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Lifestyle Changes for Managing Thyroid Disease | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine

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.

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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.

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How Lifestyle Changes Can Improve Thyroid Disease | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine

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.

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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.

By Dr. Alex Jimenez

Additional Topics: Wellness

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Turmeric Root Side Effects

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Turmeric

Turmeric: Let us ease your mind a bit. As with any dietary supplement, there are right ways to take turmeric root that could best benefit your health. We review things to keep in mind to limit any potential side effects.�

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Potential Benefits Of Turmeric Root�

The compound that gives turmeric root its signature bright yellow hue is also the compound that packs the potential health benefits punch: curcumin. Curcumin � and therefore turmeric root � is believed to provide some pretty attractive health benefits, including support of joint and muscle comfort, promotion of healthy aging of the brain, support of a healthy digestive tract, and maintenance of healthy cholesterol levels already in the normal range.

But that doesn�t mean that taking 10 turmeric root supplement capsules at once would give you 10 times the potential benefit. Quite the opposite. There are right � and wrong � ways to consume the supplement in an effort to reduce possible side effects.

Avoiding Turmeric Root Side Effects

According to�MentalHealthDaily.com, if you�re supplementing with turmeric root, especially at high doses, it is possible that you may encounter some unwanted side effects at one point or another. The two most common side effects associated are diarrhea and nausea. High on the list of possible side effects are also:

Thinning of the blood. Some research shows that curcumin may have anticoagulant effects which can slow blood clotting. If you�re already taking a blood thinner, speak to your doctor about your desire to add a turmeric root supplement, and discontinue use at least two weeks before any surgery.
Some estimates indicate that one in four turmeric root users will notice an increase in bloating and passing gas. To reduce the likelihood of experiencing this particular side effect, consider a dose less than 6 grams per day, and avoid taking your supplement on an empty stomach.
Low blood sugar. Especially in those with health concerns related to blood glucose, turmeric root supplements may yield this unwanted effect. Some experts believe that the curcumin may even act to amplify pre-existing blood sugar issues.

Less common side effects may also include facial flushing, fever, headaches, skin rash and even low testosterone.

But as with any supplement or medication, remember that the severity and number of side effects you experience is likely subject to a variety of causes and factors. Keep in mind that some individuals may not experience any side effects at all.

Recommendations And Dosages

As with all medications and supplements, we encourage you to consult with your healthcare professional before adding a turmeric root supplement to your regimen. He or she can personalize dosing recommendations for you based on your desired outcomes and other factors � like other medications and supplements you are taking. That said,�WebMD.com�offers a few general guidelines for using turmeric and avoiding possible side effects:

This root is likely safe when applied to the skin appropriately for up to eight months.
It should only be considered as a mouthwash for short-term use.
For high cholesterol levels: 1.4 grams of turmeric extract in two divided doses each day for three months has been used for those 15 years or older.

Let�s Get Technical

While there are still many studies to be done and results to be reported, BCM-95 � a highly-absorbent form of curcumin, which is the active ingredient in turmeric root � has been�clinically proven�to help temporarily relieve minor pain. When used at a dosage of 2 grams per day, volunteers participated in the study without any mild adverse reactions. To try BCM-95 out for yourself, we recommend�CuraMed�and other daily supplements from�Terry Naturally. And as always, we�re proud to provide you with free shipping anywhere in the U.S.

by�Theresa Groskopp, CN�in�Health Challenges,�Health Tips,�Nutrition Supplements

Metabolic Syndrome And Chiropractic

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

Metabolic Syndrome:

Key indexing terms:

Metabolic syndrome X
Insulin resistance
Hyperglycemia
Inflammation
Weight loss

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

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

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

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

Introduction: Metabolic Syndrome

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

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

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

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

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

metabolic table 1

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

Methods

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

Discussion

Insulin Resistance Overview

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

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

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

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

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

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

Visceral Adiposity And Insulin Resistance

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

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

Hypothalamic Inflammation And Insulin Resistance

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

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

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

Clinical Correlates Diet-Induced Inflammation & Insulin Resistance

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

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

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

MetS And Disease Expression

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

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

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

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

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

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

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

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

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

Key Nutrients That Promote Insulin Sensitivity

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

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

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

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

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

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

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

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

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

G Sylvestre

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

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

Vanadyl Sulfate

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

Chromium

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

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

?-Lipoic Acid

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

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

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

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

Limitations

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

Conclusion: Metabolic Syndrome

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

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

Chiropractic Care

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

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

Funding Sources and Conflicts of Interest

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

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of the metabolic and physiologic response to chromium 
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nutritional roles and safety. Nutr Today 2005;40(4):180�95. 
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effects of omega-3 fatty acids, alpha lipoic acid and vitamin E 
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The Best Exercises for Hypothyroidism | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Chiropractic, Functional Medicine, Wellness

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.

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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.

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Muscle Fasciculation Improvement With Dietary Change: Gluten Neuropathy

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Gluten Free Diet, Neuropathy

Muscle Fasciculations:

Key indexing terms:

Fasciculation
muscular
Gluten
Celiac disease
Chiropractic
Food hypersensitivity

Abstract
Objective: The purpose of this case report is to describe a patient with chronic, multisite muscle fasciculations who presented to a chiropractic teaching clinic and was treated with dietary modifications.

