insulin resistance

  • Going WILD with Bitter Melon for Blood Sugar Support

    Not long ago, ScienceDaily published an article entitled, “A Ton of Bitter Melon Produces Sweet Results For Diabetes.” This headline is but one of many recent announcements regarding the benefits of an ancient vegetable that is a culinary treat throughout much of the world. Unfortunately, bitter melon and its many benefits remain unknown to most Americans.

    Bitter melon grows in the tropical and subtropical areas of the East Africa, Asia, India, South America and the Caribbean. It is used traditionally as both food and medicine in all of these areas. Momordica charantia goes by many names and is known as bitter melon, bitter gourd, balsam pear, karela, and pare. Most Westerners will identify bitter melon as looking like a pale green or green cucumber with warts. Indian varieties may be whitish to gray-green, as well. Commercial cultivars can range up to a foot or more in length, whereas wild bitter melon varieties may measure only an inch or so, more than making up for their small size with greater bitterness and intense flavor. The gourd becomes more bitter as it ripens. As a food, unripe bitter melon is used fresh in salads, cooked into soups and curries, employed as a flavoring for eggs, meat and so forth.

    Long popular as part of the cuisine of South Asia and China, bitter melon today is conquering new gastronomic territories. Okinawans, renowned for longevity, are extremely fond of a small local variety reputed to confer health benefits. From Okinawa and other sources, bitter melon is becoming increasingly widespread on the Japanese mainland. This reflects an East Asian trend typical of Korea as well as Japan: Highly flavored and colored nutrient-dense foods are being adopted as everyday sources of health. Hence black and red rice, black garlic, bitter melon and other such foods and condiments are being embraced.

    A Plethora of Benefits
    Almost every part of the Momordica charantia plant has been used in traditional medical practices, including not just the fruit, but also the leaves/vines, seeds and roots. Folk and traditional systems often suggest bitter melon for microbial infections, sluggish digestion and intestinal gas, menstrual stimulation, wound healing, inflammation, fever reduction, hypertension, and as a laxative and emetic. All these benefits are from a plant with fruit that has been proven safe by centuries of oral consumption. The only concern generally of note is that bitter melon seed consumption is not recommended for those seeking to become pregnant.

    In South Asia, bitter melon is recommended to support immune health. Some of the effects are direct and some are indirect. Benefits include the inhibition of the growth of a variety of gram-negative and gram-positive bacteria, including E. coli, Salmonella, Staphylococcus, Streptococcus and H. pylori. Extracts, similarly, according to in vitro studies, appear to have an impact on a number of viruses. For instance, bitter melon constituents may prevent viral penetration of the cell wall. Immune effects include support for healthy T-helper cell ratios, natural killer cell populations and related mechanisms.

    With current problems involving overweight and obesity, some of the more attractive actions of bitter melon involve controlling weight gain in the face of the consumption of excessive calories. Animal studies have demonstrated that bitter melon can reduce insulin resistance and visceral obesity caused by a high-fat diet. Similarly, bitter melon may be protective against many damaging results of high fructose diets, including diet-induced hyperglycemia, hyperleptinemia, hyperinsulinemia, and hypertriglyceridemia. The American Medical Association currently is recommending that added sugars should not account for more than five percent of the diet, yet added sugar, especially fructose and “corn” sugars, are found everywhere in the American food supply, although often hidden. Bitter melon may offer some nutritional protection against these added sugars.

    Traditional uses and preclinical research provide a very positive picture of bitter melon. Human trials have confirmed many of these findings. In clinical trials, the fresh fruit, its freshly squeezed juice and the homogenized suspension of bitter melon have led to significant reductions in both fasting and postprandial blood glucose. The caveat is that the successful trials in the literature as a rule have used almost exclusively fresh preparations. For whatever reasons, dry extracts have not fared well in clinical trials. Perhaps this is due to the fact that dry extracts usually are concentrated for charantins even though, according to some research, charantins, the saponins commonly selected for “standardized” preparations, may be inactive or only weakly active. Another possibility is that the most active compounds in bitter melon rapidly deteriorate in most dried powders and extracts.

    If you like the taste of bitter melon, the success of freshly prepared materials in clinical trials is great news because it means that the vegetable may deliver not just a taste treat, but also health benefits when consumed raw and cooked in salads, soups, curries, egg and meat dishes, etc. There also remains another option. Recent research suggests that a special form of bitter melon, especially with proper handling, may deliver on the promise of the fresh material even when dried and delivered in capsules and tablets.

