Elements Of Health

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Iodine supplementation reduces PCOS, fibrocysts and diabetes symptoms

Orthoiodosupplementation in a Primary Care Practice

Jorge D. Flechas, M.D.

This article will focus on my experience with the use of inorganic non-radioactive iodine/iodide, thereafter referred to as iodine in a primary care practice. My medical practice is situated in the Appalachian Mountains close to Asheville, North Carolina. This area is considered to be a goiter belt. One of the major problems that we encounter in this location is a problem with hypothyroidism. Back in 1997 hypothyroidism involved 11.7% of the U.S. population . By 1994 severe iodine deficiency also involved 11.7% of the population . Both of these studies were done at separate times by separate groups showing the exact number of 11.7%. This reinforces what we were taught, that iodine deficiency goes hand in hand with the manifestation of hypothyroidism. I have on a weekly basis at least one phone call from a healthcare practitioner questioning whether the intake of iodine causes hypothyroidism and goiter. I often have to go back over the basics of thyroid physiology with these healthcare practitioners, and explain to them that iodine is essential for normal thyroid functions and that it is the manmade organic forms of iodine that are toxic (3).

My practice is family medicine with an integrative medicine twist. I have been using iodine supplementation in my practice over the last four years in amounts needed for whole body sufficiency (orthoiodosupplementation). Orthoiodosupplementation is the daily amount of iodine required for whole body sufficiency (3-5). Whole body sufficiency for iodine is assessed by an iodine/iodide loading test (3). Prior to implementing orthoiodosupplementation, I perform a complete history and physical examination. During a physical examination, I always check the patient’s thyroid. If a mass is picked up on physical then another test that I order is an ultrasound of the thyroid. While undergoing ultrasound to evaluate the mass I will have my technician measure the thyroid volume. Each lobe will have its length measured in centimeters, width measured in centimeters and height measured in centimeters. All three measurements are multiplied times each other and this gives the volume in cubic centimeters. Due to the non-spherical shape of each lobe a correctional factor of 0.52 is used. The two lobe volumes are added together for the total thyroid size. A total volume of 18 cc or more is considered a goiter (6). A volume size of 5 cc or less is suggestive of thyroid atrophy, another manifestation of iodine deficiency.

Any solid mass that is picked up on ultrasound and shows itself to be greater in size than one centimeter by one centimeter will require a radioactive I-123 uptake and scan. This test should be done previous to starting any patient on iodine if a nodule is suspected. A nodule that does not pick up radioactive iodide is considered to be a cold nodule and would suggest the presence of thyroid cancer. A needle biopsy of the cold nodule should be done by an E.N.T. doctor, general surgeon or endocrinologist. If cancer is present the thyroid gland should be surgically removed. Thyroid carcinoma is the most common malignancy of the endocrine system. Malignant tumors derived from the follicular epithelium are classified according to histological features.

The incidence of thyroid cancer is approximately nine per 100,000 in the population per year and this usually increases with age plateau after about age 50. Age is also an important prognostic factor. Thyroid cancer at a young age (less than 20) or in older people (greater than 65) is usually associated with a worse prognosis. Thyroid cancer is twice as common in women as men but the prognosis is worse in men. Additional important risk factors include a history of childhood head or neck irradiation, large nodule size greater than four centimeters, evidence for local tumor fixation or invasion into lymph nodes, and the presence of metastasis . In my small practice of around 5,000 patients, I have found five thyroid cancers in one year. If multiple nodules of the thyroid gland are found at the time of ultrasound then the diagnosis of multinodular thyroid goiter is considered even if the gland is normal in size.

I request serum T4 (the main hormone produced by the thyroid), free T3 (the biologically active thyroid hormone at the cellular level) and a thyroid stimulating hormone (TSH) level. The T3 level inside the cell correlates very well with the free T3 that is in the serum. Following orthoiodosupplementation, serum T4 and TSH levels usually go down and free T3 stays steady . I have seen TSH sometimes go up rather than down while T4 and free T3 did not change or may have gone up some. This does not mean that the patient was developing hypothyroidism but that the brain was stimulating the body to make more sodium iodide symporters (NIS). The NIS are channels in the cell membrane that transport atoms into a cell as compared to a calcium channel or a sodium channel or a chloride channel where the channel only admits one atom to go through. The NIS transports sodium iodide into cells and has been found in all cell lines tested so far. Thyroid stimulating hormone, prolactin and oxytocin have been found to stimulate the making of NIS . While taking iodide, one may see an elevated TSH but we have to recognize that this is not a bad thing. TSH has many actions outside the thyroid that have been discovered . While taking iodine, the vast majority of patients lose fat and gain muscle weight . Very rarely has weight gain occur. Often a check of the patient’s T4, free T3 and TSH shows the T4 to go down, free T3 going down and TSH going up. Iodide is an essential nutrient that is absorbed by all cell lines. Its highest concentration is seen in the thyroid.

The nutritional status of the patient will determine its response to orthoiodosupplementation (3). It is crucial that the thyroid gland has plenty of antioxidants in its cells and many other nutrients. We have found that giving a multivitamin for women with PMS (Optiviteâ ) improves the response to orthoiodosupplementation. One of my patient’s is a classic example of the above scenario. She is a CNA who is 5’1″. At the time she started taking iodine, she experienced an increase in appetite. Within a short period of time, six to eight weeks she gained about 15 pounds. She then was started on this supplementation. Within six weeks the patient lost 15 pounds with a decrease in her appetite.

Breast tissue has an affinity for iodine . Iodine deficiency causes fibrocystic breast disease (FBD) with nodules, cyst enlargement, pain and scar tissue . FBD can be characterized by a lumpy painful breast, generally in reproductive aged women. Initially, this syndrome occurs in the premenstrual phase of a cycle or involves the whole cycle. These symptoms can also occur in menopausal women on estrogen therapy. In 1928 an autopsy series reported a three percent incidence of FBD, whereas in 1973 an autopsy report quoted an 89% incidence . A review by the American Academy of Pathology gives a minimum incidence for FBD of 50% but suggests that 80% of North American women are afflicted with the syndrome during their reproductive lifetime .

Ghent et al in 1993, presented data showing that iodine works great to reduce (FBD)(14). He was able to develop a protocol and a scoring system that helps doctors assess how severe a woman’s FBD is. I would recommend that this scoring system be utilized by physicians in their own medical practice. A precise method of recording the patient’s data will help both physicians and patients see the improvement that occurs following orthoiodosupplementation. This simple method numbers the quadrants of each breast one to four. The pathological changes that can occur in FBD are noted as micronodularity, tenderness, fibrous tissue plaques, macrocysts and turgidity. The presence or the absence of changes is recorded. For example if the micro nodularity of macrocysts disease was present in the upper half of the breasts the numerical score would be one for micro nodularity and two for the two breast quadrants scoring a total of three. If all five changes occurred in all quadrants in one breast the score would be 4 (all four breast quadrants) x5 (all five changes) equals 20 and for both breasts would be 40. Patients are also encouraged to evaluate their own symptomology as expressed by a number of zero equals symptoms worse, one equals symptoms unchanged, two equals less pain only premenstrual discomfort, three equals no pain unable to predict menstruation. The subjective scoring system was employed and graded as follows. Zero equals no palpable abnormalities normal, one equals is score of less than 7.2 and a score greater than 7 but less than the pretreatment score and three equals a score greater than the pretreatment score (See Table I).

In my practice, I have over the last four years worked with some 200 women who have FDB. On average, patients come to my office practice with a mean Ghent score of 15.7 and an average age of 41.4 years. On 12.5 mg of iodine, the score after six months will drop from a mean of score 15 down to about 12.8. On 25 mg, the score will drop down to a mean of score is 10.2. On 37.5 mg the score was 8.6. When we prescribe 50 mg of Iodoralâ

(4 tablets) for 3 to 6 months, the average patient will have a score of 7.6 with a p-value less than 0.001 compared to baseline scores. After a full year at 50 mg iodine per day (4 tablets of Iodoralâ ), the patients mean score dropped to 3.8. We saw many patients with a score of zero, meaning no evidence of FBD. We often see patients’ breast pain disappear in a 1 to 30 days at a dose of 50 mg. At lower doses, the pain persisted for a much longer time. The other findings of micronodularity, tenderness, fibrous tissue plaques, macrocysts and turgidity will take almost a full year to fully go away. Ghent felt that a score of seven or below was normal. We did not see any of the patients reach the score of zero, meaning the absence of all of the pathological symptoms and physical findings of fibrocystic breast disease while taking between 12.5 to 37.5 mg per day. Once FBD is gone, a patient may opt to drop iodine intake to 12.5 to 25 mg per day. There is a chance that the cysts will return. Optimum amount for most patients for FBD is 50 mg (4 tablets) per day continued indefinitely. Monitoring the patient’s serum TSH, T4 and free T3 is done every three to six months. We did not see any major changes in serum T4, TSH and free T3 in these patients.

It was while treating a large 320-pound woman with insulin dependent DIABETES that we learned a valuable lesson regarding the role of iodine in hormone receptor function. This woman had come in via the emergency room with a very high random blood sugar of 1,380 mg/dl. She was then started on insulin during her hospitalization and was instructed on the use of a home glucometer. She was to use her glucometer two times per day. Two weeks later on her return office visit for a checkup of her insulin dependent DIABETES she was informed that during her hospital physical examination she was noted to have FBD. She was recommended to start on 50 mg ofiodine(4 tablets) at that time. One week later she called us requesting to lower the level of insulin due to having problems with hypoglycemia. She was told to continue to drop her insulin levels as long as she was experiencing hypoglycemia and to monitor her blood sugars carefully with her glucometer. Four weeks later during an office visit her glucometer was downloaded to my office computer, which showed her to have an average random blood sugar of 98. I praised the patient for her diligent efforts to control her diet and her good work at keeping her sugars under control with the insulin. She then informed me that she had come off her insulin three weeks earlier and had not been taking any medications to lower her blood sugar. When asked what she felt the big change was, she felt that her DIABETES was under better control due to the use of iodine. Two years later and 70 pounds lighter this patient continues to have excellent glucose control on iodine 50 mg per day. We since have done a study of twelve diabetics and in six cases we were able to wean all of these patients off of medications for their DIABETES and were able to maintain a hemoglobin A1C of less than 5.8 with the average random blood sugar of less than 100. To this date these patients continue to have excellent control of their Type II DIABETES. The range of daily iodine intake was from 50 mg to 100 mg per day. All diabetic patients were able to lower the total amount of medications necessary to control their DIABETES. Two of the twelve patients were controlled with the use of iodine plus one medication. Two patients have control of DIABETES with iodine plus two medications. One patient had control of her DIABETES with three medications plus iodine 50 mg. The one insulin dependent diabetic was able to reduce the intake of Lantus insulin from 98 units to 44 units per day within a period of a few weeks.