Clinical features: A 28-year-old man had muscle fasciculations of 2 years. The fasciculations began in his eye and progressed to the lips and lower extremities. In addition, he had gastrointestinal distress and fatigue. The patient was previously diagnosed as having wheat allergy at the age of 24 but was not compliant with a gluten-free diet at that time. Food sensitivity testing revealed immunoglobulin G�based sensitivity to multiple foods, including many different grains and dairy products. The working diagnosis was gluten neuropathy.

Intervention and outcome: Within 6 months of complying with dietary restrictions based on the sensitivity testing, the patient�s muscle fasciculations completely resolved. The other complaints of brain fog, fatigue, and gastrointestinal distress also improved.

Conclusions: This report describes improvement in chronic, widespread muscle fasciculations and various other systemic symptoms with dietary changes. There is strong suspicion that this case represents one of gluten neuropathy, although testing for celiac disease specifically was not performed.

Contents

Introduction:�Muscle Fasciculations

muscle fasciculations wheat-flour There are 3 known types of negative reactions to wheat proteins, collectively known as wheat protein reactivity: wheat allergy (WA), gluten sensitivity (GS),�and celiac disease (CD). Of the 3, only CD is known to involve autoimmune reactivity, generation of antibodies, and intestinal mucosal damage. Wheat allergy involves the release of histamine by way of immunoglobulin (Ig) E cross-linking with gluten peptides and presents within hours after ingestion of wheat proteins. Gluten sensitivity is considered to be a diagnosis of exclusion; sufferers improve symptomatically with a gluten-free diet (GFD) but do not express antibodies or IgE reactivity.1

The reported prevalence of WA is variable. Prevalence ranges from 0.4% to 9% of the population.2,3 The prevalence of GS is somewhat difficult to determine, as it does not have a standard definition and is a diagnosis of exclusion. Gluten sensitivity prevalence of 0.55% is based on National Health and Nutrition Examination Survey data from 2009 to 2010.4 In a 2011 study, a GS prevalence of 10% was reported in the US population.5 In contrast to the above 2 examples, CD is well defined. A 2012 study examining serum samples from 7798 patients in the National Health and Nutrition Examination Survey database from 2009 to 2010 found an overall prevalence of 0.71% in the United States.6

Neurologic manifestations associated with negative reactions to wheat proteins have been well documented. As early as 1908, �peripheral neuritis� was thought to be associated with CD.7 A review of all published studies on this topic from 1964 to 2000 indicated that the most common neurologic manifestations associated with GS were ataxia (35%), peripheral neuropathy (35%), and myopathy (16%). 8 Headaches, paresthesia, hyporeflexia, weakness, and vibratory sense reduction were reported to be more prevalent in CD patients vs controls.9 These same symptoms were more prevalent in CD patients who did not strictly follow a GFD vs those who were compliant with GFD.

At present, there are no case reports describing the chiropractic management of patient with gluten neuropathy. Therefore, the purpose of this case study is to describe a patient presentation of suspected gluten neuropathy and a treatment protocol using dietary modifications.

Case Report

A 28-year-old man presented to a chiropractic teaching clinic with complaints of constant muscle fasciculations of 2 years� duration. The muscle fasciculations originally started in the left eye and remained there for about 6 months. The patient then noticed that the fasciculations began to move to other areas of his body. They first moved into the right eye, followed by the lips,�and then to the calves, quadriceps, and gluteus muscles. The twitching would sometimes occur in a single muscle or may involve all of the above muscles simultaneously. Along with the twitches, he reports a constant �buzzing� or �crawling� feeling in his legs. There was no point during the day or night when the twitches ceased.

The patient originally attributed the muscle twitching to caffeine intake (20 oz of coffee a day) and stress from school. The patient denies the use of illicit drugs, tobacco, or any prescription medication but does drink alcohol (mainly beer) in moderation. The patient ate a diet high in meats, fruits, vegetables, and pasta. Eight months after the initial fasciculations began, the patient began to experience gastrointestinal (GI) distress. Symptoms included constipation and bloating after meals. He also began to experience what he describes as �brain fog,� a lack of concentration, and a general feeling of fatigue. The patient noticed that when the muscle fasciculations were at their worst, his GI symptoms correspondingly worsened. At this point, the patient put himself on a strict GFD; and within 2 months, the symptoms began to alleviate but never completely ceased. The GI symptoms improved, but he still experienced bloating. The patient�s diet consisted mostly of meats, fruit, vegetables, gluten-free grains, eggs, and dairy.

At the age of 24, the patient was diagnosed with WA after seeing his physician for allergies. Serum testing revealed elevated IgE antibodies against wheat, and the patient was advised to adhere to a strict GFD. The patient admits to not following a GFD until his fasciculations peaked in December 2011. In July of 2012, blood work was evaluated for levels of creatine kinase, creatine kinase�MB, and lactate dehydrogenase to investigate possible muscle breakdown. All values were within normal limits. In September of 2012, the patient under- went food allergy testing once again (US Biotek, Seattle, WA). Severely elevated IgG antibody levels were found against cow�s milk, whey, chicken egg white, duck egg white, chicken egg yolk, duck egg yolk, barley, wheat gliadin, wheat gluten, rye, spelt, and whole wheat (Table 1). Given the results of the food allergy panel, the patient was recommended to remove this list of foods from his diet. Within 6 months of complying with the dietary changes, the patient�s muscle fasciculations completely resolved. The patient also experienced much less GI distress, fatigue, and lack of concentration.