    Sometimes Wild Is Better!
    With many grains, fruits and vegetables, wild genotypes retain healthful qualities that have been bred out of cultivated varieties. For instance, Khorasan wheat (Kamut), a much older form of wheat, provides more protein, minerals and more complex carbohydrates with lower gluten levels than is true of modern wheat. Similarly, carrots initially most often were purple rather than orange because of the vastly greater amounts of phytonutrients in the form of anthocyanidins. Lettuce was more bitter, and so forth and so on.

    With bitter melon, much the same is true. There are literally hundreds of different forms of bitter melon found in China and India. In many ways, the most interesting of these nutritionally are the “wild” forms found in India.

    Recently, a comparative trial in animals looked specifically at the differences among commercial herbal extracts of bitter melon of Chinese, Indian and Indian wild genotype origin. The goal was to establish benefits with regard to blood sugar and insulin regulation and also parameters linked to blood pressure. Very little work has been performed with wild genotypes of bitter melon, even though there are a great many of these in India alone. Most information available tends to cover topics such as the effect of the wild forms on inflammatory responses. Hints in the literature suggest that the blood sugar effects of some of these wild genotypes could be more potent than in the cultivars commonly used for extraction. For instance, it has been found that extracts of bitter gourd activate cellular machinery to regulate energy production (technically, Amp-activated protein kinase) and the way that fats are handled by the liver. These components can account for as much as 7.1 g/ kg of the dried wild material.

    In a just published trial that did look at wild bitter melon, over a period of 60 days the effect of an extract from the wild genotype of bitter melon offered commercially under the name Glycostat proved to be more efficacious than the varietals typically used in Chinese and Indian preparations and certainly more consistent in influencing all the health parameters tested. Wild bitter melon was compared with two commercially available Chinese and Indian preparations in an animal model with a standard test called a Glucose Tolerance Test (GTT). In this test, a fixed amount of glucose is consumed and then the amount that accumulates in the blood (Area Under the Curve/AUC) is measured and the change (delta) is calculated. A smaller change is good because it means that the body is rapidly taking the glucose into the tissues and that there is good insulin sensitivity. All the bitter melon extracts reduced the increase in blood sugar. However, wild bitter melon was superior to both the Chinese and Indian extracts and it was the only extract to deliver statistically significant results. Of particular note, this greater benefit was achieved without elevating insulin levels.

    Other interesting findings included the wild extract’s significant influence on the nitric oxide system (influencing whether the blood vessels can dilate), a system that controls blood fluid volume known as the renin-angiotensin system (RAS) and the closely related angiotensin converting enzyme (ACE) activity. These three systems and activities influence blood pressure and cardiovascular health and in each of them, wild bitter melon either was the only extract that exhibited significant activity or it was more active compared to the Chinese and Indian extracts.

    Concluding Thoughts
    Bitter melon is yet another example of a traditional food and health aid that has made good when tested against modern Western standards. The benefits are real in areas such as blood glucose and blood pressure support—with the caveat that until now bitter melon needed to be eaten in large amounts or the freshly prepared juice consumed regularly in order for the benefits to be realized. Extracts and dried powders have been less successful, perhaps because unstable or for other reasons. A specially prepared wild bitter melon extract produced with special processing appears to have solved this limitation. Wild bitter melon extract supports both blood sugar and blood pressure health, all without the bitter taste.

  • Is the Metabolic Syndrome a Consequence of Aging?

    Is the Metabolic Syndrome a Consequence of Aging? Dallas Clouatre

    Insulin ranks as one of the great discoveries of the Twentieth Century. Initially, it was thought of primarily in terms of providing an explanation and a solution to diabetes. Subsequent research reduced expectations that insulin was a "cure" to diabetes, yet broadened the range of conditions in which insulin appeared to be active. Similarly, organs beyond the pancreas became recognized as being linked to insulin’s activities. These included the muscles as repositories for glucose disposal after meals and even the bones as regulators of insulin’s actions. The concept of insulin resistance, meaning poor responses to insulin’s actions in peripheral tissues, emerged as a major explanation for a variety of conditions under the headings Syndrome X and metabolic syndrome. Just as insulin resistance is a major component in the course of diabetes type 2, it also now is linked to many other conditions.

    Commonly over the long term in type 2 diabetes mellitus, insulin resistances increases blood glucose levels followed by a compensatory rise in circulating insulin concentrations with the latter being the body’s attempt to adapt to the former. Consequences include high blood sugar levels, prolonged high insulin levels, the appearance of medical complications and the exhaustion of the pancreas’ ability to produce insulin.