In the Type 1 diabetics that we have been following we have noted that if C-peptide is measurable, this would suggest that the individual is making their own insulin. I have been able to help this group of patients to get off insulin or to greatly reduce the amount they need for good glucose control with Iodoralâ at 4 tablets/day (50 mg). If C-peptide is absent then we feel there is no insulin being produced and we have not been able to help this particular group of patients to get off their insulin. We have been able to help these patients lower the total amount of insulin needed to control their glucose.

When patients take between 12.5 to 50 mg of iodine per day, it seems that the body becomes increasingly more responsive to thyroid hormones (3-5). T3 and steroid hormones show the same family of receptors as hydrophobic small molecules . Clur (17) has postulated that iodization of tyrosine residues in the hydrophobic portion of these receptors normalize their response to the corresponding hormone. Optimal intake of iodine in amounts two orders of magnitude greater than iodine levels needed for goiter control may be required for iodization of these receptors (4). Insulin resistance is on the increase. The insulin receptor tyrosine kinase plays a major role in signal transduction distal to the receptor as the primary event leads to subsequent phosphorylation of cytoplasmic proteins, called insulin receptors substrate proteins (IRS). The IRS proteins are cytoplasmic proteins, with multiple tyrosine phosphorylation sites, and phosphorylation of IRS proteins has been implicated as the first post receptor step in insulin signal transmission. The IRS proteins have been referred to as the metabolic switch of the cell (18).

Another organ that can concentrate iodine is the liver. An enterohepatic circulation of iodine has been reported recently 19. I have one patient with liver fatty infiltration who had varicosities of the esophagus with bleeding. Once she started on iodine for FDB we noticed that her GI bleeding stopped and the varicose veins of her stomach and esophagus disappeared.

Iodine deficiency may cause the ovaries to develop cysts , nodules and scar tissue. At its worse this ovarian pathology is very similar to that of polycystic ovarian syndrome (PCOS). As of the writing of this article I have five PCOS patients. The patients have successfully been brought under control with the use of 50 mg of iodine per day. Control with these patients meaning cysts are gone, periods every 28 days and type 2 DIABETES mellitus under control.

Ideally, all patients should have an iodine loading test prior to orthoiodosupplementation. This test is one in which 50 mg of iodine is given after discard of the first morning void. All urine is collected for the next 24 hours including the first morning urine void the next day. The urine sample is then sent to my laboratory, FFP Laboratory for testing (21). The lab is a CLIA approved high complexity testing laboratory in the state of North Carolina. The testing that is done is using the method as described in previous articles . To date we have done over 3,000 loading tests. Iodine therapy is then instituted using 50 mg/day. The body becomes iodine sufficient in about three months. Please be aware of the difference between micrograms (mcg) and milligrams (mg). One milligram is equal to 1,000 micrograms. The majority of the loading tests that are performed at FFP Lab are on women ages 31 – 70 years old. In 667 patients analyzed, the mean level of excretion was about 18 mg for all age groups no patient achieved whole body sufficiency prior to orthoiodosupplementation. The mean excretion drops, as the population gets older (See Fig. 1-6). This suggests that of a total 50 mg of iodine given, the patients on the average retained a mean of 32 mg into their body on the first go around.

We have received many comments over the last two years. Following orthoiodosupplementation, patients have described vivid dreams, dissipated depression, no more cold extremities, more energy and less fatigue.

Patients have noticed an overall feeling of well-being. Patients have noticed a loss of weight. One patient after taking four pills of iodine lost eight pounds of fluid weight in 24 hours. We have had patients note better bowel function. Patients who have been constipated for over ten years have now noted daily bowel movements. We have also had patients noted relief from leg cramps at night. In less than 1% of all the patients treated with I, have we seen an allergic reaction. More often than not, the allergic reaction is hives. After treating over 1,000 patients with iodine, I have at no time seen the Wolff-Chaikoff Effect.

Iodine induces apoptosis and inhibits cells from forming cancer. The absence of iodine in the thyroid causes goiter(3,4). Goiter is associated with breast cancer, stomach cancer, esophageal cancer, ovarian cancer and endometrial cancer . It is felt by many researchers that the absence of iodine is a promoter of cancer. I feel that those patients with the lowest excretion rates and the highest absorption of iodine on the iodine loading test are the ones with the highest risk for development of cancer. From literally hundreds of phone interviews with patients over the last two years, the levels of iodine excretion that seem to raise the highest alarm are those in which the excretion is somewhere around 10 mg or less per 24 hours in patients age 35 and up. My observations at this point show that there is a definite increase in the incidence of breast cancer, stomach cancer, ovarian cancer or thyroid cancer. If a patient has the iodine loading test and has an iodine excretion of 10 mg or less in a 24-hour period, I initiate a cancer workup. In 1976, a JAMA article showed that 6% of the female population was at risk for breast cancer (25)). Women who received thyroid supplementation doubled their risk of breast cancer to 12%. The age groups we used to separate the patients in Figures 1-6 were based on this article. As women get older, the risk of breast cancer increases. In Figures 2-6 the iodine/iodide loading test shows that the older the women are, the lower the rate of iodine excretion.

  1. Cefalu WT. Insulin Resistance. In: Leahy JL, Clark NG, Cefalu WT, editors. Medical Management of DIABETES Mellitus. New York: Marcel Dekker, Inc., 2000; 57-75.

How to cure diabetes type 2


How to cure Type II Diabetes by Dr. Joseph Mercola

With one in four people in the US suffering from type II diabetes right now, I found this to be too valuable not to repost. The following is an exerpt from a recent article by Dr. Joseph Mercola. I encourage you to check out the complete article here if you or a loved one is suffering from this cureable disease.


You CAN Cure Diabetes!

As I said earlier, type 2 diabetes is virtually 100 percent avoidable and can be effectively treated without medications in about the same percentage of cases by recovering your leptin and insulin sensitivity. Leptin, a relatively recently discovered hormone produced by fat, tells your body and brain how much energy it has, whether it needs more (saying "be hungry"), whether it should get rid of some (and stop being hungry) and importantly what to do with the energy it has (reproduce, upregulate cellular repair, or not). In fact, the two most important organs that may determine whether you become (type 2, insulin resistant) diabetic or not are your liver and your brain, and it is their ability to listen to leptin that will determine this. And guess what... The only known way to reestablish proper leptin and insulin signaling is through a proper diet and exercise! There is NO drug that can accomplish this, but following the lifestyle strategies listed below can help you do at least three things that are essential for successfully treating diabetes: Recover your insulin/leptin sensitivity Help normalize your weight, and Naturally normalize your blood pressure.

None of these will drastically raise your risk of a heart attack the way Avandia will. Rather, they will benefit your heart and your entire body: Severely limit or eliminate sugar and grains in your diet, especially fructose, which is far more detrimental than any other type of sugar. Finding out your nutritional type will help you do this without much fuss. While nearly all type 2 diabetics need to swap out their grains for other foods, some people will benefit from using protein for the substitution, while others will benefit from using more vegetable-only carbohydrates. Therefore, along with reducing grains and sugars, determining your nutritional type will give you some insight into what foods you should use to replace the grains and sugars.

Exercise regularly -- a must for anyone with diabetes or pre-diabetes. Typically, you'll need large amounts of exercise, until you get your blood sugar levels under control. You may need up to an hour or two a day. Naturally, you'll want to gradually work your way up to that amount, based on your current level of fitness.

Avoid trans fats

Get plenty of omega-3 fats from a high quality, animal-based source.

Get enough high-quality sleep every night.

Optimize your vitamin D levels. Recent studies have revealed that getting enough vitamin D can have a powerful effect on normalizing your blood pressure and that low vitamin D levels may increase your risk of heart disease.

Optimizing your vitamin D levels may also eliminate the risk of type 1 diabetes in your children if you are pregnant. It’s also vital for infants to receive the appropriate amounts of vitamin D in their early years for these same reasons. Ideally, you’ll want to do this by exposing a large amount of your skin to appropriate amounts of sunshine (or a safe tanning bed) on a regular basis, year-round. Your body can safely create up to 20,000 units of vitamin D a day this way. However, if neither of these options are available, you may want to use an oral vitamin D3 supplement. But remember, if you choose to take an oral supplement it’s essential that you get your levels tested regularly by a proficient lab to make sure you’re not reaching toxic levels, and are within the therapeutic range. Maintaining your vitamin D levels around 60-80 ng/ml can significantly help control your blood sugar.

Address any underlying emotional issues and/or stress. Non-invasive tools like the Emotional Freedom Technique (EFT) can be extremely helpful and effective.

Monitor your fasting insulin level. This is every bit as important as your fasting blood sugar. You'll want your fasting insulin level to be between 2 to 4. The higher your level, the worse your insulin receptor sensitivity is. These are the top steps you should take, starting today, if you have type 2 diabetes. Doing so will virtually guarantee that your diabetes will disappear. And if you want to make sure you are not one of the millions impacted by the coming diabetes epidemic, these same steps will help you to stay healthy and diabetes-free.

Complete article is athttp://articles.mercola.com/sites/articles/archive/2010/10/11/fda-curbs-avandia-diabetes-drug-use.aspx

Until next time,



Vitamins and Minerals that are Lacking in Diabetes Patients 


Select Vitamins and Minerals in the Management of Diabetes


In Brief

The use of vitamin, mineral, and other complementary nutrition-based therapies has increased dramatically in the United States. Many health care providers are also beginning to explore the use of these therapies in their practices. For those of us who work in conventional health care settings, this is a new venture. But for many of our patients who have been self-medicating with supplements, it is not. This article reviews how micronutrient requirements are determined and summarizes current recommendations for supplementation and the most pertinent research on the use of key vitamins and minerals in diabetes management.

Vitamins and minerals play diverse roles in our bodies. Initially, the nutrition community focused on the roles micronutrients play in preventing deficiency diseases such as scurvy, pellagra, and rickets. As our understanding of nutritional science grew, it became clear that nutrients act in far broader ways. We now know that micronutrients can regulate metabolism and gene expression and influence the development and progression of many chronic diseases.1 Eventually, we may be able to tailor nutritional recommendations to individuals’ unique genetic makeup, thus increasing the potential benefit and positive outcomes of medical nutrition therapy.


Micronutrients are vitamins and minerals that our bodies require in small quantities for specific functions. They most commonly function as essential coenzymes and cofactors for metabolic reactions and thus help support basic cellular reactions (i.e., glycolysis, the citric acid cycle, lipid and amino acid metabolism) required to maintain energy production and life.1 Even moderate deficiencies can lead to serious disease states. Micronutrients have been investigated as potential preventive and treatment agents for both type 1 and type 2 diabetes and for common complications of diabetes.2,3

Micronutrient requirements can be difficult to determine because many noninvasive assessment methods, such as the measurement of plasma nutrient levels, do not accurately reflect the quantities of nutrients present in functionally important nutrient pools, and many dietary assessment methods and databases are not perfectly accurate.14

These and other methodological concerns have limited researchers’ ability to conduct well-designed, targeted studies of micronutrient supplements in individuals who are deficient and therefore most likely to benefit from supplementation. This has likely contributed to the varied results obtained in research studies of micronutrients in people with diabetes.