Discussion

muscle fasciculations wheat protein loaf The authors could not find any published case studies related to a presentation such as the one�described here. We believe this is a unique presentation of wheat protein reactivity and thereby represents a contribution to the body of knowledge in this field.

This case illustrates an unusual presentation of a widespread sensorimotor neuropathy that seemed to respond to dietary changes. Although this presentation is consistent with gluten neuropathy, a diagnosis of CD was not investigated. Given the patient had both GI and neurologic symptoms, the likelihood of gluten neuropathy is very high.

There are 3 forms of wheat protein reactivity. Because there was confirmation of WA and GS, it was decided that testing for CD was unnecessary. The treatment for all 3 forms is identical: GFD.

The pathophysiology of gluten neuropathy is a topic that needs further investigation. Most authors agree it involves an immunologic mechanism, possibly a direct or indirect neurotoxic effect of antigliadin anti- bodies. 9,10 Briani et al 11 found antibodies against ganglionic and/or muscle acetylcholine receptors in 6 of 70 CD patients. Alaedini et al12 found anti-ganglioside antibody positivity in 6 of 27 CD patients and proposed that the presence of these antibodies may be linked to gluten neuropathy.

It should also be noted that both dairy and eggs showed high responses on the food sensitivity panel. After reviewing the literature, no studies could be located linking either food with neuromuscular symp- toms consistent with the ones presented here. There- fore, it is unlikely that a food other than gluten was responsible for the muscle fasciculations described in this case. The other symptoms described (fatigue, brain fog, GI distress) certainly may be associated with any number of food allergies/sensitivities.

Limitations

One limitation in this case is the failure to confirm CD. All symptoms and responses to dietary change point to this as a likely possibility, but we cannot confirm this diagnosis. It is also possible that the�symptomatic response was not due directly to dietary change but some other unknown variable. Sensitivity to foods other than gluten was documented, including reactions to dairy and eggs. These food sensitivities may have contributed to some of the symptoms present in this case. As is the nature of case reports, these results cannot necessarily be generalized to other patients with similar symptoms.

Conclusion:�Muscle Fasciculations

This report describes improvement in chronic, widespread muscle fasciculations and various other systemic symptoms with dietary change. There is strong suspicion that this case represents one of gluten neuropathy, although testing for CD specifically was not performed.

Brian Anderson DC, CCN, MPHa,?, Adam Pitsinger DCb

Attending Clinician, National University of Health Sciences, Lombard, IL Chiropractor, Private Practice, Polaris, OH

Acknowledgment

This case report is submitted as partial fulfillment of the requirements for the degree of Master of Science in Advanced Clinical Practice in the Lincoln College of Post-professional, Graduate, and Continuing Education at the National University of Health Sciences.

Funding Sources and Conflicts of Interest

No funding sources or conflicts of interest were reported for this study.

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disorders: consensus on new nomenclature and classification.
BMC Med 2012;10:13.
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secondary immunoglobulin E sensitization to soy and wheat in
the Multi-Centre Allergy Study cohort. Clin Exp Allergy
2008;38:493�500.
3. Vierk KA, Koehler KM, Fein SB, Street DA. Prevalence of
self-reported food allergy in American adults and use of food
labels. J Allergy Clin Immunol 2007;119:1504�10.
4. DiGiacomo DV. Prevalence and characteristics of non-celiac
gluten sensitivity in the United States: results from the
continuous National Health and Nutrition Examination Survey
2009-2010. Presented at: the 2012 American College of
Gastroenterology Annual Scientific Meeting; Oct. 19-24, Las
Vegas.; 2012.
5. Sapone A, Lammers KM, Casolaro V. Divergence of gut
permeability and mucosal immune gene expression in two
gluten-associated conditions: celiac disease and gluten sensitivity.
BMC Med 2011;9:23.
6. Rubio-Tapia A, Ludvigsson JF, Brantner TL, Murray JA,
Everhart JE. The prevalence of celiac disease in the United
States. Am J Gastroenterol 2012 Oct;107(10):1538�44.
7. Hadjivassiliou M, Grunewald RA, Davies-Jones GAB. Gluten
sensitivity as a neurological illness. J Neurol Neurosurg
Psychiatr 2002;72:560�3.
8. Hadjivassiliou M, Chattopadhyay A, Grunewald R, et al.
Myopathy associated with gluten sensitivity. Muscle Nerve
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9. Cicarelli G, Della Rocca G, Amboni C, et al. Clinical and
neurological abnormalities in adult celiac disease. Neurol Sci
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associated with gluten sensitivity. J Neurol Neurosurg
Psychiatry 2006;77:1262�6.
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ganglionic acetylcholine receptors in celiac disease. Autoimmunity
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12. Alaedini A, Green PH, Sander HW, et al. Ganglioside reactive
antibodies in the neuropathy associated with celiac disease.
J Neuroimmunol 2002;127(1�2):145�8.

Foods to Avoid When Managing Hypothyroidism | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine

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.

Contents

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..