    The core of the metabolic syndrome thus is the dysregulation and dysfunction involving glucose and insulin. Aside from these, secondary characteristics encompass central obesity, hypertension, and dyslipidemias—especially hypertriglyceridemia and low levels of HDL cholesterol. In addition to participating in the development of many facets of the metabolic syndrome, impairment in insulin sensitivity also appears to be involved in the aging process by promoting inflammation, endothelial dysfunction, the production of advanced glycation end products (AGE), and oxidative stress. Downstream consequences of these dysfunctions include cardiovascular disease and cancer.

    Several major questions have emerged regarding the appearance of the metabolic syndrome. Western medicine, unlike, for instance, traditional Chinese and Indian medicine, tends to pursue and treat the various arms of the metabolic syndrome as distinct clinical entities. Much of the research on the syndrome within allopathic medicine over the past three decades has been aimed at arguing against this separation. Another issue is the level of insulin resistance that should be taken as requiring attention. Most clinicians consider a level of circulating glucose under fasting conditions in the range of 100–125 mg/dl to be pre-diabetic. And then there is the issue of inevitability, which is to say, does the metabolic syndrome arise as a consequence of aging?

    Early Signs of the Metabolic Syndrome in Non-Diabetics

    For some time, there have been questions as to what should be acceptable as a normal fasting glucose level. Circulating glucose within levels generally accepted as normal can influence brain function in an unfavorable manner and increasing hemoglobin AlC (HbAlC) and insulin levels even in the non-diabetic range may affect blood pressure adversely. Such observations lead to suspicions that minor insulin resistance predicts the early onset of many disturbed health parameters involved in the metabolic syndrome. Recently Harry G. Preuss and co-authors, of whom I am one, addressed just such questions in "Fasting Circulating Glucose Levels in the Non-Diabetic Range Correlate Appropriately with Many Components of the Metabolic Syndrome." 1 Those with special interests should consult that journal and a forthcoming more detailed article.

    To be sure, despite access to a large number of medical records, our study faced technical limitations. Because we worked exclusively with subjects possessing non-diabetic fasting glucose concentrations, the other measured clinical values, for the most part, fell in the accepted normal range. Therefore, correlations rather than exact numbers were largely used to determine alterations in health modalities. For corroboration, however, we examined statistical differences in the various parameters between the highest and lowest quartiles associated with these fasting glucose levels. Our data in this preliminary study are representative of the general population in middle and late middle age. The hypothesis is that glucose/insulin perturbations are at the heart of the increased incidence and severity of the various constituents making up the metabolic syndrome and could hasten/ worsen the aging process. A major goal in the study was to cast light on the issue of whether aging itself is associated with the development of the components of the metabolic syndrome or whether, to the contrary, containment of fasting insulin/glucose levels to a relatively low level reduced the appearance of the metabolic syndrome components despite advancing age.

    Findings
    Despite the fact that the population sample consisted entirely of individuals with fasting blood glucose readings below those of diabetes, there was a clear positive correlation between rising glucose levels and metabolic syndrome components. As expected, the average, baseline values of most parameters were in the accepted normal range. Nevertheless all of the following increased more or less in tandem with rising glucose levels: body weight, body fat mass, systolic/diastolic BP, HbA1C, circulating levels of insulin, triglycerides, hsCRP (highly sensitive C-reactive protein) and along with a number of other components representing inflammation and liver health. Elevated non-diabetic glucose levels were associated with signs of augmented inflammation (increased hsCRP, white cell and neutrophil cell counts) and liver perturbations (increased ALT) proposed to play a role in the metabolic syndrome.

    On the reverse side, high-density lipoprotein (HDL) showed a negative correlation, meaning that higher blood glucose levels lead to lower HDL levels. Put another way, unlike fasting glucose, when total cholesterol became the independent variable, the majority of these health parameters improved showing beneficial correlations compared to fasting glucose. However, when examining the total cholesterol minus HDL-cholesterol correlations, all benefits of total cholesterol are lost, suggesting that the benefits noted with total cholesterol are primarily due to the presence of HDL-cholesterol.

    We concluded that the early onset of the various risk factors correlating with circulating fasting glucose suggests a significant role for insulin resistance in the development of the metabolic syndrome. HbA1C and insulin values are also be linked to insulin resistance, but we chose to follow a more common, clinically available marker—circulating fasting glucose levels. Fasting glucose concentrations and the levels of HbA1C and insulin are significantly correlated, therefore findings are similar whether one tests using fasting glucose levels or insulin levels.