Other research variables that may also contribute to the lack of consensus in study results include the use of diverse populations of patients with diabetes stemming from different biochemical origins, differences in glycemic control, variations in doses and forms of micronutrients used, variable study length, lack of control for dietary contribution of micronutrients, and use of different biochemical assays and methods of analysis.14 We are unlikely to have conclusive data until these methodological concerns are resolved.

The American Diabetes Association (ADA) and the American Dietetic Association recommend that healthy people at low risk for nutritional deficiencies meet their nutritional requirements with natural food sources. These organizations do not generally support the use of micronutrient supplements for people with diabetes, and the supplements they do recommend are the same as those recommended for the general public. The ADA does note that people who are at increased risk for micronutrient deficiencies, such as those following very-low-calorie diets, the elderly, strict vegetarians, and other special populations, may benefit from multivitamin supplements.2,3

Current nutritional guidelines are based on Dietary Reference Intakes (DRIs). DRIs, established in 1998, expand on the previously used Recommended Dietary Allowances (RDAs). DRIs are composed of four values: the RDA, the Adequate Intake (AI), the Estimated Average Require-ment (EAR), and the Tolerable Upper Intake Level (UL).

The RDA is the level of nutrient intake believed to meet the needs of nearly all healthy individuals. It is most appropriately used as a target intake goal. However, intakes that fall below the RDA are not necessarily deficient because the RDA, by definition, is significantly greater than the needs of many people. The AI is used in place of the RDA for nutrients for which we do not yet have sufficient scientific evidence to establish an RDA.

The EAR is the level of nutrient intake believed to meet the requirements of half of the healthy individuals in a given life stage or gender group. It is most appropriately used to assess the likelihood of a nutritional deficiency. Diets that fall below the EAR for a given nutrient have a ≥50% chance of being inadequate. Supporting clinical and biochemical evidence is needed to establish the presence of an actual deficiency.

The UL is the greatest level of nutrient intake for which no adverse side effects have been noted. It is based on the members of a healthy population who are most likely to experience toxicity. The UL is usually based on total daily nutrient intake from both food and supplements. It is most appropriately used to assess the level of chronic daily nutrient intake that is likely to cause significant negative side effects. (For more information on DRIs, visit the National Institutes of Health Office of Dietary Supplements Website: http://odp.od.nih.gov/ods. Full text of all the DRI documents can be accessed without charge from the National Academy Press Website: www.nap.edu.)

Vitamin and mineral supplements are regulated by the Food and Drug Administration under the 1994 Dietary Supplement Health and Education Act (DSHEA). This act provides for only minimal regulatory oversight of supplement manufacturing and processing, focusing instead on the labeling and marketing of these products.



The trace element trivalent chromium (Cr+3) is required for the maintenance of normal glucose metabolism. Experimental chromium deficiency leads to impaired glucose tolerance, which improves upon the addition of chromium to the diet.5Because there is no accurate biochemical indicator of chromium status, the determination of clinical chromium deficiency is difficult.2,5 Effects of chromium on glycemic control, dyslipidemia, weight loss, body composition, and bone density have all been studied.4,5

The current AI for chromium is 25 μg for women and 35 μg for men. No UL has been established. Previous recommendations placed a daily intake of ≤200 μg/day within a safe and adequate range. Usual dietary intakes in the United States are estimated to range between 20 and 30 μg/day.5

There is no evidence that people with diabetes have increased rates of deficiency, although several risk factors for micronutrient deficiencies are common in people with diabetes. These include hyperglycemia and glycosuria, low-calorie diets, and increased age. Other factors that may increase chromium requirements include pregnancy, lactation, stress, infection, physical trauma, and chronic vigorous exercise.4,5 Because chromium is a nutrient, supplements will only benefit individuals who have a deficiency.

Mechanism of action.

Chromium appears to act by enhancing or potentiating insulin’s actions.6 No chromium-containing enzyme has been discovered, and the biologically active form of chromium is still uncertain. Chromium’s actions have been attributed to an increase in the number of insulin receptors,5 increased binding of insulin to the insulin receptor, and increased activation of the insulin receptor in the presence of insulin.6 In vitro studies using organic forms of chromium have documented altered activity of phosphotyrosine phosphatase and phosphotyrosine kinase.5,6

Evidence-based research.

Numerous researchers have investigated the effects of chromium supplements on glycemic control in type 2 diabetes,713 type 1 diabetes,8 gestational diabetes,14insulin resistance,15 reactive hypoglycemia,16 the elderly,17 and steroid-induced diabetes.18 Chromium has also been shown to improve various aspects of dyslipidemia in diabetic subjects.7,9,10 There are few well-controlled, well-designed studies.

The most definitive support for chromium supplementation in type 2 diabetes was provided by a 1997 randomized, double-blind, placebo-controlled study conducted in China by Anderson et al.7 One hundred and eighty subjects were randomized to placebo, 200 μg/chromium picolinate/day, or 1,000 μg chromium picolinate/day for 4 months. HbA1c significantly declined in both groups at 4 months compared to placebo (P <0.05) (placebo 8.5%, 200 μg 7.5%, 1,000 μg 6.6%). Fasting blood glucose (FBG) levels, 2-h oral glucose tolerance test, and insulin and cholesterol levels all decreased in the high-dose-supplement group at 4 months.

The dose-dependent response and clinically significant decreases in HbA1c(decreases are similar in magnitude to those seen with many oral hypoglycemic agents) seen in this study are encouraging, although questions remain about its applicability in the United States, where ethnicity, dietary chromium intakes, and average body mass index of people with diabetes differ from those of the Chinese subjects.

Overall, the results of research studies are mixed,5 with some showing positive effects7,8,1014 and others having clearly negative or ambiguous results.9,10,16,18 Studies using higher doses7,11,12 and more bioavailable forms of chromium7,8,1113 have had more positive effects than those using other forms of chromium.10,16,18 Studies in which subjects were possibly consuming low-chromium diets or had other risk factors for deficiency were also more likely to show positive effects.7,11,13,14

Research on chromium is summarized in Table 1. When evaluating these studies, one must pay particular attention to the form and dose of chromium used; the etiology of diabetes in the population studied; subjects’ duration of diabetes, ethnicity, and weight; study duration; subjects’ relative glycemic control; statistical and clinical relevance of the data; and the study design (with randomized, double-blind, placebo-controlled studies that control for dietary intake preferred). Emphasis should be placed on studies conducted after 1980, when methodological limitations in measuring chromium were resolved.

Side effects and contraindications.

The toxicity of dietary chromium (Cr+3) is believed to be low in comparison to other trace elements.2 (Hexavalent chromium [+6], a known human carcinogen, is not present in the food supply in significant quantities.) The Environmental Protection Agency sets toxicity rates at intakes >1 mg/kg body weight/day.5

Cell culture studies have suggested that high doses of chromium picolinate may cause increased rates of chromosomal damage.19 It is not certain whether chromium or picolinate were responsible for these effects, which have not been seen in in vivo human or animal studies.

There are case reports of renal and hepatic toxicity, rhabdomylosis, psychiatric disturbances, and hypoglycemia with large doses of chromium.20 In many, chromium has not been unequivocally established as the sole etiological agent.

High doses of chromium have been shown to decrease zinc absorption and may compete with iron for transport on transferrin.4,19 Vitamin C and aspirin may increase chromium absorption, but in cell culture studies, vitamin C enhanced chromium’s genotoxic effects.19

Clinical application.

Accurate biochemical indices of chromium status are not available, so assessment of status and responsiveness to supplementation can only be established by a supplement trial. Positive effects should be seen within 6–12 weeks of supplementation.5 If clear evidence of benefit is not established, supplementation should be discontinued because chronic use of chromium may increase the risk for as-yet-unidentified toxicities.

Supplements of up to 200 μg are unlikely to be harmful, but the safety of higher doses, which have been shown to be more effective, is less certain. Chromium picolinate and chromium nicotinate appear to have increased bioactivity when compared to inorganic forms of chromium, such as chromium chloride. The ADA does not recommend chromium supplementation for people with diabetes.21

The prevalence of chromium deficiency is unknown, but consuming good sources of chromium, such as whole grains, cheese, dried beans, nuts/seeds, mushrooms, beef, wheat germ, and broccoli, will increase the likelihood of meeting nutritional recommendations.4 Adequate blood glucose control and decreased intake of simple sugars may reduce urinary chromium loss.4,5

Because chromium appears to increase the activity of the insulin receptor, it is logical to expect that adequate levels of insulin must also be present. Patients using chromium supplements should be cautioned about the potential for hypoglycemia, and monitoring renal function is prudent.


The trace element vanadium has not been established as an essential nutrient, and human deficiency has not been documented.4,22 Vanadium exists in several valence states, with vanadate (+4) and vanadyl (+5) forms most common in biological systems. Vanadyl sulfate and sodium metavanadate are the most common supplemental forms, but other organic vanadium compounds have been developed.

In animal models, vanadium has been shown to facilitate glucose uptake and metabolism, facilitate lipid and amino acid metabolism, improve thyroid function, enhance insulin sensitivity, and negatively affect bone and tooth development in high doses.23,24 In humans, pharmacological doses alter lipid and glucose metabolism by enhancing glucose oxidation, glycogen synthesis, and hepatic glucose output.23,24 Vanadium acts primarily as an insulinmimetic agent, although enhanced insulin activity and increased insulin sensitivity have also been noted.23,24 More recent research suggests that insulin may be required for its effects.24

Vanadium is ubiquitous in the environment but is present in extremely small quantities. This makes it difficult to accurately measure status or to induce deficiencies.4,22 There are no accurate assays for clinical settings.22 There is also no RDA. The usual U.S. diet is estimated to provide 10–60 μg/day.22

Vanadium is stored primarily in bone and transported in the bloodstream on transferrin.22 It is cleared primarily through the kidney.22

Mechanism of action.

Vanadium’s chemical structure is similar to that of phosphorus, which appears to influence its biochemical actions. It may act as a phosphate analog and has been shown to alter the rate of activity of a number of adenosine triphosphatases, phosphatases, and phosphotransferases.23

Vanadium appears to affect several points in the insulin signaling pathway and may lead to upregulation of the insulin receptor and subsequent intracellular signaling pathways.23,24 Suggested effects include insulin receptor autophosphorylation, increased protein tyrosine and serine threonine kinase activity, inhibition of phosphotyrosine phosphatase activity, increased adenylate cyclase activity, altered glucose-6-phosphatase activity, inhibition of hepatic gluconeogenesis, and increased glycogen synthesis.23,24

Evidence-based research.