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How Diet Can Help the Thyroid | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Chiropractic, Functional Medicine

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.

Contents

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

TRENDING TOPIC: EXTRA EXTRA: About Chiropractic

Key Nutrition for Thyroid Disease | Wellness Clinic

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Functional Medicine

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.

Contents

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.

By Dr. Alex Jimenez

Additional Topics: Wellness

TRENDING TOPIC: EXTRA EXTRA: About Chiropractic

The Role Of Epigenetics In Obesity And Metabolic Disease

by Dr Alex Jimenez DC, APRN, FNP-BC, CFMP, IFMCP | Basal Metabolic Index (BMI), Epigenetic's, Metabolic Syndrome, Weight Loss, Wellness

Epigenetic Abstract:

The increased prevalence of obesity and related comorbidities is a major public health problem. While genetic factors undoubtedly play a role in determining individual susceptibility to weight gain and obesity, the identified genetic variants only explain part of the variation. This has led to growing interest in understanding the potential role of epigenetics as a mediator of gene-environment interactions underlying the development of obesity and its associated comorbidities. Initial evidence in support of a role of epigenetics in obesity and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which reported epigenetic changes in key metabolically important tissues following high-fat feeding and epigenetic differences between lean and obese animals and by human studies which showed epigenetic changes in obesity and T2DM candidate genes in obese/diabetic individuals. More recently, advances in epigenetic methodologies and the reduced cost of epigenome-wide association studies (EWAS) have led to a rapid expansion of studies in human populations. These studies have also reported epigenetic differences between obese/T2DM adults and healthy controls and epigenetic changes in association with nutritional, weight loss, and exercise interventions. There is also increasing evidence from both human and animal studies that the relationship between perinatal nutritional exposures and later risk of obesity and T2DM may be mediated by epigenetic changes in the offspring. The aim of this review is to summarize the most recent developments in this rapidly moving field, with a particular focus on human EWAS and studies investigating the impact of nutritional and lifestyle factors (both pre- and postnatal) on the epigenome and their relationship to metabolic health outcomes. The difficulties in distinguishing consequence from causality in these studies and the critical role of animal models for testing causal relationships and providing insight into underlying mechanisms are also addressed. In summary, the area of epigenetics and metabolic health has seen rapid developments in a short space of time. While the outcomes to date are promising, studies are ongoing, and the next decade promises to be a time of productive research into the complex interactions between the genome, epigenome, and environment as they relate to metabolic disease.

Keywords: Epigenetics, DNA methylation, Obesity, Type 2 diabetes, Developmental programming

Contents

Introduction

Epigenetic mechanisms Obesity is a complex, multifactorial disease, and better understanding of the mechanisms underlying the interactions between lifestyle, environment, and genetics is critical for developing effective strategies for prevention and treatment [1].

In a society where energy-dense food is plentiful and the need for physical activity is low, there is a wide variation in individuals� susceptibility to develop�obesity and metabolic health problems. Estimates of the role of heredity in this variation are in the range of 40�70 %, and while large genome-wide association studies (GWAS) have identified a number of genetic loci associated with obesity risk, the ~100 most common genetic variants only account for a few percent of variance in obesity [2, 3]. Genome-wide estimates are higher, accounting for ~20 % of the variation [3]; however, a large portion of the heritability remains unexplained.

Recently, attention has turned to investigating the role of epigenetic changes in the etiology of obesity. It has been argued that the epigenome may represent the mechanistic link between genetic variants and environmental�factors in determining obesity risk and could help explain the �missing heritability.� The first human epigenetic studies were small and only investigated a limited number of loci. While this generally resulted in poor reproducibility, some of these early findings, for instance the relationship between PGC1A methylation and type 2 diabetes mellitus (T2DM) [4] and others as discussed in van Dijk et al. [5], have been replicated in later studies. Recent advances and increased affordability of high- throughput technologies now allow for large-scale epigenome wide association studies (EWAS) and integration of different layers of genomic information to explore the complex interactions between the genotype, epigenome, transcriptome, and the environment [6�9]. These studies are still in their infancy, but the results thus far have shown promise in helping to explain the variation in obesity susceptibility.

There is increasing evidence that obesity has develop mental origins, as exposure to a suboptimal nutrient supply before birth or in early infancy is associated with an increased risk of obesity and metabolic disease in later life [10�13]. Initially, animal studies demonstrated that a range of early life nutritional exposures, especially those experienced early in gestation, could induce epigenetic changes in key metabolic tissues of the offspring that persisted after birth and result in permanent alterations in gene function [13�17]. Evidence is emerging to support the existence of the same mechanism in humans. This has led to a search for epigenetic marks present early in life that predict later risk of metabolic disease, and studies to determine whether epigenetic programming of metabolic disease could be prevented or reversed in later life.

This review provides an update of our previous systematic review of studies on epigenetics and obesity in humans [5]. Our previous review showcased the promising outcomes of initial studies, including the first potential epigenetic marks for obesity that could be detected at birth (e.g., RXRA) [18]. However, it also highlighted the limited reproducibility of the findings and the lack of larger scale longitudinal investigations. The current review focuses on recent developments in this rapidly moving field and, in particular, on human EWAS and studies investigating the impact of (pre- and postnatal) nutritional and lifestyle factors on the epigenome and the emerging role of epigenetics in the pathology of obesity. We also address the difficulties in identifying causality in these studies and the importance of animal models in providing insight into mechanisms.