    What is the ideal range of fasting blood glucose? Based on our preliminary study, the health data were significantly better with glucose levels in the range of 67–86 mg/dL than at 98–125 mg/dL. Across a wide range of variables, lower definitely was better. Another finding, one only touched on in the provisional version of the study described here, is that aside from blood pressure, age did not seem to play a significant independent role in determining metabolic syndrome health risks and even with regard to increasing systolic blood pressure (the top figure) the influence was less than expected. Glucose and insulin levels were the primary drivers of risk factors, not age.

    Conclusion
    If glucose and insulin levels are the primary sources of metabolic syndrome risks, then enhancing insulin sensitivity and lowering circulating glucose levels are steps that should be taken to promote and maintain health. Fortunately, many of the means to encourage better glucose control are relatively easy. Diet no doubt is key. Sugar, refined carbohydrates and excessive calorie consumption definitely are not friends of good health. Neither are bad eating habits, which include skipping breakfast, eating late in the day and snacking, especially at bedtime. Exercise can be very helpful, particularly taking at least a 15-minute brisk walk before lunch and again later in the day. All of these measures amount to the ounce of prevention advice that actually does work, but only so long as it is followed!

    References:

    1. Preuss, H. G., Clouatre, D, et al. Fasting Circulating Glucose Levels in the Non-Diabetic Range Correlate
    2. Appropriately with Many Components of the Metabolic Syndrome. The Original Internist June 1, 2016, pp. 78ff.
  • The Missing Pieces of the Weight Loss Puzzle

    Obesity has gone prime time. We Find evidence of its presence where ever we look: in every neighborhood, every mall, every school and every workplace. Hardly a day goes by without the news reporting on some aspect of the looming obesity crisis. However, the epidemic is not confined to just the wealthy developed world. Even desperately poor countries such as Nigeria and Uganda are wrestling with the dilemma of obesity. China, which was once one of the world’s leanest countries, is not immune. In fact, it has one of the fastest-growing obesity rates in the world and one quarter of its urban youth is presently overweight. It is projected that by 2015, 200 million Chinese will be not just obese, but morbidly obese. The looming obesity epidemic is sending chills through the global community. Worldwide, more than 1.3 billion people are overweight, whereas only 800 million are underweight—and these statistics are diverging rapidly.

    The problem of expanding waistlines is more than merely a vanity concern. There are serious health consequences from sporting that beer belly. Being overweight can radically change the course of a person’s life. Fat is toxic and potentially lethal. Just carrying as few as an extra 4.5 kilos (10 pounds), over your ideal weight is considered a serious risk factor for heart disease, diabetes, high blood pressure, dementia and Alzheimer’s disease, liver disease, hormonal imbalances depression and cancer. In fact, at least 30 different diseases are related to being overweight. So, what’s going on here? If people were to follow the advice offered by medical professional, public health officials and the experts from the weight loss industry, the problem should be easily solved. Their call to action basically involves turning your back on all those sugary, high carbohydrate, processed, junk foods and switch to a low calorie diet fortified by plenty of exercise. They say it all boils down to a very simple equation: take in fewer calories and burn more.

    Sounds logical. The only problem is that this decades old approach is a dismal failure. For the vast majority of people, it doesn’t work. In fact, long-term success for attaining permanent weight loss is only achieved by a mere 2–5 percent of those very determined and lucky dieters.

    A definition of insanity is doing the same thing over and over again and expecting a different outcome. It certainly appears that the traditional approach to winning the battle of the bulge does indeed, seem insane.

    If there are answers and successful strategies to stem the tide of this serious health epidemic, they will need to be sought elsewhere.

    It’s time to discover some of the missing pieces of the weight loss puzzle.

    Secrets of the Brain-Belly Connection
    Do you value your brainpower? Certainly the one faculty that everyone wants to hold onto throughout a life’s lifetime is a fully functioning, intact brain. Unfortunately belly fat can deliver a serious blow to your aspirations.

    Overwhelming evidence now reveals that your expanding waistline will put a serious crimp on your brain size as well as brainpower.

    Researchers set out to discover if being overweight posed a danger to the brain. They scanned the brains of 94 people over the age of 70. They were looking to see the differences in the brains of people who were of normal weight (BMI under 25), overweight (BMI 25–30), and obese (BMI over 30). (BMI stands for body mass index, an approximation of body fat based on height and weight.)

