Diabetes

Diabetes

DIABETES

There seem to be certain connections linking diabetes with thyroid disease. I'm pretty certain that most cases of diabetes are the result of nutrient deficiencies. If you look on this page there is a study (Title: High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes) showing that biotin and chromium picolinate work very well together to control diabetes. What is interesting about this is that we've seen that biotin is very important for copper metabolism and is often deficient in hyperT. Further down on this page there is a study showing that copper levels are high in diabetics. Generally when copper levels are high it means that copper is not being used properly because of other deficiencies. Copper is essential for the production of insulin, so it's possible that the lack of other nutrients which work with copper are preventing copper from being used to produce insulin, and therefore an insulin deficiency (diabetes) results. Possibly this is where biotin and chromium fit in.

Another interesting possible connection between diabetes and hyperT is that experimenters have found that diabetes can be controlled by administering tungsten. A quote from one study: "Results of uncontrolled trials on volunteers accumulated in Japan also suggest that tungstate effectively regulates diabetes mellitus without detectable side effects." There are other bits of information about tungsten and a possible connection between tungsten and copper which leads me to suspect that a tungsten deficiency is involved in hyperT also. Tungsten seems to be extremely difficult to get from foods and is unavailable as a supplement. The only sources I've found are the trace mineral supplements that list tungsten (over 1 mg per liter), and water from the eastern Sierra Nevada mountains (like Crystal Geyser--a brand found here in California).

Another hint that tungsten is involved in diabetes is that tungsten seems to play a role in the retina, perhaps for the detection of light (tungsten makes a good filament for light bulbs) and diabetics can get retinopathy.

Besides possible deficiencies of biotin, chromium, and tungsten, it's possible that diabetes could also result from a copper deficiency, since copper is necessary for insulin production. It may be that many diabetics have high copper, but some have low.

Med Hypotheses 1999 May;52(5):401-6

High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes.

McCarty MF

NutriGuard Research, Encinitas, CA 92024, USA.

Glucokinase (GK), expressed in hepatocyte and pancreatic beta cells, has a central regulatory role in glucose metabolism. Efficient GK activity is required for normal glucose-stimulated insulin secretion, postprandial hepatic glucose uptake, and the appropriate suppression of hepatic glucose output and gluconeogenesis by elevated plasma glucose. Hepatic GK activity is subnormal in diabetes, and GK may also be decreased in the beta cells of type II diabetics. In supraphysiological concentrations, biotin promotes the transcription and translation of the GK gene in hepatocytes; this effect appears to be mediated by activation of soluble guanylate cyclase. More recent evidence indicates that biotin likewise increases GK activity in islet cells. On the other hand, high-dose biotin suppresses hepatocyte transcription of phosphoenolpyruvate carboxykinase, the rate-limiting enzyme for gluconeogenesis. Administration of high-dose biotin has improved glycemic control in several diabetic animals models, and a recent Japanese clinical study concludes that biotin (3 mg t.i.d. orally) can substantially lower fasting glucose in type II diabetics, without side-effects. The recently demonstrated utility of chromium picolinate in type II diabetes appears to reflect improved peripheral insulin sensitivity--a parameter which is unlikely to be directly influenced by biotin. Thus, the joint administration of supranutritional doses of biotin and chromium picolinate is likely to combat insulin resistance, improve beta-cell function, enhance postprandial glucose uptake by both liver and skeletal muscle, and inhibit excessive hepatic glucose production. Conceivably, this safe, convenient, nutritional regimen will constitute a definitive therapy for many type II diabetics, and may likewise be useful in the prevention and management of gestational diabetes. Biotin should also aid glycemic control in type I patients.

Thyroid disease and diabetes

A DGReview of :"Practical Pointers: Thyroid Disease and Diabetes"
Clinical Diabetes

02/22/2000
By Mark Greener

Thyroid disease is widespread and prevalence increases with advancing age. However, as assessing thyroid function is reliable and inexpensive, certain high-risk groups - such as neonates, the elderly and diabetics - should undergo regular screening, a recent review notes.

Thryoid dysfunctions complicate diabetes management and the diagnosis of diabetes complications, the paper adds. For example, 6.6 per cent of the general population suffers from thyroid dysfunction, compared to between 10.8 and 13.4 per cent of people with diabetes. It is easy to understand the high prevalence of thyroid disease in women with type 1 diabetes - they are at greater risk because of their diabetes and because thyroid disease is more prevalent in women. In addition, postpartum thyroiditis is three times more common among women with diabetes than the non-diabetic population.