Several small trials2528 have evaluated the use of oral vanadium supplements in diabetes. Most focused on type 2 diabetes,2528 although animal studies suggest that vanadium also has potential benefit in type 1 diabetes.23

In subjects with type 2 diabetes, vanadium increased insulin sensitivity as assessed by euglycemic, hyperinsulinemic clamp studies in some,2527 but not all,28 trials. Glucose oxidation and glycogen synthesis were increased, and hepatic glucose output was suppressed in two studies.26,27

In type 1 diabetes, vanadium did not affect insulin sensitivity, although daily insulin doses declined.25 Supplementation decreased FBG,2628 HbA1c,26,27 and cholesterol levels25 and stimulated kinase activity.25

Pharmacological doses appear to have a mild effect on insulin sensitivity and glucose utilization in type 2 diabetes. Effects in animal models are stronger than in humans, and there is no information on the long-term effects in diabetes.

Research on vanadium is summarized in Table 2. When evaluating these studies, one should pay particular attention to the form of vanadium utilized, specific animal model of diabetes used or type of diabetes in humans, doses, physiological relevance of the results, length of study, and the impact on food intake and weight caused by the anorexiant effects of vanadium. It is also important to look at study design, controls, washout period, and assay methods, especially in vitro phosphorylation assays, which are notoriously difficult to conduct well.

Side effects and contraindications.

Because it is needed in such small quantities (in animals 50–500 ppb supports growth) and body stores are so low (100 μg), relatively small doses of supplemental vanadium are potentially toxic.22 Patients using oral supplements most commonly report nausea, vomiting, cramping, flatulence, and diarrhea.2528 These effects are transient and improve with a decrease in dose.

Longer-term use has been associated with anorexia, decreased food and fluid intake, and weight loss. Animal studies indicate that long-term, high-dose supplementation (>10 mg/day of elemental vanadium) can be toxic, with neurological, hematological, nephrotoxic, hepatotoxic, and reproductive and developmental effects.4,22

Vanadium may enhance the activity of digoxin and anticoagulant medications.20Excessive intakes may result in a green discoloration of the tongue.4 Limiting daily intake to <100 μg/day has been recommended.22

Clinical application.

There is insufficient information on the long-term effects of pharmacological doses of vanadium to recommend its use in diabetes. Chronic intake of relatively small doses could have significant adverse effects.

Researchers are working to develop forms of vanadium that are better absorbed and have fewer side effects. Good dietary sources include black pepper, dill, parsley, mushrooms, spinach, oysters, shellfish, cereals, fish, and wine.4


Niacin (vitamin B3) occurs in two forms: nicotinic acid and nicotinamide. The active coenzyme forms (nicotinamide adenine dinucleotide [NAD] and NAD phosphate) are essential for the function of hundreds of enzymes and normal carbohydrate, lipid, and protein metabolism.2,4

As a vitamin, the two compounds function similarly, but in pharmacological doses they have distinct effects. Nicotinic acid (1–3 g/day) is an effective treatment for dyslipidemia,4 although its use in people with diabetes has been limited because of its negative effect on glycemic control. Pharmacological doses of nicotinamide are being studied for their potential benefit in the prevention2932 and treatment3337 of diabetes.

The DRIs for niacin are reported in niacin equivalents (NE) because niacin can be synthesized by the body from tryptophan. The RDA is 14 mg NE for women and 16 mg NE for men. The UL is 35 mg NE/day for adults. Niacin deficiency (pellagra) is not common in the United States.

Mechanism of action.

Animal studies suggest that nicotinamide acts by protecting pancreatic β-cells from autoimmune destruction by maintaining intracellular NAD levels and inhibiting the enzyme poly (ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair. Excessive PARP induction results in depletion of cytoplasmic NAD levels, induction of immunoregulatory genes, and cellular apoptosis (programmed cell death). Nicotinamide may additionally act as a weak antioxidant of nitric oxide radicals.38,39

Evidence-based research.

The effects of nicotinamide supplementation have been studied in several trials focusing on the development2932 and progression3436 of type 1 diabetes; a meta-analysis;33 and one small trial in type 2 diabetes.37 Results have been mixed, and the largest clinical trial, the European Nicotinamide Diabetes Intervention Trial (ENDIT), is not yet complete.32

Nicotinamide appears to be most effective in newly diagnosed diabetes and in subjects with positive islet cell antibodies but not diabetes. People who develop type 1 diabetes after puberty appear to be more responsive to nicotinamide treatment.3336 Study results have offered more support for the idea that nicotinamide helps to preserve β-cell function33 than for its possible role in diabetes prevention.30

Research on nicotinamide is summarized in Table 3. When evaluating these studies, one should pay particular attention to subjects’ age of diabetes onset, duration of diabetes, and form of diabetes; the dose and form of nicotinamide used; the clinical significance of effects; and effects on growth in pediatric populations.

Side effects and contraindications.

Nicotinamide is a water-soluble vitamin and thus is not stored in the body.2 It is relatively safe with few significant side effects.39 Adverse effects have included skin reactions (flushing), abnormal prothrombin times, hepatotoxicity, nausea, vomiting, diarrhea, headache, dizziness, blurry vision, heartburn, sore mouth, and fatigue.1,4,20

Nicotinamide interacts with some anticonvulsants by increasing serum concentrations.20 Its use is contraindicated in active liver disease and may worsen gallbladder disease, gout, peptic ulcer disease, and allergies.20 In animal models, high doses have caused growth retardation, but this has not been seen in human studies.39 One trial noted decreases in first-phase insulin release30 with nicotinamide supplementation, and a second trial noted decreased insulin sensitivity.29

Clinical application.

Nicotinamide may help to preserve residual β-cell function in people with type 1 or type 2 diabetes, but it does not lead to clinically significant improvements in metabolic control. Typical doses are 25–50 mg/kg/day. Of concern are potential negative effects on insulin release, insulin sensitivity, and growth.

Any role that nicotinamide may have in prevention of type 1 diabetes should be elucidated at the conclusion of the ENDIT study sometime after 2003.39 Until then, the efficacy and safety of long-term, high-dose nicotinamide supplementation are unclear. Monitoring liver enzymes and platelet function is prudent if using high-dose nicotinamide supplements. Good dietary sources of niacin include fortified grains, some cereals, meats, fish, and dried beans.4


The mineral magnesium functions as an essential cofactor for more than 300 enzymes. It is essential for all energy-dependent transport systems, glycolysis, oxidative energy metabolism, biosynthetic reactions, normal bone metabolism, neuromuscular activity, electrolyte balance, and cell membrane stabilization.40The kidney primarily regulates magnesium homeostasis.

Magnesium deficiency has been associated with hypertension, insulin resistance, glucose intolerance, dyslipidemia, increased platelet aggregation, cardiovascular disease, complications of diabetes, and complications of pregnancy.2,3,40,41Whether poor magnesium status plays a causal role in these disorders or is simply associated with them has not been determined.

Less than 0.3% of the body’s magnesium pool is found in serum, and extracellular magnesium levels do not reflect functionally important body pools. This makes assessment of magnesium status difficult.2,40,41 Serum magnesium is a specific, but not sensitive, indicator of magnesium deficiency; low serum magnesium levels indicate low magnesium stores, but a deficiency must be severe before serum levels decline. More sensitive assays are being developed.2,40,41

Magnesium is one of the more common micronutrient deficiencies in diabetes.2,3,40,41 Decreased magnesium levels and increased urinary magnesium losses have been documented in both type 1 and type 2 diabetic patients.2,4045Low dietary magnesium intake has been associated with increased incidence of type 2 diabetes in some,46 but not all,47 studies.

Hypomagnesemia in diabetes is most likely due to increased urinary losses.40,41Additional risk factors include ketoacidosis, use of certain medications including digitalis and diuretics, malabsorption syndromes, congestive heart failure, myocardial infarction (MI), electrolyte disturbances, acute critical illness, alcohol abuse, and pregnancy.40,41 Low-calorie and poor-quality diets are more likely to be inadequate in magnesium. People with diabetes may have diets low in magnesium.48 Hypermagnesemia may occur with renal insufficiency that impairs magnesium clearance.40,41

The RDA is 400 mg/day for men under age 30, 420 mg/day for men over age 30, 310 mg/day for women under 30, and 320 mg/day for women over age 30. The UL is 350 mg/day as supplemental magnesium. Daily intake from food and water is not included in the UL.

Mechanism of action.

The mechanisms by which magnesium affects insulin resistance, hypertension, and cardiovascular disease are unknown. However, the widespread use of magnesium in normal metabolism of macronutrients, cellular transport systems, intracellular signaling systems, platelet aggregation, vascular smooth muscle tone and contractility, electrolyte homeostasis, and phosphorylation and dephosphorylation reactions1 suggests that these effects are multifactorial.

Evidence-based research.

Research has focused on the following areas:

  • Glycemic control. An inverse relationship between plasma magnesium levels and indices of glycemic control has been noted in both type 1 and type 2 diabetes.42,43 Clinical studies evaluating the effect of supplemental magnesium on glycemic control are mixed, with some studies reporting improvements44,49 and others showing no improvement.45,50,51

  • Insulin sensitivity. Diets low in magnesium are associated with increased insulin levels,52 and clinical magnesium deficiency is strongly associated with insulin resistance.40,41 It is not known if low magnesium levels play a role in the development of insulin resistance, are a result of insulin resistance, or are simply a coexisting condition. In vitro evidence suggests that insulin plays a role in magnesium transport, and insulin resistance has been shown to decrease magnesium uptake in type 2 diabetes.40 Conversely, magnesium supplementation has a mild positive effect on insulin sensitivity.40,49,53 Animal models show decreased insulin receptor tyrosine kinase activity and decreased glucose uptake and oxidation in magnesium deficiency.40 Supplement-ation trials have primarily focused on type 2 diabetes.

  • Hypertension. Observational studies indicate an inverse relationship between magnesium levels and hypertension in people with and without diabetes. Clinical trials have produced inconsistent results.54

  • Cardiovascular disease. Magnesium deficiency is associated with dyslipidemias, atherosclerosis, acute MI, and cardiovascular disease (CVD)41,55 and has been shown to alter platelet aggregation and activity.3,40,41,55 Most trials in type 2 diabetes have shown little effect of supplementation on lipid levels,45,50,51 although improvement in the magnesium status of subjects with type 1 diabetes was associated with mild improvements in triglycerides.55

  • Complications. Some,47 but not all,56 research suggests that subjects with common microvascular complications of diabetes have lower serum magnesium levels than subjects without complications. Patients with retinopathy have been found to have lower magnesium levels than control subjects or diabetic subjects without retinopathy.40 Intracellular magnesium levels were lower in patients with neuropathy.44 In type 2 diabetic subjects, micro- and macroalbuminuria were associated with lower serum ionized magnesium levels than was normoalbuminuria.57

Research on magnesium is summarized in Table 4. When evaluating these studies, one should pay particular attention to the characteristics of the population studied; the etiology of diabetes; the presence of obesity; subjects’ age, renal function, diet composition, oral hypoglycemic or insulin use, and degree of glycemic control; the dose and form of magnesium, subjects’ baseline magnesium status and response to supplementation; assessment methods; length of trial; and the study design and ability to identify causality.