Review

Epigenetic Changes In Animal Models Of Obesity

rabbit eating Animal models provide unique opportunities for highly controlled studies that provide mechanistic insight into�the role of specific epigenetic marks, both as indicators of current metabolic status and as predictors of the future risk of obesity and metabolic disease. A particularly important aspect of animal studies is that they allow for the assessment of epigenetic changes within target tissues, including the liver and hypothalamus, which is much more difficult in humans. Moreover, the ability to harvest large quantities of fresh tissue makes it possible to assess multiple chromatin marks as well as DNA methylation. Some of these epigenetic modifications either alone or in combination may be responsive to environmental programming. In animal models, it is also possible to study multiple generations of offspring and thus enable differentiation between trans-generational and intergenerational transmission of obesity risk mediated by epigenetic memory of parental nutritional status, which cannot be easily distinguished in human studies. We use the former term for meiotic transmission of risk in the absence of continued exposure while the latter primarily entails direct transmission of risk through metabolic reprogramming of the fetus or gametes.

Animal studies have played a critical role in our current understanding of the role of epigenetics in the developmental origins of obesity and T2DM. Both increased and decreased maternal nutrition during pregnancy have been associated with increased fat deposition in offspring of most mammalian species studied to date (reviewed in [11, 13�15, 19]). Maternal nutrition during pregnancy not only has potential for direct effects on the fetus, it also may directly impact the developing oocytes of female fetuses and primordial germ cells of male fetuses and therefore could impact both the off- spring and grand-offspring. Hence, multigenerational data are usually required to differentiate between maternal intergenerational and trans-generational transmission mechanisms.

Table 1 summarizes a variety of animal models that have been used to provide evidence of metabolic and epigenetic changes in offspring associated with the parental plane of nutrition. It also contains information pertaining to studies identifying altered epigenetic marks in adult individuals who undergo direct nutritional challenges. The table is structured by suggested risk transmission type.

(i) Epigenetic Changes In Offspring Associated With Maternal Nutrition During Gestation

Maternal nutritional supplementation, undernutrition, and over nutrition during pregnancy can alter fat deposition and energy homeostasis in offspring [11, 13�15, 19]. Associated with these effects in the offspring are changes in DNA methylation, histone post-translational modifications, and gene expression for several target genes,�especially genes regulating fatty acid metabolism and insulin signaling [16, 17, 20�30]. The diversity of animal models used in these studies and the common metabolic pathways impacted suggest an evolutionarily conserved adaptive response mediated by epigenetic modification. However, few of the specific identified genes and epigenetic changes have been cross-validated in related studies, and large-scale genome-wide investigations have typically not been applied. A major hindrance to comparison of these studies is the different develop mental windows subjected to nutritional challenge, which may cause considerably different outcomes. Proof that the epigenetic changes are causal rather than being associated with offspring phenotypic changes is also required. This will necessitate the identification of a parental nutritionally induced epigenetic �memory� response that precedes development of the altered phenotype in offspring.

(ii)Effects Of Paternal Nutrition On Offspring Epigenetic Marks

baby sleeping holding hands Emerging studies have demonstrated that paternal plane of nutrition can impact offspring fat deposition and epigenetic marks [31�34]. One recent investigation using mice has demonstrated that paternal pre-diabetes leads to increased susceptibility to diabetes in F1 offspring with associated changes in pancreatic gene expression and DNA methylation linked to insulin signaling [35]. Importantly, there was an overlap of these epigenetic changes in pancreatic islets and sperm suggesting germ line inheritance. However, most of these studies, although intriguing in their implications, are limited in the genomic scale of investigation and frequently show weak and somewhat transient epigenetic alterations associated with mild metabolic phenotypes in offspring.

(iii)Potential Trans-generational Epigenetic Changes Promoting Fat Deposition In Offspring

excess nutrition Stable transmission of epigenetic information across multiple generations is well described in plant systems and C. elegans, but its significance in mammals is still much debated [36, 37]. An epigenetic basis for grand- parental transmission of phenotypes in response to dietary exposures has been well established, including in livestock species [31]. The most influential studies demonstrating effects of epigenetic transmission impacting offspring phenotype have used the example of the viable yellow agouti (Avy) mouse [38]. In this mouse, an insertion of a retrotransposon upstream of the agouti gene causes its constitutive expression and consequent yellow coat color and adult onset obesity. Maternal transmission through the germ line results in DNA methylation�mediated silencing of agouti expression resulting in wild-type coat color and lean phenotype of the offspring [39, 40]. Importantly, subsequent studies in these mice demonstrated that maternal exposure to methyl donors causes a shift in coat color [41]. One study has reported transmission of a phenotype to the F3 generation and alterations in expression of large number of genes in response to protein restriction in F0 [42]; however, alterations in expression were highly variable and a direct link to epigenetic changes was not identified in this system.