Clinically, thyroid dysfunction may undermine diabetes control. For example, hyperthyroidism may worsen glycaemic control and increase insulin requirements. Indeed, thyrotoxicosis may unmask subclinial diabetes. The author points to three issues which arise from this:

· Hyperglycaemia may improve during thyrotoxicosis treatment.
· Unexplained worsening hyperglycaemia may be due to hyperthyroidism.
· Hyperthyroidism may lead to poor glycaemic control.

While hypothyroidism markedly alters carbohydrate metabolism, such changes are rarely clinically significant. However, as less insulin is degraded, the exogenous insulin requirement may be lower. Moreover, hypothyroidism often produces dyslipidaemias, including elevated triglyceride and low-density lipoprotein (LDL) cholesterol concentrations. Therefore, hypothyroidism can exacerbate coexisting dyslipidaemias in type 2 diabetes. Thyroxine reverses these lipid abnormalities.

Postpartum transient thyroid dysfunction is common. As glucose control may fluctuate, the author stresses the importance of monitoring thyroid function - approximately 30 per cent of women do not recover and require thyroxine replacement.

The author notes that diagnosing thyroid dysfunction can be difficult. For example, poor glycaemic control produces symptoms similar to hyperthyroidism, such as weight loss despite increased appetite as well as fatigue. Clinicians need to be careful not to confuse severe diabetic nephropathy and hypothyroidism: both produce oedema, fatigue, pallor and weight gains. Finally, poorly controlled diabetes may alter thyroid function.

Against this background, the serum TSH immunoassay offers the most reliable and sensitive screening test for thyroid dysfunction. However, screening for anti-thyroid peroxidase (TPO) antibodies in people with type 1 diabetes may predict autoimmune thyroid disorders.

Management is generally similar to that in the non-diabetic population. However, the author warns that L-thyroxine therapy may exacerbate angina by increasing myocardial contractility and heart rate. She adds that clinicians should consider treating subclinical hypothyroidism if patients either have elevated serum LDL cholesterol exacerbated by hypothyroidism or detectable serum anti-TPO antibodies.

The author concludes that thyroid dysfunction is common among diabetic patients and can produce metabolic disturbances. Therefore, regularly screening diabetic patients allows early treatment. Type 1 patients expressing anti-TPO antibodies should be screened annually. In anti-TPO negative patients, a TSH assay every two to three years suffices. Among patients suffering from type 2 diabetes, clinicians should consider a TSH at diagnosis and then at least every five years.

Pediatrician 1983-85;12(4):213-9: The role of trace elements in juvenile diabetes mellitus.

Tuvemo T, Gebre-Medhin M.

There is accumulating evidence that the metabolism of several trace elements is altered in insulin-dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic heart disease and severe retinopathy. Increased urinary loss of zinc is a commonly encountered feature of diabetes. High-dose oral zinc might enhance wound healing, although data regarding diabetes are lacking. Chromium increases tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL) cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in processes which protect the cell against oxidative damage by peroxides produced from lipid metabolism. There is one report of elevated serum selenium in diabetic children although the clinical significance of this finding is still unclear. An insulin-like effect has recently been attributed to vanadium in experimental animals, a finding of potential interest to man. Current knowledge does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride, molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element supplementation might prove beneficial in ameliorating some physiological deficiencies associated with diabetes and prevent or retard secondary complications. However, properly designed and well-documented trials, especially on magnesium supplementation, need to be performed before rationales for such supplementation are developed. The potential roles of vanadium, chromium and selenium in diabetes constitute challenging areas for further experimental and clinical research.

Diabetes Res Clin Pract 1990 Aug-Sep;10(1):59-63

Early increase in histamine concentration in the islets of Langerhans isolated from rats made diabetic with streptozotocin.

Azevedo MS, Silva IJ, Raposo JF, Neto IF, Falcao JG, Manso CF

Instituto de Quimica Fisiologica, Faculdade de Medicina, Lisboa, Portugal.

Sprague-Dawley rats were separated in 4 groups. G1 received streptozotocin (ST). G2 received nicotinamide (NC) followed by ST. G3 was a NC control and G4 was a citrate control. The rats were sacrificed after 28 h and the islets isolated. Histamine and histaminase were determined. In the islets there was an increase in histamine content in G1 and a smaller increase in G2. The first two groups differ significantly and also in relation to the control groups. A decrease in islet histaminase does not seem responsible for the increased histamine, since group 2 (NC + ST) which had no diabetes, had a lower activity than group 1 (ST). It is suggested that histamine liberation by ST may be related to the diabetogenic effect of this drug.