Side effects and contraindications.

Magnesium is relatively nontoxic in people with normal renal function. Chronic supplementation and use of magnesium-containing medications such as laxatives and antacids can lead to hypermagnesemia in people with impaired renal function, defined as creatinine clearance <30 ml/min.40 Hypermagnesemia can result in hypotension, headaches, nausea, altered cardiac function, central nervous system disorders, and death.1,4

Clinical application.

The ADA recommends assessment of magnesium status in patients at risk for deficiency and supplementation for documented deficiencies.41

Oral supplements are available in numerous forms, but some research suggests that magnesium citrate is more bioavailable.4 Supplements up to the UL of 350 mg/day are appropriate; intakes >500 mg/day of elemental magnesium may cause diarrhea.4

Effects of supplementation on indices of magnesium status are mixed,40,41 but some research suggests that relatively high doses of magnesium for 1–3 months followed by lower daily supplements are needed to restore and maintain magnesium in people with diabetes.44,45

In patients with renal insufficiency, supplementation must be monitored closely. Adequate dietary intakes and good glycemic control should be encouraged to prevent deficiency. Good dietary sources include whole grains, leafy green vegetables, legumes, nuts, and fish.4 Diets high in saturated fat, fructose, caffeine, and alcohol may increase magnesium needs.1,4,40

Vitamin E

This essential fat-soluble vitamin functions primarily as an antioxidant.1 Free radical damage is believed to play a role in many diseases, such as CVD and cancer, as well as in normal cellular aging. Antioxidants have been proposed as preventive and treatment agents for these conditions.4

Low levels of vitamin E are associated with increased incidence of diabetes,58 and some research suggests that people with diabetes have decreased levels of antioxidants.59 People with diabetes may also have greater antioxidant requirements because of increased free radical production with hyperglycemia.60,61

Increased levels of oxidative stress markers have been documented in people with diabetes.62,63 Improvement in glycemic control decreases markers of oxidative stress,60 as does vitamin E supplementation.60,64,65

Clinical trials involving people with diabetes have investigated the effect of vitamin E on diabetes prevention,66 insulin sensitivity,67,68 glycemic control,6971 protein glycation,72 microvascular complications of diabetes,73,74and cardiovascular disease and its risk factors.64,65,75,76

Vitamin E refers to a group of compounds that includes tocopherols and tocotrienols. Alpha-tocopherol is the most abundant and biologically active.4Usual dietary intakes are estimated at 7–11 mg/day.4 The RDA for alpha-tocopherol is 15 mg/day for people 15 years of age and older. The UL for alpha-tocopherol is 1,000 mg/day from supplemental sources. Natural vitamin E (d-alpha tocopherol) has approximately twice the bioactivity of synthetic forms of the vitamin (dl-alpha tocopherol).4

Mechanism of action.

Vitamin E is a potent lipophilic antioxidant. It acts to neutralize free radical species produced during normal cellular metabolism, protecting cellular membranes and lipoproteins—LDL in particular—from oxidative damage. It also interacts with water-soluble antioxidants such as glutathione.1,4 It may play a role in preventing and treating common complications of diabetes, such as CVD, nephropathy, and neuropathy, by decreasing protein glycation, lipid oxidation, and inhibition of platelet adhesion and aggregation.64,65,7274,76

Evidence-based research.

Studies have focused on the following areas:

  • CVD. People with diabetes are at increased risk for CVD.64,65 Dietary vitamin E has been associated with decreased incidence of CVD,77,78and in subjects without diabetes, supplementation has improved cardiovascular outcomes in some,79 but not all, studies. A large recent intervention trial including 3,577 people with diabetes found no beneficial effect on cardiovascular outcomes with 400 IU of natural vitamin E/day for 4.5 years.75

    The effects of supplementation on CVD risk factors in diabetes are mixed.96 Positive effects on lipid levels or lipid oxidation have been noted in some,64,70,71 but not other,69 studies. Improvements have been noted in cell adhesion,65 platelet aggregation,65 monocyte proatherogenic activity,65 and endothelial function.76 Vitamin E has improved LDL oxidation, but positive effects may be greater for buoyant LDL than for the highly atherogenic dense LDL.64

  • Microvascular complications. Limited research suggests that vitamin E may be beneficial in preventing or treating microvascular complications of diabetes.73,74

  • Insulin resistance and glycemic control. Some studies have documented improvements in glycemic control67,7072 and insulin resistance67 with vitamin E supplementation, whereas others have noted no effect64,69 or negative effects.68

Research on vitamin E is summarized in Table 5. When evaluating these studies, one should pay particular attention to the population studied, presence of preexisting CVD, type of diabetes, form and dose of vitamin E, duration of supplementation, level of glycemic control, use of a pre-study run-in period, levels of antioxidant body pools, degree of incorporation into lipoproteins, degree of protection from oxidation conferred, assay method for oxidative markers, effects on mortality, presence of smoking or alcohol use, and supplement use and usual diets of subjects.

Side effects and contraindications.

Vitamin E is relatively nontoxic.5 Most long-term trials have found no negative side effects with supplementation.4,7980

Vitamin E has been shown to have anticoagulant properties, and patients using medications and herbal supplements known to decrease blood clotting, such as warfarin, aspirin, gingko biloba, garlic, and ginseng, may be at increased risk for bleeding with high-dose supplements.20 Doses of vitamin E up to 400 IU are believed to be safe.1 Doses >800 IU may alter blood clotting, although trials that have monitored prothrombin times have noted no increases.4

Vitamin E has been associated with increased risk of hemorrhagic stroke (and decreased incidence of ischemic stroke) in smokers.4 In vitro assays suggest that vitamin E can have some pro-oxidant activity, but this has not been shown in in vivo studies.4

Clinical application.

Good sources of vitamin E are primarily higher-fat foods, such as vegetable oils, margarines, wheat germ, seeds, and nuts.2 Adequate intakes for antioxidant activity may be difficult to achieve for those following low-fat diets.

Supplements containing natural (d-alpha tocopherol) vitamin E are more bioavailable. Doses may need to be increased as much as two times that of natural vitamin E if the synthetic form of the vitamin (dl-alpha-tocopherol) is used.4

Patients using medications such as orlistat, which decrease vitamin E absorption, may require vitamin E supplements. The ADA does not recommend regular supplementation of vitamin E in people with diabetes.21

B Vitamins Involved in Homocysteine Metabolism

Hyperhomocysteinemia (Hhcys) is positively correlated with coronary heart disease, cerebrovascular disease, and peripheral vascular disease.81 It has not been determined whether the presence of Hhcys precedes or follows vascular diseases.

A recent prospective, population-based study found that Hhcys is a risk factor for overall mortality in type 2 diabetic patients independent of other known risk factors. Hhcys was a twofold stronger risk factor for death in diabetic patients as compared to nondiabetic patients. For each 5 μmol/l increment of homocysteine, risk of mortality rose by 17% in nondiabetic and 60% in diabetic subjects.82

Adequate levels of the vitamins pyridoxine (vitamin B6), cobalamin (vitamin B12), and folate are necessary for normal homocysteine metabolism.1 Folate refers to a family of naturally occurring compounds. Folic acid is the synthetic form of the vitamin. Folate is an essential coenzyme for reactions involving the transfer of one-carbon-units in amino acid and nucleic acid synthesis.1,4

The RDA for folate is 400 μg/day folate equivalents for adults and 600 μg per day in pregnancy. The UL is 1,000 μg/day of folic acid from supplements and does not include dietary sources. Folate is widely available in the food supply but as much as 50–95% of it may be destroyed by processing.1 Folic acid is the preferred supplemental form.

Conditions that increase the risk of folate deficiency include pregnancy and lactation; alcoholism; anorexia; older age; chronic use of medications such as anticonvulsants, antiproliferative drugs, and oral contraceptives; malabsorption disorders; and gastrointestinal surgery.1,4

The biguanide metformin may reduce folate and vitamin B12 absorption and increase homocysteine levels.83,84 The clinical significance of this effect is unknown. Folic acid supplements in patients using metformin decreased homocysteine levels,85 and calcium supplements improved serum B12 levels presumably by reversing the negative effects of metformin on vitamin B12absorption.86

B12 has been used as a treatment for peripheral neuropathy in diabetes, but there is insufficient evidence to support this use. Many of the symptoms of B12deficiency are similar to those associated with aging and neuropathy (ataxia, memory changes).1 Thus, clinicians must be alert to the possibility of and specifically test for B12 deficiency in these populations. Risk of vitamin B12deficiency is increased with elderly age, achlorhydria, alcohol abuse, long-term gastric acid inhibitors, vegan diet, partial gastrectomy, celiac sprue, and autoimmune disorders including type 1 diabetes, AIDS/HIV, and thyroid disorders.1,4

The adult RDA for B12 is 2.4 μg/day. A UL has not been set, but daily doses up to 100 μg/day have not been associated with toxicity.4

Risk of B6 deficiency is increased with elderly age, alcoholism, high-protein intakes, liver disease, dialysis, and use of medications such as corticosteroids, penicillamine, anticonvulsants, and isoniazid.1,4 Poor glycemic control may also lead to increased urinary losses.

B6 acts as an essential cofactor for hundreds of enzymes and plays a role in glucose, lipid, and amino acid metabolism and neurotransmitter synthesis. The active coenzyme form of the vitamin, pyridoxal 5’phosphate, in muscle tissue is closely associated with glycogen phosphorylase.1 Deficiency of B6 in humans and animals is associated with glucose intolerance, but supplementation does not result in improved glycemic control.2 B6 is not an effective treatment for diabetic neuropathy.3 The RDA for B6 is 1.3 mg/day for adults up to the age 50.

The RDA increases to 1.5 mg/day for women and 1.7 mg/day for men over age 50. The UL for B6 is 100 mg/day for adults.

Mechanism of action.

The amino acid homocysteine can be metabolized through transulfuration or remethylation. In the remethylation pathway, methionine synthase converts homocysteine to methionine using folate as the methyl donor.1,81 B12 acts as an essential cofactor for this reaction. In the transulfuration pathway, homocysteine and serine combine to form cystathione. This reaction is catalyzed by cystathione B-synthase and requires B6 as a coenzyme.1,81

The mechanism by which increased homocysteine levels increase CVD risk has not been determined but is believed to result from pro-oxidant activity of the amino acid, endothelial dysfunction, and increased platelet activation.81

Evidence-based research.

