thyroid function even in people with adequate iodine intake. If a dietary recall indicates frequent millet ingestion in patients with hypothyroidism, it may be wise to indicate they choose another grain.
Foods, Supplements, and Medication Interactions
When it comes to thyroid medications, it is very important to RDs to know the drugs can interact with common nutritional supplements. Calcium supplements have the capacity to interfere with absorption of thyroid medications, so when taking the two patients need to consider the timing. Studies recommend limiting calcium supplements and thyroid drugs by at least four hours. Coffee and fiber nutritional supplements reduced the absorption of thyroid drugs, so patients should take them one hour apart. Dietitians should affirm whether customers have received and are adhering to these guidelines for optimum wellness.
Chromium picolinate, which is marketed for blood sugar control and weight reduction, also impairs the absorption of thyroid medications. If clients decide to take chromium picolinate, then they ought to take it three to four hours apart from thyroid drugs. Flavonoids in vegetables, fruits, and tea have been shown to have potential cardiovascular benefits. But, high-dose flavonoid supplements can suppress thyroid function. The Natural Standards Database provides a comprehensive list of nutritional supplements with a possible impact on thyroid function, thus taking precautions and coordinating patient care with a knowledgeable practitioner is sensible.
Exercise
A discussion on thyroid disorder and good health is not complete without stressing the importance of physical activity. Lisa Lilienfield, MD, a thyroid disorder specialist in the Kaplan Center for Integrative Medicine in McLean, Virginia, and a certified yoga teacher, is a firm believer in the value of exercise, especially. “With hypothyroid patients, certainly exercise can assist with weight gain, fatigue, and depression. With hyperthyroidism, anxiety and sleep disturbances are so common, and exercise might help regulate both.”
In addition to the obvious impact exercise has on weight and metabolism, a study of patients with Graves’ disease found that a structured exercise plan revealed remarkable improvements in fatigue levels, and significantly more patients have been able to successfully quit taking antithyroid medications with no relapse.
In Conclusion
Celiac disease presents unique challenges as a result of unwanted weight changes, significant cardiovascular disease, and symptoms such as fatigue, mood changes, and gastrointestinal upset, which can hinder the growth of healthful behaviors. It’s vital that dietitians focus when counselling clients on setting goals that are realistic for adjustments and routine exercise. With so many nutrient deficiencies and interactions with medications and nutritional supplements, it will be important for dietitians to coordinate with their clients’ health care team for health outcomes.
The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
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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.
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
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
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
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
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
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, 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.
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
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.
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
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
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 