PMID: 1701117, UI: 91065188

REGULAR PHYSICAL ACTIVITY HALVES DIABETES RISK IN POSTMENOPAUSAL WOMEN

Postmenopausal women who engage in any physical activity on a regular basis

are approximately half as likely to develop type 2 diabetes as those who

rarely or never exercise, according to study results published in the

January issue of the American Journal of Public Health.

http://diabetes.medscape.com/15503.rhtml

WESTPORT, Mar 30 (Reuters Health) - Despite concerns that thiazide diuretics and

beta-blockers may promote the development of type 2 diabetes mellitus, the

results of a new study indicate that only beta-blockers are associated with an

increased risk.

The findings appear in the March 30th issue of the New England Journal of

Medicine. One of the study's authors told Reuters Health, "We want to sound a

yellow alert about beta-blockers," but the risk of diabetes should nevertheless

be weighed against the proven cardiovascular benefits of beta-blockers.

Dr. Frederick L. Brancati, of Johns Hopkins School of Medicine in Baltimore,

said that the findings should alleviate concerns about most antihypertensive

medications, including diuretics. He and his and colleagues with the

Atherosclerosis Risk in Communities Study, analyzed data on 12,550 nondiabetic

subjects age 45 to 64 years. Examination at baseline included blood-pressure

measurement and assessment of medications.

At 3 and 6 years, participants were screened for diabetes based on fasting serum

glucose concentrations.

Overall, patients with hypertension were 2.5 times more likely than

nonhypertensives to develop type 2 diabetes mellitus, the researchers report.

After adjustment for potential confounders, patients taking a thiazide diuretic,

angiotensin-converting-enzyme (ACE) inhibitor or calcium-channel antagonist did

not have a greater risk of developing diabetes than those not taking any

antihypertensive medications. But the relative hazard for diabetes mellitus was

1.28 among

patients taking a beta-blocker.

Based on the results, "concern about increasing the risk of diabetes should not

discourage physicians from prescribing thiazide diuretics for the treatment of

hypertension in adults," the authors write. They also note while beta-blockers

do appear to raise the risk of diabetes, "but this adverse effect must be

weighed against the proven benefits of beta-blockers in reducing the risk of

cardiovascular events."

In an editorial accompanying the study, Dr. James R. Sowers, of the State

University of New York Health Science Center at Brooklyn, and Dr. George L.

Bakris, of Rush-Presbyterian-St. Luke's Medical Center in Chicago, Illinois,

call for prospective studies to determine whether using ACE inhibitors along

with beta-blockers might counteract the increased risk of diabetes.

"Until such studies are conducted, beta-blockers will continue to have an

important therapeutic role in patients with hypertension who have known coronary

artery disease and in hypertensive patients who have diabetes, a population in

which the prevalence of underlying coronary disease is high," they conclude.

N Engl J Med 2000;342:905-912,969-970.

Title: Alterations of antioxidant tissue defense enzymes and related metabolic parameters in streptozotocin-diabetic rats--effects of iodine treatment.
Author: Winkler R; Moser M
Address: Department of Physiology, Paracelsus Institute, Bad Hall.
Source: Wien Klin Wochenschr, 104(14):409-13 1992
Abstract

This study reports on the effect of streptozotocin (STZ) induced diabetes on water soluble-SH and -SS, as well as on hepatic glutathione peroxidase (GSH-Px), catalase and superoxide dismutase (SOD) activity and on malondialdehyde (MDA) content. In addition, we determined serum concentrations of glucose, cholesterol, triglycerides and thyroxine, and thyroid weight. To elucidate the possible impact of exogenous iodine on impaired free radical tissue defense mechanisms STZ-diabetic rats were exposed to iodine brine providing for a daily iodide uptake of about 300 micrograms/kg body weight. STZ-exposure caused a decline in thyroid weight (p less than 0.01) and in total serum thyroxine (p less than 0.001), as well as a fall in hepatic catalase (CAT) activity (p less than 0.01) versus control group. Impairment of catalase activity was related to serum glucose level (r = -0.569, p less than 0.01), while hepatic MDA was positively related to serum glucose (r = + 0.5, p less than 0.01). No protective effects of iodine brine were seen with regard to impairment by STZ of antioxidant enzyme status. We conclude that impairment by STZ of antioxidant enzymes may contribute to STZ-dependent experimental diabetes.

WESTPORT, Mar 22 (Reuters Health) - Regardless of dietary patterns, African-American children have an increased risk of type 2 diabetes compared with white children, according to a report in the March issue of the American Journal of Clinical Nutrition.