This summary focuses on folate because it is the primary nutritional determinant of homocysteine levels. The prevelance of Hhcys may vary between 5 and 30% in the general population. Hhcys has been found in type 2 diabetes,87 and in some,88 but not all,89 studies of type 1 diabetes. Differences in renal filtration rates may explain some of the variable results seen in serum homocysteine levels in diabetes; hyperfiltration decreases homocysteine levels, and impaired filtration rates increase homocysteine levels.

Elevated plasma levels of homocysteine have been positively associated with CVD in some studies of people with diabetes.87,88 Hhcys is also associated with increased incidence of nephropathy, decreased renal function,87,88,90 and other microvascular complications of diabetes.88,90,91 Others have found no association between homocysteine levels and CVD,90,91 retinopathy,90 and indices of renal function92 or neuropathy.87

It has not been determined whether the presence of Hhcys precedes or follows the development of these conditions, although impairment of renal function clearly contributes to Hhcys. Elevated homocysteine levels in diabetes have also been associated with menopausal status, increased body mass index, smoking, and age.

In people without diabetes, there is an inverse correlation between serum folate and homocysteine levels, even in subjects with adequate nutrition.81 In diabetes, serum folate and homocysteine levels have been found to be inversely correlated in some,87,90 but not all,89 studies. Serum B12 levels90 are also inversely correlated with homocysteine levels, and serum pyridoxal 5’phosphate (B6) is inversely correlated with post-methionine-load homocysteine levels.

In patients with diabetes and Hhcys, increased folate intake decreases and in some cases normalizes serum homocysteine levels85,93 A meta-analysis found that treatment with 0.5–5 mg/day of folic acid lowers homocysteine levels by 15–40% within 6 weeks.94 Others have estimated that decreasing homocysteine levels by 5 μmol/l may reduce cardiovascular death by 10%.95 It is not known if supplementation is effective in prevention or treatment of micro- and macrovascular complications associated with Hhcys.

When evaluating research in this area, one should pay particular attention to the folate, B12, and B6 status of subjects; dose and form of folate used; effects of supplementation on folate and homocysteine levels; subjects’ age, type of diabetes, use of biguanides, duration of diabetes, menopausal status, weight, and glycemic control; presence of impaired renal function or hyperfiltration; and length of supplementation, with more than 4 weeks and possibly up to 3 months necessary for full effects. The impact of ethnicity and methylenetetrahydrofolate reductase (MTHFR) gene mutation incidence could also affect results. (MTHFR is an enzyme essential for the metabolism of folate and is important in the metabolism of homocysteine. A common mutation in the MTHFR gene is associated with Hhcys in homozygous subjects.)

Side effects and contraindications.

Doses of folate ≤15 mg/day have not been associated with adverse effects in healthy adults.4 However, folate supplementation may mask the anemia associated with B12 deficiency and result in permanent nerve damage.1 High-dose folate supplements may also interfere with anticonvulsant medications.1 High-dose B6 supplements are not recommended as a treatment for neuropathy; in fact, toxicity symptoms include neuropathy.2

Clinical application.

Long-term trials are needed to determine the effects of folic acid on micro- and macrovascular complications, both early and late in the disease process. Early research suggests that folate supplements decrease Hhcys levels and may be beneficial in the prevention and management of vascular complications in diabetes. Folic acid supplements are recommended for all women of childbearing age.

The primary risk of supplementation relates to the potential for undiagnosed B12deficiency. Since impaired B12 absorption is estimated to occur in 10–30% of people over the age of 50, assessment of B12 status in patients with peripheral neuropathy is prudent. In elderly people with achlorhydria, synthetic forms of oral B12 supplements are better absorbed than food-bound B12 and are therefore preferred. The use of biguanides may decrease folate and B12 absorption.

All patients with diabetes should be encouraged to consume adequate quantities of dietary folate, B12, and B6 and to modify factors such as alcohol intake and smoking, which increase homocysteine levels. All “enriched” cereal grain products (rice, flour, breakfast cereals, pasta, bread) in the United States have been fortified with folic acid since 1998. Good dietary sources of folate include fortified grain and cereal products, spinach, orange juice, strawberries, and peanuts.4 Good dietary sources of B12 are animal products, and good sources of B6 include whole grains, animal products, and legumes.4


As health care providers interested in promoting the optimal health of people with diabetes, we need to act as an unbiased resource on the numerous treatments available to our patients. We need to be open to new treatment regimens while also serving as careful watchdogs for ineffective or dangerous therapies. Above all, we need to encourage our patients’ involvement in and ownership of their diabetes, and help them to focus their efforts where they are likely to receive the greatest benefits. In the future, this will likely include nutritional supplements for people whom research has identified as having the genetic or clinical potential to benefit from them.


Celiac Disease and Type 1 Diabetes Symptoms, Links, and Cures



 Celiac disease is an autoimmune condition in which the body cannot tolerate certain proteins, specifically those contained in wheat, barley, and rye. These common cereal grains contain a certain gluten protein, which is why celiac disease is often called gluten intolerance. Individuals with celiac disease will have allergic reaction to gluten, manifesting itself in digestive discomfort, anemia, and other nutritional concerns. The only known remedy for people with celiac disease is to refrain from eating any food which contains glutens.

A gluten-free diet requires a whole lot of careful looking at nutrition information, ingredients, and package labels. A person with celiac disease must avoid all kinds of breads, bagels, muffins, cereals, crackers, pasta and even items like canned soups, salad dressings, gravy, season mixes, and deli meat, since these products may contain traces of wheat and/or other glutens.

Noticing the Link Between Celiac Disease and Type 1 Diabetes
Although the symptoms of celiac disease are somewhat different from the symptoms of type 1 diabetes, the two diseases are linked. Before scientists were researching the link between gluten intolerance and type 1 diabetes, it was simply observed that many people who had type 1 diabetes also had celiac disease. Approximately 1 out of every 250 people have celiac disease. The statistics for type 1 are lower; approximately 1 in every 500 individuals has diabetes. But when someone does have type 1 diabetes, their likelihood for having celiac disease skyrockets. In fact, 1 out of every 20 persons with type 1 diabetes also has celiac disease.

Finding the Link Between Celiac Disease and Type 1 Diabetes
After substantial research, scientists were able to isolate the link between celiac disease and type 1 diabetes. Both conditions are genetically related. Both conditions are diseases of the autoimmune system. Like diabetes, celiac disease has to do with the inability of the body’s immune system to absorb or utilize certain essential nutrients. For the person with celiac disease, the body’s immune system rejects gluten and attacks the lining of the small intestine once the small intestine is tainted with foods containing gluten. This is similar to the way that the immune system of someone with diabetes will reject the insulin-producing cells of the pancreas. It goes back to an individual’s genes. Celiac disease and type 1 diabetes share a susceptibility gene, namely HLA-DQB1.

What’s ahead?
Because many individuals with diabetes also have celiac disease, it forces them into a position to take extra measures to ensure their optimal health. Since the two diseases are linked, this can be an advantage. Celiac disease requires that individuals take precautions in their diet. The same level of dietary precautions are necessary for someone with type 1 diabetes. Gluten-free foods and a diet with less wheat is a healthier diet. Besides, a lower gluten diet will naturally help to keep blood sugar levels lower. The fact that the two diseases are linked may also suggest that the cure for both diseases are linked. As scientists race to find a cure for diabetes and celiac disease, they may just discover that the cure for one is the cure for the other.

By Daniel Threlfall


Factors affecting the Expression of Asthma

Factors Affecting the Expression of Asthma




Abstracts of Relevant Scientific Studies

"...The problem is that there is never going to be a perfect study. Questions always remain unanswered no matter how many references you cite. And there are so many opposing theories that it would be virtually impossible to counter every one of them. I realize that I would never come to my own conclusions about accelerated metabolic aging if I had focused on studies rather than true science..... " Diana Schwarzbein, 1999

Studies published in peer-reviewed journals are pieces of evidence, the currency of modern science. Not all are equal in significance and their value depends on many factors. Unfortunately, few studies show simple, direct relations of lifestyle to asthma and allergic conditions. Only rarely does a single study prove something which a subsequent study cannot refute. It takes a number of studies to constitute a body of evidence which can lead to general acceptance. From there, the trail to practical treatment is long and winding.

Studies included here pertain, directly or indirectly, to categories including breathing, diet, hydration, sleep, physical conditioning, emotional attitudes, stresses, and other basic aspects of life. Practical application of these studies depends on interpretation; and any lifestyle modification must be weighed against costs and risks.

The lay reader need not be intimidated. Even without complete understanding, much can be learned.

Welcome to the Soup Kettle! Dive in and have a look.


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MSM for Diabetes, Asthma, Candida, Parasites



Natural Health and Longevity Resource Center



Sulfur (MSM)


A Basic Essential Nutrient Needed Now, More than Ever Before

Methylsulfonylmethane is a relatively new dietary supplement form of sulfur that is found in our living tissues. MSM supports healthy connective tissues like tendons, ligaments, and muscle. Thus, it is important in conditions such as arthritis, muscle pains, bursitis, etc. MSM should be considered an integral part of any health care practice because of its physiological action, indirect importance, and current / future uses.

To understand MSM, some background information is necessary. MSM is a "naturally-occurring nutrient found in normal human diets" (1). It gets into the diet through the sulfur cycle. Ocean plankton release sulfur compounds which rise into the ozone where ultra-violet light makes MSM and DMSO. DMSO, dimethyl sulfoxide, is a precursor to MSM. MSM and DMSO return to the surface of the earth in rain (1). Plants concentrate MSM and return it to the earth and the sea. Evaporation into the air results in their return to the earth (1).

MSM has a unique action on body tissues. It decreases the pressure inside the cell. In removing fluids and toxins, sulfur affects the cell membrane. MSM is an organic form of sulfur, whereas sulfites in foodstuffs are inorganic. Sue Williams states "sulfur is present in all cells" and is in the form of "organic compounds throughout the body’ (2). However, sulfur can be found in the body in sulfate forms. It forms sulfate compounds with sodium, potassium, magnesium, and selenium. MSM has a significance, because sulfur compounds are found everywhere throughout the body and in nature.

Sulfur has an indirect importance, because sulfur compounds play a role in many body organs and systems. Sulfur is in the hair, skin, and nails. Many amino acids, the building blocks of protein, have sulfur as a component. Taurine is a sulfur-containing amino acid formed from methionine (2). Taurine stabilizes cell membranes (2). Methionine contains sulfur, detoxifies cells, and is involved in pain relief (2). Carnitine comes from methionine and transports long chain fatty acids preventing accumulations of lipoproteins (2). Many B-complex vitamins interact with or contain sulfur. Sulfur is needed for insulin production.