(iv) Direct Exposure Of Individuals To Excess Nutrition In Postnatal Life

modern western lifestyle While many studies have identified diet-associated epigenetic changes in animal models using candidate site-specific regions, there have been few genome-wide analyses undertaken. A recent study focussed on determining the direct epigenetic impact of high-fat diets/ diet-induced obesity in adult mice using genome-wide gene expression and DNA methylation analyses [43]. This study identified 232 differentially methylated regions (DMRs) in adipocytes from control and high-fat fed mice. Importantly, the corresponding human regions for the murine DMRs were also differentially methylated in adipose tissue from a population of obese and lean humans, thereby highlighting the remarkable evolutionary conservation of these regions. This result emphasizes the likely importance of the identified DMRs in regulating energy homeostasis in mammals.

Human Studies

anatomy 3D model

Drawing on the evidence from animal studies and with the increasing availability of affordable tools for genome- wide analysis, there has been a rapid expansion of epigenome studies in humans. These studies have mostly focused on the identification of site-specific differences in DNA methylation that are associated with metabolic phenotypes.

A key question is the extent to which epigenetic modifications contribute to the development of the metabolic phenotype, rather than simply being a con- sequence of it (Fig. 1). Epigenetic programming could contribute to obesity development, as well as playing a role in consequent risk of cardiovascular and metabolic problems. In human studies, it is difficult to prove causality [44], but inferences can be made from a number of lines of evidence:

fig 1 (i) Genetic association studies. Genetic polymorphisms that are associated with an increased risk of developing particular conditions are a priori linked to the causative genes. The presence of differential�methylation in such regions infers functional relevance of these epigenetic changes in controlling expression of the proximal gene(s). There are strong cis-acting genetic effects underpinning much epigenetic variation [7, 45], and in population-based studies, methods that use genetic surrogates to infer a causal or mediating role of epigenome differences have been applied [7, 46�48]. The use of familial genetic information can also lead to the identification of potentially causative candidate regions showing phenotype-related differential methylation [49].

(ii)Timing of epigenetic changes. The presence of an epigenetic mark prior to development of a phenotype is an essential feature associated with causality. Conversely, the presence of a mark in association with obesity, but not before its development, can be used to exclude causality but would not exclude a possible role in subsequent obesity-related pathology.

(iii)Plausible inference of mechanism. This refers to epigenetic changes that are associated with altered expression of genes with an established role in regulating the phenotype of interest. One such example is the association of methylation at two CpG sites at the CPT1A gene with circulating triglyceride levels [50]. CPT1A encodes carnitine palmitoyltransferase 1A, an enzyme with a central role in fatty acid metabolism, and this is strongly indicative that differential methylation of this gene may be causally related to the alterations in plasma triglyceride concentrations.

Epigenome-Wide Association Studies: Identifying Epigenetic Biomarkers Of Metabolic Health

A number of recent investigations have focused on exploring associations between obesity/metabolic diseases�and DNA methylation across the genome (Table 2). The largest published EWAS so far, including a total of 5465 individuals, identified 37 methylation sites in blood that were associated with body mass index (BMI), including sites in CPT1A, ABCG1, and SREBF1 [51]. Another large-scale study showed consistent associations between BMI and methylation in HIF3A in whole blood and adipose tissue [52], a finding which was also partially replicated in other studies [9, 51]. Other recently reported associations between obesity-related measures and DNA methylation include (i) DNA methylation differences between lean and obese individuals in LY86 in blood leukocytes [53]; (ii) associations between PGC1A promoter methylation in whole blood of children and adiposity 5 years later [54]; (iii) associations between waist-hip ratio and ADRB3 methylation in blood [55]; and (iv) associations between BMI, body fat distribution measures, and multiple DNA methylation sites in adipose tissue [9, 56]. EWAS have also shown associations between DNA methylation sites and blood lipids [55, 57�59], serum metabolites [60], insulin resistance [9, 61], and T2DM [48, 62, 63] (Table 2).

table 2 contd From these studies, altered methylation of PGC1A, HIF3A, ABCG1, and CPT1A and the previously described RXRA [18] have emerged as biomarkers associated with, or perhaps predictive of, metabolic health that are also plausible candidates for a role in development of metabolic disease.

Interaction Between Genotype And The Epigenome

Genotype Epigenome Epigenetic variation is highly influenced by the underlying genetic variation, with genotype estimated to explain ~20�40 % of the variation [6, 8]. Recently, a number of studies have begun to integrate methylome and genotype data to identify methylation quantitative trait loci (meQTL) associated with disease phenotypes. For instance, in adipose tissue, an meQTL overlapping�with a BMI genetic risk locus has been identified in an enhancer element upstream of ADCY3 [8]. Other studies have also identified overlaps between known obesity and T2DM risk loci and DMRs associated with obesity and T2DM [43, 48, 62]. Methylation of a number of such DMRs was also modulated by high-fat feeding in mice [43] and weight loss in humans [64]. These results identify an intriguing link between genetic variations linked with disease susceptibility and their association with regions of the genome that undergo epigenetic modifications in response to nutritional challenges, implying a causal relationship. The close connection between genetic and epigenetic variation may signify their essential roles in generating individual variation [65, 66]. However, while these findings suggest that DNA methylation may be a mediator of genetic effects, it is also important to consider that both genetic and epigenetic processes could act independently on the same genes. Twin studies [8, 63, 67] can provide important insights and indicate that inter-individual differences in levels of DNA methylation arise predominantly from non-shared environment and stochastic influences, minimally from shared environmental effects, but also with a significant impact of genetic variation.