    Their results were quit shocking. Overweight people have 4 percent less brain tissue than people of normal weight. And, for obese people, the findings were even worse. They had 8 percent less brain tissue than people of normal weight.

    The study not only showed that carrying extra weight degenerated the brain but it also accelerated its aging. Researcher Paul Thompson shared his observation, “The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people. Type 2 diabetes, which is common in the overweight, is known to accelerate the aging of the brain and the onset of dementia. But the relationship between brain size and weight still stood when the researchers accounted for this, suggesting it is the fat itself that is causing the problem. It is thought that high levels of fat raise the odds of the arteries clogging up, cutting the flow of blood and oxygen to the brain. This could cause brain cells to die and the organ to shrink.” The high demands put on these brain areas may make them more sensitive to changes in oxygen levels.

    Another study used magnetic resonance imaging to compare the brains of 44 obese individuals with those of 19 lean people of similar age and background. The obese individuals had more water in the amygdale—a part of the brain involved in eating behavior. It also showed smaller orbitofrontal cortices in obese individuals, important for impulse control and also involved in eating behavior. These findings strengthen the “slippery slope” theory of obesity. The neural changes that occur when you are overweight, affects the parts of your brain that influence and control so many behaviors necessary to make healthy choices.

    Further studies indicate that those with the most belly fat (visceral fat mass) suffer the greatest mental declines over time—and that central or abdominal obesity, in particular, accounts for more than a three-fold increase in dementia risk.

    What’s even more worrying is that increased belly fat is linked to decreases in total brain volume, independent of BMI. This can cause changes in another area of the brain, called the hippocampus, which is responsible for long-term memory, spatial memory and navigation. Finally, excess belly fat also appears to contribute to lesions in the brain’s white matter, especially in diabetic patients—linking it not just to memory loss, but also to increased risk of stroke.

    Obesity is also causes changes to the immune system, which are fanning the flames of inflammation throughout the body. This increased inflammation can impact the brain and lead to a vicious cycle of gaining more and more weight: obesity leads to inflammation, which damages certain parts of the brain, which in turn leads to more uncontrolled eating and more obesity.

    There are many areas of the brain that are affected by being overweight.

    • Frontal and temporal lobes—critical for planning, memory and impulse control
    • Anterior cingulate gyrus—responsible for attention and executive functions
    • Hippocampus—important for long-term memory, spatial memory and navigation
    • Basal ganglia—essential for proper movement and coordination

    Here is the catch-22. Those extra kilos impair brain function and compromise the particular areas of brain that impact a person’s ability to have a keen memory, control impulses and follow through on any kind of planning. It, therefore, becomes more difficult to successfully commit to any kind of program, especially a weight loss program. Since the impulse control part of the brain is affected, controlling those urges to help yourself to another donut or a second helping of mashed potatoes is a Herculean effort and generally doomed to fail.

    Vitamin D —A Key to a Healthy Metabolism
    There is one really important nutritional player when it comes to our health. This superstar nutrient is the sunshine hormone, vitamin D. (Vitamin D is really a steroid hormone rather than an actual vitamin.)

    Vitamin D truly deserves the title of superstar. Each year, vitamin D research discovers additional health benefits conferred by this sunshine vitamin. Vitamin D receptors are found throughout the body including the brain. Optimal levels are absolutely necessary to insure healthy bones, healthy arteries, a robust immune system, balanced moods, optimal cognitive function, protection from hypertension, allergies, multiple sclerosis, Alzheimer’s disease, autoimmune conditions, and fertility and PMS. Most significantly, vitamin D has been proven to be protective against 13 different kinds of cancer.

    Optimal Levels of Vitamin D Are Critical for Health Here are some basic facts you need to know about vitamin D. It is a fat-soluble steroid hormone that is both made by the body and from our diet. In order for the body to produce vitamin D (cholecalciferol), the skin must be exposed to ultraviolet light, primarily from the sun. Vitamin D is further metabolized in the liver and kidneys to create the fully active form of vitamin D. Thus variations in sun exposure due to latitude, season, time of day, sunscreen use, skin pigmentation, and age will determine how much vitamin D the body makes.

    Although it is known that vitamin D play a vital role for the well-being of infants, children, adults and the elderly, we presently have a global pandemic of chronically low vitamin D levels. It’s estimated that 85 percent of the American public are deficient, and as much as 95 percent of all its senior citizens. Vitamin D deficiencies are also widespread throughout the UK, with 86 percent of the population deficient in the winter and 57 percent in the summer.