One current use of MSM is for joint problems, as sulfur is found in and near osseous structures. Sulfur supports healthy muscles, tendons, and ligaments. Arthritic conditions have responded to oral MSM. Some researchers note results from MSM when used for post-exercise muscle pain (1). MSM normalizes pressure inside cells and removes toxins. Oregon Health Sciences University has conducted arthritis studies with mice. The mice which received MSM had "no degeneration of articular cartilage" (1). The other non-MSM mice had cartilaginous degeneration. The university has used MSM on over 12,000 patents. Researchers make no claim about MSM as a supplement, but osteoarthritis, rheumatoid arthritis, muscle soreness and muscle pain respond to oral MSM.

One researcher claims MSM is about as safe as water. One should drink extra water with MSM use. There are other dietary factors to consider.

Avoiding nightshade plants has helped arthritis patients (tomatoes / potatoes / green pepper/eggplant). Biotin and vitamin C help the body assimilate MSM. Biotin and vitamin C are found in fresh fruits. Eating fresh fruits while taking MSM could be helpful.

In addition to arthritis, it may have other future uses. Dr. Stanley Jacob believes ,'most people are deficient' in sulfur (1). Insulin synthesis depends upon sulfur. Many vitamins require or contain sulfur. Some researchers claim it has many future uses such as in allergies (1).

A good MSM product is both safe and effective. The MSM source for MSM supplements is often lignin from pine trees. Lignin is a molecule in plants that is part of a plant's cell wall. Lignin oxidation in oak wine barrels results in the vanilla flavors of wines. The pine tree lignin is an ideal source for a good MSM product.

For those who do not want to take MSM as a supplement, food sources of sulfur are as follows: sunflower seeds, garlic, lentils, soybeans, and yogurt. Persons with kidney problems or recurrent kidney stones may not want to take MSM. Certain renal tubular defects can make a person susceptible to recurrent kidney stones (2). Other kidney defects include errors of metabolism in which processing of sulfur amino acids is altered (2). Such persons may wish to avoid MSM.

One thousand to three thousand milligrams per day is a typical dosage range, but some people take well above that amount. This author takes MSM alone.

From the cell walls of pine trees to the cells of the human body, a good MSM supplement can contribute to good health.


Conditions That Have Reportedly Responded to MSM Supplements
    • Acne
    • Allergies
    • Arthritis
    • Asthma
    • Candida Yeast Infections
    • Carpal Tunnel Syndrome
    • Chronic Fatigue
    • Constipation
    • Diabetes
    • Digestive Disorders
    • Fragile Hair & Nails
    • Migraine Headaches
    • Muscle Pain & Cramps
    • Parasites
    • Skin Damage & Aging
    • Toxic Build-up
    • Ulcers

A body made up of healthy, flexible cells will not only feel better, it will look better too. The body is continuously at work replacing old, worn out cells with new ones. The process goes on 24 hours a day, 7 days a week, without stop. When all the raw materials needed for cell-building are available, it is a very efficient process. When there are deficiencies, the new cells may be weak, rigid or deformed.

One of the most important raw materials for building healthy new cells is a form of organic sulfur known as methyl sulfonyl methane (MSM). This element is so essential to life that it is found in every cell of every plant and every animal. Sulfur makes up 0.25% of human body weight. However neither plants nor animals can use elemental sulfur directly. Sulfur is not easily available to living organisms in its inorganic form.

MSM is not a medicine, a drug, or a food additive. It is a food. MSM is an organic form of sulfur that can be easily absorbed and utilized by the body. Although DMSO and MSM are chemically similar, each is unique. MSM is a pure, stable, white crystalline powder without the unpleasant smell or taste of DMSO. (1-3) Also, MSM does not give you a strong body odor like DMSO.

Since sulfur is a component of all cells, it is essential that the body have a plentiful supply of this mineral in its usable form. There is a positive synergistic effect on building healthier cells when MSM is taken in combination with vitamin C. The new cells are more pliable and permeable, allowing fluids to pass through the tissue more easily. (1) Internally this means more efficient elimination of toxins, a reduction in inflammation and pain - so you feel better. On the outside it shows up as a softer, smoother complexion, stronger hair and nails - so you look better.

MSM for Relief of Pain and Inflammation

Approximately half of the total body sulfur is concentrated in the muscles, skin and bones. One of the most significant uses of MSM as a supplement is its demonstrated ability to relieve pain and inflammation. When rigid fibrous tissue cells swell and become inflamed, pressure and pain result. Since MSM can restore flexibility and permeability to cell walls, fluids can pass through the tissues more easily. This helps equalize pressure and reduce or eliminate the cause of pain. Harmful substances such as lactic acid and toxins are allowed to flow out, while nutrients are permitted to flow in. This prevents the pressure buildup in cells that causes inflammation. (1)

MSM has shown a remarkable ability to reduce or eliminate muscle soreness and cramps both in geriatric patients and in athletes. It's even given to race horses before a race to prevent muscle soreness, and afterward to reduce the risk of cramping. People with arthritis report substantial and long-lasting relief with MSM supplements. Taken along with glucosamine, a key substance in the process of rebuilding cartilage, MSM can relieve pain and help repair worn or damaged cartilage in joints, ligaments and tendons with healthy, flexible new cells. (1)

How Does MSM Work?

MSM makes cell walls permeable, allowing water and nutrients to freely flow into cells and allowing wastes and toxins to properly flow out.   The body uses MSM along with Vitamin C to create new, healthy cells, and MSM provides the flexible bond between the cells. Without proper levels of MSM, our bodies are unable to build good healthy cells, and this leads to problems such as lost flexibility, scar tissue, wrinkles, varicose veins, hardened arteries, damaged lung tissues, dry cracking skin, digestive disorders, joint problems, and inability to defend against allergic reactions to food, animals and plants.

MSM is an anti-oxidant that helps to clean the blood stream and flush toxins trapped in our cells.  It is also a foreign protein and free radical scavenger.  In order to maintain good health, we need to supplement our diets with MSM, to enable the body to heal itself.   The body uses what it needs, and after 12 hours will flush out any excess amounts.

The Beauty Mineral for Hair, Skin and Nails

Sulfur has been called nature's "beauty mineral" because it is needed to keep the hair glossy and smooth and keeps the complexion clear and youthful. It is needed for synthesis of collagen and is prevalent in keratin, a tough protein substance necessary for health and maintenance of the skin, nails and hair.

MSM is responsible for the flexible disulfide bonds between cells, including those that make up the skin. It blocks undesirable chemical and physical cross-linking or bonding of collagen which is associated with tough, aging skin. Con consequently MSM enhances tissue pliability and encourages repair f damaged skin. If there is insufficient sulfur in the body when new cells are being manufactured, the new cells will be rigid. This rigidity can contribute to cracking, wrinkling and unsightly scar tissue. When sufficient sulfur is present for new cells, the skin is softer, smoother and more flexible. MSM provides that sulfur.

Acne, including the severe acne rosacea, responds favorably to MSM supplements. Adequate sulfur and vitamin C are also needed for healing. When the body is deficient in these nutrients, the new tissue will be elevated leaving an unattractive, raised scar. Because MSM makes the skin more permeable and pliant, it can also help prevent blistering and promote faster healing from sunburn or wind damage.

With MSM supplements, nails show not only an increase in growth rate, but also increased toughness and resistance to chipping and cracking. This effect has been seen both in human nails and horses hoofs.

Allergens, Toxins and Parasites

Flexible, permeable cells are also important in that they allow toxins, allergens and foreign substances to be flushed out of the body more easily . When skin cells are soft and permeable, many toxins can be eliminated through the sweat glands, which takes some of the load off the liver and kidneys. While MSM is not a cure for allergies, supplementation may reduce symptoms by allowing allergens to be removed from the body more quickly. Even reactions to insect bites, poison ivy and poison oak are less severe when the diet is supplemented with MSM. Vitamin C is also synergistic in this application in that it can lower histamine levels.

MSM has also shown amazing anti-parasitic action against Giardia, Trichomonas, roundworms, nematodes, Enterobius and other intestinal worms. When parasites attach themselves to the intestinal lining, they can live, reproduce and rob the body of nutrients indefinitely. MSM blocks parasites by competing for receptor sites on the mucous membrane. When parasites can not attach themselves, they are simply flushed out of the system.

The same is true with food allergens. MSM coats mucosal surfaces and occupies the binding sites that could otherwise be used by challenging food allergens. It can also bind with offending agents to produce harmless substances which are then excreted from the body. This facilitates normal digestion and assimilation and allows the body to get maximum nutritional value from foods that would otherwise cause a reaction. Individuals who experience an allergic response to certain foods have reported improved or complete tolerance to those foods when they take MSM supplements. Healthy flexible colon tissues along with improved digestion, can also relieve constipation.


Sulfur is also a component of insulin, the hormone that regulates carbohydrate metabolism and insufficient sulfur may result in decreased insulin production. It is also possible that a lack of bio-available sulfur would make the cells so rigid and impermeable that they become unable to absorb sugar from the blood efficiently, leaving blood sugar levels elevated. Studies indicate that regular MSM supplements which cause the cell to become permeable, could help balance blood sugar and allow the overworked pancreas to return to normal.

Why Supplement?

Since sulfur is present in every cell of every living thing, it might seem that we would get plenty of this essential mineral from dietary sources and should not need supplements, but that may not be the case. Meat, poultry, fish, eggs and dairy products are the main sources of dietary sulfur, but we have been advised to restrict or remove many of those foods from our diets. Vegetarians, especially those who do not eat eggs, are at particular risk for sulfur deficiency. Plants cells contain sulfur but not in abundant quantities and much of the MSM present in unprocessed foods is lost in washing, cooking or steaming. And, of course, MSM levels decline noticeably with age - doesn't everything? So, the older you get, the more important it becomes to maintain adequate sulfur levels in the body.

Usage and Toxicity

Due to its positive effects, particularly in maintaining healthy cell formation, 2,000 to 6,000 mg. of supplemental MSM daily is recommended. Of course, the optimum daily dosage of MSM depends largely on body size, age and the nature and severity of any deficiency symptoms you may be experiencing. Since vitamin C provides a positive synergistic it should be taken along with MSM.

MSM ranks in the "extremely low" toxicity category with a toxicity profile similar to that of water. When oral supplements are taken, the body will distribute MSM where it is needed. After about 12 hours, any excess amounts will be flushed out of the body. MSM, a member of the sulfur family, should never be confused with sulfa drugs to which some people are allergic.