Dr. Michael I. Goran and colleagues at the University of Southern California in Los Angeles, California, evaluated the diets of 54 white children and 41 African-American children based on three 24-hour recalls. They also measured total cholesterol, triacylglycerol, insulin sensitivity and acute insulin response.

Cholesterol levels were not significantly different between the groups, the researchers report, and triacylglycerol levels were significantly lower among African Americans. However, acute insulin response was increased among African Americans, and insulin sensitivity was lower.

"Intake of fruit and vegetables was significantly higher, and dairy intake lower, in African Americans than in white children after adjustment for social class and total energy intake," Dr. Goran's team found. "However, neither macronutrient nor food group intake accounted for the ethnic differences in triacylglycerol and acute insulin response."

The investigators did find several associations between diet and insulin. According to the report, "carbohydrates and fruit intakes were positively associated with insulin sensitivity...and vegetable intake was negatively associated with acute insulin response."

In an editorial in the same journal, Dr. Sidika E. Kasim-Karakas, from the University of California at Davis writes, "Although [these researchers suggest] that dietary factors are not responsible for the insulin resistance in African Americans, it also shows that a high vegetable intake may have a favorable effect on insulin sensitivity. Further understanding of the mechanisms of the ethnic differences in insulin resistance will be important to reducing the morbidity and mortality related to diabetes mellitus and coronary artery disease."

Am J Clin Nutr 2000;71:725-732.

VEGAN DIET HELPS CONTROL DIABETES

WESTPORT, Sep 13 (Reuters Health) - A low-fat, vegetarian diet can help improve glycemic control in patients with type diabetes, and reduce the need for oral hypoglycemic medication even in the absence of exercise or controlled energy consumption.

In addition, patients who adhere to the vegan diet lose more weight than those consuming a conventional low-fat diet for 12 weeks, Dr. Andrew S. Nicholson, of the Physicians Committee for Responsible Medicine in Washington, DC, and colleagues report in the August issue of Preventive Medicine.

The investigators randomized 12 patients with noninsulin-dependent diabetes mellitus to one of the two diets for 12 weeks.

During the study, fasting serum glucose dropped an average of 28% in patients on the low-fat vegan diet and 12% in those randomized to the conventional low-fat diet. Mean weight loss was 7.2 kg in the vegan group and 3.8 kg in the conventional group, according to the report.

One of six patients in the vegan group completely discontinued oral hypoglycemic medication during the study while three patients were able to reduce their dosage of these agents. By comparison, "[n]o patients in the control group reduced medication use," the investigators point out.

High-density lipoprotein (HDL) cholesterol levels declined in both groups during the study, more so in vegan patients, but this change did not appear "...to be associated with elevated atherosclerotic risk in the context of a low total serum cholesterol concentration."

Although the findings appear promising, the study was small and the authors warn that the results require confirmation through further research.

Prev Med 1999;29:87-91.

Title: Preliminary observation on the metabolism in spontaneous hereditary diabetic Chinese hamster (Shanyi colony).
Author: Hu M; Wu Y; Wu H
Address: Institute of Metabolism and Endocrinology, Second Affiliated Hospital, Hunan Medical University, Hunan Province, China.
Source: Chin Med J (Engl), 110(9):711-4 1997 Sep
Abstract: OBJECTIVE: To observe the changes of tissue lithium content and its relationship with glucose metabolism in spontaneous hereditary diabetic Chinese hamsters (SHDCH). METHODS: Twenty diabetic and ten normal Chinese hamsters were paired and separated randomly into four groups: controls (C), diabetics (D), controls treated with lithium carbonate (CT) and diabetics treated with lithium carbonate (DT). The lithium carbonate treatment was administrated with drinking water containing lithium carbonate (0.2 mg/ml). Blood glucose levels were determined at 0, 1, 3, 5, 6th month, and insulin levels at 1, 3, 6th month. The lithium contents in liver, kidney and muscles were determined at the end of 6th month, using wet digestion assay and ICP-AES. Concentrations of fructosamine, lactic acid, GPT, BUN were also evaluated. RESULTS: The data showed that in Group D the lithium levels in hepatic tissue were lower than in Group C (P < 0.05), and lithium contents in kidney and muscle also decreased. In Group DT, the lithium contents in tissues were higher than in Group D (P < 0.05) and similar to Group C. Blood glucose levels and fructosamine concentrations decreased while insulin and lactic acid levels did not alter significantly. GPT and BUN levels did not change in both Group CT and Group DT. CONCLUSIONS: There is lithium deficiency in hepatic, renal and muscular tissues from diabetic Chinese hamsters. Low-dose and six-month-treatments of lithium carbonate can improve tissue lithium deficiency and glucose metabolism, and do not damage liver and kidney functions.