    Even though Australia’s is described as “sun burnt” country and is one of the sunniest countries in the world, a surprising number of its citizens are severely lacking in vitamin D. A recent report stated that as many as 1 in 3 Australians may have low vitamin D levels.

    For all those on a weight loss quest, vitamin D is one of those missing pieces you have been searching for. There is overwhelming evidence that confirms the importance of keeping your vitamin D levels up to get your extra kilos down. Not only does it help achieve weight loss, it also improves other risk factors such as insulin resistance, metabolic syndrome and blood sugar imbalances. If you are feeling hungry all the time no matter how much you eat, you might want to have your vitamin D levels checked. What drives insatiable hunger is the relationship between low vitamin D levels and a hormone called leptin. Leptin is a messenger molecule made in fat cells that communicates to the hypothalamus, letting it know how much fat is stored in the body. It is the hormone that communicates that you are full.

    Low vitamin D levels interfere with the effectiveness of leptin. Researchers at Aberdeen University, Scotland found that obese people produced 10 per cent less vitamin D than people of average weight. The study discovered that low levels of the vitamin in blood interfered with the function of leptin, which tells the brain when the stomach is full. The study also found that excess body fat absorbs vitamin D, stopping it from entering the bloodstream. Dr Helen MacDonald, of Aberdeen University’s department of medicine and therapeutics, said: “Obese people had less vitamin D and the link between obesity and vitamin D deficiency was statistically significant.” Overweight people, shirking the sun or not taking adequate vitamin D supplementation thwart their dieting efforts in another way. Low vitamin D levels have been shown to increases fat storage. A 2009 Canadian study found that weight and body fat were significantly lower in women with normal vitamin D levels than women with insufficient levels.

    It seems that fat people may be less able to convert vitamin D into its hormonally active form. A Norway study found that the more participants weighed, the lower their vitamin D levels tended to be. The researcher, Zoya Lagunova, MD, believes that obesity is associated with lower vitamin D levels since vitamin D is a fat-soluble vitamin. “Much of the vitamin D produced in the skin or ingested is distributed in fat tissue, so obese people may take in as much vitamin D from the sun, food, or supplements as people who are not obese, but their [blood] levels will tend to be lower. Obese people may need more vitamin D to end up with the same levels as a person whose weight is normal.”

    How much less vitamin does an overweight person make? As it turns out, increased fatty cells can decrease the ability to make vitamin D by a factor of 4. That means that if you are carry extra weight, you may make only one quarter the amount of vitamin D compared to a leaner person. Vitamin D is also an important factor in diabetes. Low levels of vitamin D has been linked to an increased risk of developing type 2 diabetes. After following more than 5,000 people for five years, an Australian research team found that those with lower than average vitamin D levels had a 57 percent increased risk of developing diabetes, compared to those within the recommended range.

    Low levels of vitamin D are also known to nearly double the risk of cardiovascular disease if you already have diabetes. Diabetics, who are deficient in vitamin D and cannot process cholesterol normally, tend to have it build up in their blood vessels, hence increasing the risk of heart attack and stroke.

    Vitamin D also helps keep blood sugar levels under control. In type 2 diabetes the body can’t use insulin it produces efficiently to control blood sugar levels. Vitamin D plays a role by increasing the release of insulin. In one study, researchers evaluated the vitamin D levels and the chance of developing unbalanced blood sugar metabolism. In this study, subjects were evaluated for serum vitamin D levels and followed for 7 years to determine the effects on blood sugar metabolism. The study showed that the subjects with the highest vitamin D levels had a 40 percent increase in supporting optimal future blood sugar balance.

    If you want to lose weight and keep it off, it is critical to check your vitamin D levels. The higher your vitamin D levels the higher your leptin levels and the more your blood sugar will remain balanced. Vitamin D helps your body respond to the correct metabolic messages. High vitamin D levels increase your ability to lose weight and losing weight will increase your vitamin D levels. All of which will reduce your risk of metabolic syndrome, insulin resistance, diabetes, and cardiovascular disease, not to mention most chronic illnesses.

    While it is important for most people to take vitamin D supplementation, especially the overweight, children and elderly, it is critically important to check your vitamin D levels. Taking a vitamin D supplement may not get you into optimal range, which is where you want to be. Its optimal blood vitamin D levels that count. The proper blood test is called 25-hydroxyvitamin D (25-OH), which is included in the basic blood workup. In Australia optimal levels should be 150–200 nmol/L. In the U.S., optimal levels should be between 70–100 ng/mL. Do not settle for less than optimal levels if your goal is the best health possible.