The Impact Of The Prenatal And Postnatal Environment On The Epigenome

Prenatal environment: Two recently published studies made use of human populations that experienced �natural� variations in nutrient supply to study the impact of maternal nutrition before or during pregnancy on DNA methylation in the offspring [68, 69]. The first study used a Gambian mother-child cohort to show that both seasonal variations in maternal methyl donor intake during pregnancy and maternal pre-pregnancy BMI were associated with altered methylation in the infants [69]. The second study utilized adult offspring from the Dutch Hunger Winter cohort to investigate the effect of prenatal exposure to an acute period of severe maternal undernutrition on DNA methylation of genes involved in growth and metabolism in adulthood [68]. The results highlighted the importance of the timing of the exposure in its impact on the epigenome, since significant epigenetic effects were only identified in individuals exposed to famine during early gestation. Importantly, the epigenetic changes occurred in conjunction with increased BMI; however, it was not possible to establish in this study whether these changes were present earlier in life or a consequence of the higher BMI.

Other recent studies have provided evidence that prenatal over-nutrition and an obese or diabetic maternal environment are also associated with DNA methylation changes in genes related to embryonic development, growth, and metabolic disease in the offspring [70�73].

While human data are scarce, there are indications that paternal obesity can lead to altered methylation of imprinted genes in the newborn [74], an effect thought to be mediated via epigenetic changes acquired during spermatogenesis.

Postnatal environment: The epigenome is established de novo during embryonic development, and therefore, the prenatal environment most likely has the most significant impact on the epigenome. However, it is now clear that changes do occur in the �mature� epigenome under the influence of a range of conditions, including aging, exposure to toxins, and dietary alterations. For example, changes in DNA methylation in numerous genes in skeletal muscle and PGC1A in adipose tissue have been demonstrated in response to a high-fat diet [75, 76]. Interventions to lose body fat mass have also been associated with changes in DNA methylation. Studies have reported that the DNA methylation profiles of adipose tissue [43, 64], peripheral blood mononuclear cells [77], and muscle tissue [78] in formerly obese patients become more similar to the profiles of lean subjects following weight loss. Weight loss surgery also partially reversed non-alcoholic fatty liver disease-associated methylation changes in liver [79] and in another study led to hypomethylation of multiple obesity candidate genes, with more pronounced effects in subcutaneous compared to omental (visceral) fat [64]. Accumulating evidence suggests that exercise interventions can also influence DNA methylation. Most of these studies have been conducted in lean individuals [80�82], but one exercise study in obese T2DM subjects also demonstrated changes in DNA methylation, including in genes involved in fatty acid and glucose transport [83]. Epigenetic changes also occur with aging, and recent data suggest a role of obesity in augmenting them [9, 84, 85]. Obesity accelerated the epigenetic age of liver tissue, but in contrast to the findings described above, this effect was not reversible after weight loss [84].

Collectively, the evidence in support of the capacity to modulate the epigenome in adults suggests that there may be the potential to intervene in postnatal life to modulate or reverse adverse epigenetic programming.

Effect Sizes And Differences Between Tissue Types

connective tissues DNA methylation changes associated with obesity or induced by diet or lifestyle interventions and weight loss are generally modest (<15 %), although this varies depending on the phenotype and tissue studied. For instance, changes greater than 20 % have been reported in adipose tissue after weight loss [64] and associations between HIF3A methylation and BMI in adipose tissue were more pronounced than in blood [52].

The biological relevance of relatively small methylation changes has been questioned. However, in tissues consisting of a mixture of cell types, a small change in DNA methylation may actually reflect a significant change in a specific cell fraction. Integration of epigenome data with transcriptome and other epigenetic data, such as histone modifications, is important, since small DNA methylation changes might reflect larger changes in chromatin structure and could be associated with broader changes in gene expression. The genomic context should also be considered; small changes within a regulatory element such as a promotor, enhancer, or insulator may have functional significance. In this regard, DMRs for obesity, as well as regions affected by prenatal famine exposure and meQTL for metabolic trait loci have been observed to overlap enhancer elements [8, 43, 68]. There is evidence that DNA methylation in famine-associated regions could indeed affect enhancer activity [68], supporting a role of nutrition-induced methylation changes in gene regulation.

A major limitation in many human studies is that epigenetic marks are often assessed in peripheral blood, rather than in metabolically relevant tissues (Fig. 2). The heterogeneity of blood is an issue, since different cell populations have distinct epigenetic signatures, but algorithms have been developed to estimate the cellular composition to overcome this problem [86]. Perhaps more importantly, epigenetic marks in blood cells may not necessarily report the status of the tissues of primary interest. Despite this, recent studies have provided clear evidence of a relationship between epigenetic marks in blood cells and BMI. In the case of HIF3A for which the level of methylation (beta-value) in the study population ranged from 0.14�0.52, a 10 % increase in methylation was associated with a BMI increase of 7.8 %�[52]. Likewise, a 10 % difference in PGC1A methylation may predict up to 12 % difference in fat mass [54].