Growth Hormone Therapy May Accelerate Onset of Type 2 Diabetes in Predisposed Children

WESTPORT, Feb 18 (Reuters Health) - Children with glucose disorders who are treated with growth hormone (GH) develop type 2 diabetes at a rate six times that of children not treated with GH, researchers report in the February 19th issue of The Lancet.

Using the Pharmacia and Upjohn International Growth Study database, Dr. Wayne S. Cutfield, of the University of Auckland in New Zealand, and a multinational team determined that 43 of 23,333 children treated with growth hormone had confirmed glucose disorders, including 11 children with type 1 diabetes and 18 with type 2. Most children who developed diabetes were in puberty and had received GH for several years.

Among the children with type 1 diabetes, the incidence of disease and age at diagnosis did not differ from expected values, Dr. Cutfield's group reports. But among type 2 diabetics, disease incidence "was 34.4 cases per 100,000 years of GH treatment, which was sixfold higher than the incidence in children not treated with GH."

Discontinuation of GH therapy did not resolve type 2 diabetes. This "excludes a transient drug-induced effect such as that seen with high-dose glucocorticoid treatment," the authors note.

Dr. Cutfield and colleagues conclude that "GH therapy may...have hastened the onset of type 2 diabetes that would have occurred in adult life without GH therapy."

The authors recommend "that each child's glucose status be determined before starting GH therapy by measurement of hemoglobin A1c and fasting plasma glucose and insulin concentration." In addition, they say, "follow-up of patients is important for children with disorders at high risk of type 2 diabetes mellitus, such as obesity, Turner's syndrome, intrauterine growth retardation, Prader-Willi syndrome, and GH deficiency secondary to other causes."

In an editorial, Dr. William Jeffcoate of City Hospital in Nottingham, UK, says that the findings add weight to the case that widespread use of GH is not justified.

"In view of the possibility of a link between serum insulin-like growth factor-1 and carcinoma of the breast, prostate, and colon, the possibility of an adverse effect of GH on lipoprotein(a)1, the relation between fasting serum GH (within the normal range) and mortality in the Paris prospective study, and, now, the chance that some patients treated with GH might develop diabetes, the sceptical minority have a case," Dr. Jeffcoate says.

Lancet 2000;355:589-590,610-613.

Title: Vanadate, molybdate and tungstate for orthomolecular medicine.
Author: Matsumoto J
Address: Department of Chemistry, University of Massachusetts, Amherst 01002.
Source: Med Hypotheses, 43(3):177-82 1994 Sep
Abstract: Recent studies indicate that oxyanions, such as vanadate (V) or vanadyl (IV), cause insulin-like effects on rats by stimulating the insulin receptor tyrosine kinase. Tungstate (VI) and molybdate (VI) show the same effects on rat adipocytes and hepatocytes. Results of uncontrolled trials on volunteers accumulated in Japan also suggest that tungstate effectively regulates diabetes mellitus without detectable side effects. Since these oxyanions naturally exist in organisms, oxyanion therapy, the oral administration of vanadate, vanadyl, molybdate, or tungstate, can be considered to be orthomolecular medicine. Therefore, these oxyanions may provide a viable alternative to chemotherapy. Many diseases in addition to diabetes mellitus might also be treated since the implication of these results is that tyrosine kinases are involved in a variety of diseases.
Title: Insulin-like actions of tungstate in diabetic rats. Normalization of hepatic glucose metabolism.
Author: Barber`a A; Rodr´iguez-Gil JE; Guinovart JJ
Address: Department of Biochemistry and Physiology, School of Chemistry, University of Barcelona, Spain.
Source: J Biol Chem, 269(31):20047-53 1994 Aug 5
Abstract: Oral administration of tungstate for 15 days normalized glycemia in streptozotocin-induced diabetic rats. Simultaneously, the alterations in hepatic glucose metabolism due to diabetes were almost completely counteracted by this treatment. Thus, 6-phosphofructo-2-kinase, L-pyruvate kinase, and glycogen phosphorylase alpha activities reached levels similar to those observed in healthy animals. Hepatic levels of fructose 2,6-bisphosphate and glycogen also recovered. However, the recovery of glucokinase activity and hepatic levels of glucose 6-phosphate was only partial. The total activity of glycogen synthase increased, although the activation state was not recovered. Moreover, mRNA levels of hepatic glucokinase, glycogen phosphorylase, and phosphoenolpyruvate carboxykinase were also normalized. Tungstate administration in healthy animals also affected all these parameters, although to a much lesser extent. All these effects were similar to those previously reported for vanadate, suggesting a common mechanism of action in vivo.