  1. Total Health. 1998. "MSM". Feb/Mar, Vol., 20 No. 1. pp. 30-31.
  2. Williams, S. 1997. Nutrition & Diet Therapy (8th ed.). Academic Press, N.Y., N.Y.
  3. Thomas, C. 1993. Taber's Cyclopedic Medical Dictionary, (1 7th Ed.). F.A. Davis Company, Philadelphia, PA.
  4. Mindell, Earl L., The MSM Miracle - Enhance your health with organic sulfur, Keats Good Health Guide, Keats Publishing, Inc., New Canaan, CT, 1997
  5. Herschler, R. J., "Methylsulfonylmethane in Cosmetics", 1984, Cardinal Associates, Inc.
  6. Whitaker, J., "Try MSM for Relief from Muscular Pain", Health and Healing, Oct. 1997
  7. Kirschmann, J. D. and Dunne, L. J., Nutrition Almanac, Second Edition, McGraw-Hill, 1984
  8. Balch, J. F. and Balch P.A., Prescription for Nutritional Healing, Avery Publishing, Garden City Park, NY, 1990







Statements about products on this website have not been evaluated by the United States Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease. Nothing stated here should be considered as medical advice for dealing with a given problem. You should consult your health care professional for individual guidance for specific health problems. This page is for informational and educational purposes only, and is simply a collection of information in the public domain. Information conveyed herein is based on pharmacological and other records - both ancient and modern. No claims whatsoever can be made as to the specific benefits accruing from the use of any herb or nutrients.





Your rights and diabetes

Diabetes And Work


Questions and Answers About Diabetes in the Workplace and the Americans with Disabilities Act

Individuals with diabetes successfully perform all types of jobs from heading major corporations to protecting public safety. Yet, many employers still automatically exclude them from certain positions based on myths, fears, or stereotypes. For example, some employers wrongly assume that anyone with diabetes will be unable to perform a particular job (e.g., one that requiresdriving) or will need to use a lot of sick leave. The reality is that, because many individuals with diabetes work with few or no restrictions, their employers do not know that they have diabetes. Some employees, however, tell their employers that they have diabetes because they need a "reasonable accommodation" - a change or adjustment in the workplace to better manage and control their condition. Most of the accommodations requested by employees with diabetes, such as regular work schedules, meal breaks, a place to test their blood sugar levels, or a rest area, do not cost employers anything to provide.

The Americans with Disabilities Act and Amendments Act

The Americans with Disabilities Act of 1990 (ADA) is a federal law that prohibits discrimination against individuals with disabilities. Because of the disputed interpretations of this act on the part of courts, the Americans with Disabilities Act Amendments Act (ADAAA) was signed into law September 25, 2008, becoming effective Jan 1, 2009. (1) The ADAAA makes significant changes to the ADA's definition of "disability" that broadens the scope of coverage under both the ADA and Section 503 of the Rehabilitation Act.

Title I of the ADA covers employment by private employers with 15 or more employees as well as state and local government employers. The Rehabilitation Act provides similar protections related to federal employment. In addition, most states have their own laws prohibiting employment discrimination on the basis of disability. Some of these state laws may apply to smaller employers and provide protections in addition to those available under the ADA.

When is diabetes a disability under the ADA?

Diabetes is a disability when it substantially limits one or more of a person's major life activities. Major life activities are basic activities that an average person can perform with little or no difficulty. Under the amendments act, major life activities include, but are not limited to, caring for oneself, performing manual tasks, seeing, hearing, eating, sleeping, walking, standing, lifting, bending, speaking, breathing, learning, reading, concentrating, thinking, communicating, and working. Major life activities also include major bodily functions which include, but are not limited to, functions of the immune system, normal cell growth, digestive, bowel, bladder, neurological, brain, respiratory, circulatory, endocrine, and reproductive functions. (2)

Diabetes also is a disability when it causes side effects or complications that substantially limit a major life activity. Even if diabetes is not currently substantially limiting because it is controlled by dietexerciseoral medication, and/or insulin, and there are no serious side effects, the condition may be a disability because it was substantially limiting in the past (i.e., before it was diagnosed and adequately treated). 

Finally, diabetes is a disability when it does not significantly affect a person's everyday activities, but the employer treats the individual as if it does. For example, an employer may assume that a person is totally unable to work because he has diabetes. Under the ADA, the determination of whether an individual has a disability is made on a case-by-case basis.

1 - The U.S. Equal Employment Opportunity Commission. Notice Concerning the Americans with Disabilities Act (ADA) Amendments Act of 2008. http://www.eeoc.gov/ada/amendments_notice.html (accessed 05/09).

2 - United States Department of Labor. The ADA Amendments Act of 2008: Frequently Asked Questions. http://www.dol.gov/esa/ofccp/regs/compliance/faqs/ADAfaqs.htm#Q3 (accessed 05/09).

3 - U.S. Equal Employment Opportunity Commission. EEOC Fact Sheet: The Americans with Disabilities Act and Diabetes. http://www.eeoc.gov/ (accessed 04/08).

Reviewed by Francine Kaufman, MD. 4/08


Diabetics Confront a Tangle of Workplace Laws

Michael Temchine for The New York Times

A Complicated Process Stephen A. Bokat, general counsel for the United States Chamber of Commerce, says businesses are torn in complying with the Family and Medical Leave Act, balancing long-term leaves of absence with the short-term needs of diabetic employees.

Published: December 26, 2006

MINNEAPOLIS — John Steigauf spent more than a decade fiddling with the innards of those huge United Parcel Service trucks until an icy day two years ago when the company put him on leave from his mechanic’s job. A supervisor escorted him off the premises.

Costs of a Crisis

Business Implications

Articles in this series are exploring the widening impact of the Type 2 diabetes epidemic.


Go to Complete Coverage »
Jamie Rose for The New York Times

A Fight for Fairness Shereen Arent, the director of legal advocacy for the American Diabetes Association, says confusion about the disease itself is a big part of the problem: “It’s not all about ignorance, but if I can get rid of ignorance, I can get rid of a lot of discrimination.”

His work was good. He hadn’t socked the boss or embezzled money. It had to do with what was inside him:diabetes.

U.P.S. framed it as a safety issue: Mr. Steigauf’s blood sugar might suddenly plummet while he tested a truck, causing him to slam into someone.

Mr. Steigauf considered it discrimination, a taint that diabetes can carry. “I was regarded as a damaged piece of meat,” he said. “It was like, ‘You’re one of those, and we can’t have one of those.’ ”

With 21 million American diabetics, disputes like this have increasingly rippled through the workplace:

¶A mortgage loan officer in Oregon was denied permission to eat at her desk to stanch her sugar fluctuations, and eventually was fired.

¶A Sears lingerie saleswoman in Illinois with nerve damage in her leg quit after being told she could not cut through a stockroom to reach her department.

¶A worker at a candy company in Wisconsin was fired after asking where he could dispose of his insulin needles.

In each instance, diabetics contend that they are being blocked by their employers from the near-normal lives their doctors say are possible. But the companies say they are struggling, too, with confusion about whether diabetes is a legitimate disability and with concern about whether it is overly expensive, hazardous and disruptive to accommodate the illness.

The debate will probably intensify. The number of diabetics in America swelled by 80 percent in the past decade. Experts say the disease is on its way to becoming a conspicuous fact of life in the nation’s labor force, raising all sorts of issues for workers and managers.

Even an outspoken advocate for diabetics like Fran Carpentier, a Type 1 diabetic and a senior editor at Parade magazine, understands the implications for business. “Knowing what it’s like to live with the disease hour by hour, day by day, I wonder if I owned my own company if I would hire someone with diabetes,” she said. “I’m being bluntly honest. And it kills me to say this.”

Doctors, though, say that with improved medications and methods of self-testing blood sugar, most diabetics can do almost any job if they properly manage their illness. Yet myths about the disease persist, advocates say, leading many companies to shun diabetic employees.

“It’s not all about ignorance, but if I can get rid of ignorance, I can get rid of a lot of discrimination,” said Shereen Arent, the director of legal advocacy for the American Diabetes Association.

Part of the confusion is a byproduct of the disease itself, a capricious illness of elevated, damaging levels of sugar in the blood. Type 1 is a malfunction of the immune system that usually appears in childhood, while the far more prevalent Type 2 is closely associated with obesity and inactivity. Many people with diabetes will face withering complications like blindness, amputations and heart disease. Others will not.

For some, particularly insulin users prone to the abnormal drops in blood sugar known as hypoglycemia, the illness can cause dizziness, fainting or muddled judgment. Doctors, however, say those constitute a tiny number of readily identifiable cases.

Nonetheless, the risk of plunging blood sugars has fueled a longstanding reluctance to employ diabetics in jobs like those of truck driver or police officer, if they are on insulin. Until this summer, the National Fire Protection Association cautioned against making it too easy for even non-insulin-dependent diabetics to become firefighters. Now the association recommends an individual assessment.

Federal law bars diabetics from joining the armed services and prevents diabetics on insulin from becoming commercial pilots.

Innumerable diabetics, though, are engaged in more mundane jobs uninvolved in matters of life and death. For these people, secretaries and factory workers and programmers, a “reasonable accommodation,” like permission to eat at one’s desk or to be excused from fluctuating shifts, can make the difference in whether they can function.

When disputes can’t be resolved, the cases often land in court or before the Equal Employment Opportunity Commission. The commission, which enforces the Americans With Disabilities Act of 1990, says diabetes-related complaints have been on the rise, one of the few conditions generally showing an increase in complaints. Diabetes accounts for nearly 5 percent of the 15,000 annual allegations that the commission gets under that act, trailing only back impairment, other orthopedic injuries and depression.

for the complete story go to: http://www.nytimes.com/2006/12/26/health/26workplace.html?_r=1

Cancer and Diabetes can be cured

Cancer or diabetes, It can be cured!

Go to www.gersontherapy.org 

Gerson Institute / Cancer Curing Society

The Gerson Institute is a non-profit organization located in San Diego, California, dedicated to providing education and training in the alternative, non-toxic treatment of cancer and other disease, using the Gerson Therapy.

The Gerson Therapy is a safe, natural treatment developed by Dr. Max Gerson in the 1920’s that uses organic foods, juicing, coffee enemas, detoxification and natural supplements to activate the body’s ability to heal itself.  Over the past 60 years, thousands of people have used the Gerson Therapy to recover from so-called “incurable” diseases such as cancer, diabetes, heart disease and arthritis.

Founded by Charlotte Gerson (Dr. Gerson’s daughter) in 1977, we are the true source of information on the original, unmodified, proven Gerson Therapy.  We refer people to licensed Gerson clinics and treatment centers, practitionersand caregivers.  We also train health professionals, patients and others who want to learn this natural therapy.  Visit ourSTORE for a wide selection of educational books, audio and video tapes. 

You have the power to heal yourself.  We can give you the tools and show you how!

The Gerson Institute 
1572 Second Avenue 
San Diego, CA 92101

For videos on Gerson Therapy go to youtube:


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