Conclusions

The study of the role of epigenetics in obesity and metabolic disease has expanded rapidly in recent years, and evidence is accumulating of a link between epigenetic modifications and metabolic health outcomes in humans. Potential epigenetic biomarkers associated with obesity and metabolic health have also emerged from recent studies. The validation of epigenetic marks in multiple cohorts, the fact that several marks are found in genes with a plausible function in obesity and T2DM development, as well as the overlap of epigenetic marks with known obesity and T2DM genetic loci strengthens the evidence that these associations are real. Causality has so far been difficult to establish; however, regardless of whether the associations are causal, the identified epigenetic marks may still be relevant as biomarkers for obesity and metabolic disease risk.

Effect sizes in easily accessible tissues such as blood are small but do seem reproducible despite variation in ethnicity, tissue type, and analysis methods [51]. Also, even small DNA methylation changes may have biological significance. An integrative �omics� approach will be crucial in further unraveling the complex interactions between the epigenome, transcriptome, genome, and metabolic health. Longitudinal studies, ideally spanning multiple generations, are essential to establishing causal relationships. We can expect more such studies in the future, but this will take time.

While animal studies continue to demonstrate an effect of early life nutritional exposure on the epigenome and metabolic health of the offspring, human data are still limited. However, recent studies have provided clear�evidence that exposure to suboptimal nutrition during specific periods of prenatal development is associated with methylation changes in the offspring and therefore have the potential to influence adult phenotype. Animal studies will be important to verify human findings in a more controlled setting, help determine whether the identified methylation changes have any impact on metabolic health, and unravel the mechanisms underlying this intergenerational/transgenerational epigenetic regulation. The identification of causal mechanisms underlying metabolic memory responses, the mode of transmission of the phenotypic effects into successive generations, the degree of impact and stability of the transmitted trait, and the identification of an overarching and unifying evolutionary context also remain important questions to be addressed. The latter is often encapsulated by the predictive adaptive response hypothesis, i.e., a response to a future anticipated environment that increases fitness of the population. However, this hypothesis has increasingly been questioned as there is limited evidence for increased fitness later in life [87].

In summary, outcomes are promising, as the epigenetic changes are linked with adult metabolic health and they act as a mediator between altered prenatal nutrition and subsequent increased risk of poor metabolic health outcomes. New epigenetic marks have been identified that are associated with measures of metabolic health. Integration of different layers of genomic information has added further support to causal relationships, and there have been further studies showing effects of pre- and postnatal environment on the epigenome and health. While many important questions remain, recent methodological advances have enabled the types of large-scale population-based studies that will be required to address the knowledge gaps. The next decade promises to be a period of major activity in this important research area.

Susan J. van Dijk1, Ross L. Tellam2, Janna L. Morrison3, Beverly S. Muhlhausler4,5� and Peter L. Molloy1*�

Competing interests

The authors declare that they have no competing interests.

Authors� contributions
All authors contributed to the drafting and critical revision of the manuscript, and all authors read and approved the final manuscript.

Authors� information
Beverly S. Muhlhausler and Peter L. Molloy are joint last authors.

Acknowledgements

This work has been supported by a grant from the Science and Industry Endowment Fund (Grant RP03-064). JLM and BSM are supported by the National Health and Medical Research Council Career Development Fellowships (JLM, APP1066916; BSM, APP1004211). We thank Lance Macaulay and Sue Mitchell for critical reading and comments on the manuscript.

Author details

1CSIRO Food and Nutrition Flagship, PO Box 52, North Ryde, NSW 1670, Australia. 2CSIRO Agriculture Flagship, 306 Carmody Road, St Lucia, QLD 4067, Australia. 3Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, GPO Box 2471, Adelaide, SA 5001, Australia�4FOODplus Research Centre, Waite Campus, The University of Adelaide, PMB 1, Glen Osmond, SA 5064, Australia. 5Women�s and Children�s Health Research Institute, 72 King William Road, North Adelaide, SA 5006, Australia.

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

G Sylvestre

Vanadyl Sulfate

Chromium

?-Lipoic Acid

Limitations

Conclusion: Metabolic Syndrome

Chiropractic Care

Funding Sources and Conflicts of Interest

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References:

Close Accordion

How can hypothyroidism affect your body?

The Hypothyroidism-Exercise Link

The Best Exercises for Hypothyroidism

Ease Into Exercise

Additional Topics: Wellness

Introduction:�Muscle Fasciculations

Case Report

Discussion

Limitations

Conclusion:�Muscle Fasciculations

Acknowledgment

Funding Sources and Conflicts of Interest

What foods can affect thyroid disease?

Foods with Soy (Edamame, Tofu, and Miso)

Cruciferous Vegetables (Broccoli and Cauliflower)

Gluten (Bread, Pasta, and Rice)

Fatty Foods (Butter, Meat, and Fried Foods)

Sugary Foods (Chocolate and Desserts)

Processed Foods in Packages

Excessive Fiber (Beans, Legumes, and Vegetables)

Coffee (Time your First Cup Carefully)

Alcohol and Thyroid Health

Additional Topics: Wellness

How do you recognize thyroid gland imbalances?

Identifying Thyroid Disease

Gluten and your Thyroid Gland

Sugar

Goitrogens

Nutrition is Vital for a Healthy Thyroid

Additional Topics: Wellness

What is the function of the thyroid gland?

Thyroid Diseases Explained

Key Nutrients for Thyroid Disease

Iodine

Vitamin D

Selenium