The following study indicates that while zinc and magnesium levels in diabetics are normal, copper levels are high. This may mean that iron levels are low, and this would be great additional information to determine what is deficient that is making copper levels high.

Copper, zinc, and magnesium levels in non-insulin dependent diabetes mellitus.

Zargar AH, Shah NA, Masoodi SR, Laway BA, Dar FA, Khan AR, Sofi FA, Wani AI

Department of Endocrinology, Institute of Medical Sciences, Soura, Srinagar, Kashmir, India.

A relationship has been reported between trace elements and diabetes mellitus. This study evaluated the role of such a relationship in 83 patients with non-insulin dependent diabetes mellitus (40 men and 43 women), with a mean duration of diabetes of 3.9 +/- 3.6 years. Patients with nephropathy were excluded. Thirty healthy non-diabetic subjects were studied for comparative analysis. Subjects were subdivided into obese and non-obese. Diabetic subjects were also subdivided into controlled and uncontrolled groups; control was based on fasting blood glucose and serum fructosamine levels. Plasma copper, zinc and magnesium levels were analysed using a GBC 902 double beam atomic absorption spectrophotometer. Plasma zinc and magnesium levels were comparable between diabetic and non-diabetic subjects, while copper levels were significantly elevated (p < 0.01) in diabetic patients. Age, sex, duration and control of diabetes did not influence copper, zinc, or magnesium concentrations. We conclude that zinc and magnesium levels are not altered in diabetes mellitus, but the increased copper levels found in diabetics in our study may merit further investigation of the relationship between copper and non-insulin dependent diabetes mellitus.

PMID: 10197198, UI: 99212947

Cow's Milk May Increase Child's Risk Of Type 1 Diabetes

June 14, 2000

NEW YORK (Reuters Health) - Consuming large quantities of cow's milk during childhood may increase the risk of developing type 1 diabetes in children who are already genetically susceptible to the disorder, results of a study suggest.

The team of Finnish researchers found that children who had a sibling with diabetes were more than five times as likely to develop the autoimmune disorder if they drank more than half a liter (about three glasses) of cow's milk a day, compared with children who drank less milk.

The study findings, published in the June issue of Diabetes, add to an ongoing debate over the role of cow's milk in the onset of type 1 diabetes.

``Our study is the first prospective study to suggest that cow's milk consumption during childhood is related to development of clinical diabetes in siblings of children with diabetes,'' lead author Dr. Suvi M. Virtanen with the University of Tampere, Finland, told Reuters Health.

However, more studies are needed to assess the possible interaction between genetic disease susceptibility and dietary exposures in the development of the disease, Virtanen added.

While it is not clear which component of cow's milk may increase risk of diabetes, researchers suspect that one of several proteins may be to blame, Virtanen explained. Similarly, it is not known how cow's milk increases the risk of type 1 diabetes, although Virtanen suspects that it may ``program the immune system in a direction favoring an immune attack against insulin producing cells.''

Type 1 diabetes is usually diagnosed in children or in adults younger than 30. The disorder is caused by an abnormal immune reaction that destroys the cells of the pancreas that produce insulin, the hormone that regulates blood sugar. People with type 1 diabetes usually take life-long insulin injections to regulate their blood sugar.

The investigators looked at children who consumed cow's milk in the first year of life and followed up when children were age 3 to 19. Some children had a sibling with type 1 diabetes and were examined for a genetic predisposition to the disorder.

Results show that children who developed diabetes were more likely to have consumed at least three glasses of milk daily before entering the study. The number of diabetics and nondiabetics who had breast-fed for at least 2 months or had received some cow's milk before 2 months of age did not differ, researchers found.

A greater number of children who developed diabetes were genetically susceptible to the disease. Seventy-nine percent of these children carried a particular genetic variation associated with diabetes while only 30% of those who did not develop diabetes were found to have this variation.

SOURCE: Diabetes 2000;49:912-917.

Niacin May Be Alternative to Statins for Diabetics With Peripheral Arterial Disease

WESTPORT, Sep 13 (Reuters Health) - Patients with type 2 diabetes who receive lipid-modifying doses of niacin show a significant increase in high-density lipoprotein cholesterol and a significant decrease in triglycerides and low-density lipoprotein cholesterol levels, according to results from the Arterial Disease Multiple Intervention Trial.

Dr. Marshall B. Elam, of the University of Tennessee, Memphis, and a multicenter team studied 468 patients with peripheral arterial disease, of whom 125 were diabetic. The team randomized all patients to receive either niacin, 3000 mg/day or the maximum tolerated dose, or placebo. Sixty-four diabetic patients received niacin, as did 173 nondiabetics. The trial ran for 60 weeks, which included a 12-week run-in period.

"Niacin use significantly increased HDL cholesterol by 29% and 29% and decreased triglycerides by 23% and 28% and LDL cholesterol by 8% and 9%, respectively, in participants with and without diabetes," the research team reports in the September 13th issue of The Journal of the American Medical Association.

In the subjects receiving placebo, Dr. Elam and colleagues detected "increases of 0% and 2% in HDL cholesterol and increases of 7% and 0% in triglycerides, and increases of 1% and 1% in LDL cholesterol." They also noted that glucose levels increased by 8.7 mg/dL in diabetics receiving niacin and by 6.3 mg/dL in the nondiabetics receiving niacin. All changes were statistically significant.

Additionally, Dr. Elam's group saw "no significant differences in niacin discontinuation, niacin dosage, or hypoglycemic therapy in participants with diabetes assigned to niacin versus placebo."

"Despite current recommendations against use of niacin in diabetes, the present study demonstrates that lipid-modifying doses of immediate-release niacin can be used safely in patients with stable, controlled, type 2 diabetes mellitus," Dr. Elam and associates conclude.

Moreover, they add, "niacin therapy may be considered as an alternative to statin drugs or fibrates in patients with diabetes in whom these agents are not tolerated, or in whom they fail to sufficiently correct hypertriglyceridemia or low HDL cholesterol."

JAMA 2000;284:1263-1270.

The following article about cinnamon combined with the anecdotal stories of cinnamon cravings in persons with thyroid disease makes me wonder if there is something more in cinnamon than mentioned here. Perhaps cinnamon accumulates some nutrient that is important in correcting thyroid imbalance.

Cinnamon May Help Control Blood Sugar

Cinnamon may significantly help people with type 2 diabetes improve their ability to regulate their blood sugar. As a matter of fact, this study found that it increased glucose metabolism 20-fold.

	In a test tube and in animal studies, the spice appeared to increase glucose metabolism by about 20 times.
	Clinical trials using a cinnamon extract on humans are due to begin in 6 months.
	Researchers maintain that this could be a good means of lowering or controlling blood glucose levels at very little cost and could prove helpful to millions of people.
	Approximately 16 million Americans suffer from diabetes with 95% of them having type 2 diabetes, where the body's cells fail to recognize insulin.
	As a result, the amount of sugar in the blood remains high, leading to fatigue, blurred vision, and other problems. Over the long term, excess blood glucose can increase the risk of heart disease, kidney failure and blindness.
	Diabetes is the seventh-leading cause of death in the US, according to the American Diabetes Association. Yet, because of its influence in raising the risk of other problems, particularly heart disease, diabetes may be responsible for many more deaths than is attributed to it.

Dr. Richard A. Anderson, lead scientist at the Beltsville, Maryland-based Human Nutrition Research Center, a branch of the US Department of Agriculture (USDA), explained that his mostly unpublished research shows that a compound in cinnamon called methylhydroxy chalcone polymer (MHCP) makes fat cells more responsive to insulin by activating an enzyme that causes insulin to bind to cells and inhibiting the enzyme that blocks this process.

While it is too soon to recommend the spice as a regular treatment for type 2 diabetes, Dr. Anderson said patients could try adding 1/4 - 1 teaspoon of cinnamon to their food. "The worst that will happen is it won't do any good and the best is that it will help dramatically," he stated.

Preliminary Findings Announced by the USDA August, 2000.

The following study offers evidence that cadmium may be a factor in diabetes. If this is true then persons with diabetes may need to restrict intake of green leafy vegetables and other high cadmium foods.

Cigarette Smoking May Increase Risk of Diabetes

WESTPORT, CT (Reuters Health) Nov 29 - The results of a prospective study of more than 21,000 physicians indicate that smoking is associated with a substantial increase in the incidence of type II diabetes mellitus, researchers report in the November issue of the American Journal of Medicine.

"Smoking increases blood glucose levels after an oral glucose challenge and may impair insulin sensitivity," Dr. JoAnn E. Manson, of Brigham and Women's Hospital, Boston, and colleagues point out, which is one of the reasons why there may be a causal association between smoking and diabetes.

To investigate, the researchers examined the relationship between smoking and type II diabetes in a prospective cohort study of 21,068 US male physicians between the ages of 40 and 84 years. At the time of enrollment in 1982, none of the subjects had a diagnosis of diabetes mellitus, cardiovascular disease or cancer.

After an average of 12 years follow-up, 770 cases of type II diabetes mellitus were identified. Compared with those who had never smoked, smokers of 20 or more cigarettes daily had a 2.1 relative risk of diabetes. For fewer than 20 cigarettes daily, the corresponding figure was 1.4. For past smokers, the relative risk was 1.2.

After adjusting for factors such as body mass index and physical activity, the relative risks were 1.7 for smokers of 20 or more cigarettes daily, 1.5 for smokers of fewer than 20 cigarettes daily, and 1.1 for past smokers, compared with those who had never smoked. Total pack-years of smoking were also associated with increased risk.

The researchers conclude that "smoking is an independent and modifiable determinant of type II diabetes mellitus." Populations at high risk of the condition, they add, "should be considered for special targeted smoking interventions."

Am J Med 2000;109:538-542.

Sci Total Environ 2000 Apr 17;249(1-3):123-31: A syndrome of molybdenosis, copper deficiency, and type 2 diabetes in the moose population of south-west Sweden.

Frank A, Sell DR, Danielsson R, Fogarty JF, Monnier VM

Department of Clinical Chemistry, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala. dr.a.frank@rocketmail.com

Since the mid-1980s, a 'mysterious' disease has been afflicting the moose (Alces alces L.) population of south-western Sweden. Molybdenosis combined with secondary copper deficiency syndrome has been suggested as the cause of the clinical signs and of necropsy findings, supported by trace element analysis. Copper deficiency has long been associated with disturbed carbohydrate metabolism and also with oxidative stress. When testing the oxidative stress hypothesis, we found increased concentrations of the glycoxidation products pentosidine and carboxymethyl-lysine (CML), both in plasma proteins and in renal tissue, when compared with control values. The concentration of glycated lysine (furosine), a marker of hyperglycaemia, was also increased. These data, together with elevated insulin levels in affected moose, strongly suggest that they are suffering from an environmentally-induced, non-insulin-dependent type 2 diabetes.

Tungstate Improves Glucose Homeostasis in Diabetic Rats

WESTPORT, CT (Reuters Health) Feb 13 - Administration of sodium tungstate markedly reduces glycemia in a rat model of type 2 diabetes, Spanish researchers report in the January issue of Diabetes.

Dr. Joan J. Guinovart from Universitat de Barcelona and colleagues have previously shown that tungstate lowers blood glucose levels in rats made insulin deficient to simulate type 1 diabetes. In the current study, the researchers administered tungstate orally to 7.5-week-old Zucker diabetic fatty rats, which are "considered the closest available rat model to human type 2 diabetes associated with obesity."

The animals had begun to show hyperglycemia, and the treatment temporarily reversed this for about 10 days. Glucose levels then rose again but stabilized at about 200 mg/dL at day 24. In contrast, the glucose level of untreated rats rose to a maximum value of 450 mg/dL.

Tungstate treatment caused serum triglyceride levels to fall by 42%, and normalized hepatic concentrations of glucose-6-phosphate. The researchers also found that the treatment led to 55% higher glycogen levels in the liver compared with untreated diabetic or healthy rats. Treatment did not cause a significant change in phosphotyrosine-modified proteins in cultured hepatocytes from diabetic animals.

"These data suggest that tungstate administration to Zucker diabetic fatty rats causes a considerable reduction of glycemia, mainly through a partial restoration of hepatic glucose metabolism and a decrease in lipotoxicity," Dr. Guinovart and colleagues conclude.

Diabetes 2001;50:131-138.

Vitamin E Shows Promise In Treating Diabetes

June 5, 2001

WASHINGTON (Hearst Newspapers) - Break out that jar of wheat germ in the back of the refrigerator because it might help save your life if you are diabetic.

Scientists are assessing research that suggests high dosages of Vitamin E - naturally found in wheat germ, vegetable oils, margarine, whole-grain breads, nuts and peanut butter - may help stave off the ravages of diabetes.

The complications from diabetes can be devastating, including heart disease, eye and nerve damage, leading to amputations and kidney failure.

About 16 million Americans have the disease, which is caused by a deficiency of insulin, a hormone secreted by the pancreas and that is essential for converting sugar, starches and other foods into energy for cells. Lacking insulin, sugars build up in the blood rather than entering cells to fuel them. The result is that the body's cells literally can starve to death, causing the complications.

At the same time, the unprocessed sugar damages the weakened cell walls.

Some 798,000 new cases of diabetes are diagnosed annually in the United States. It is a chronic disease that has no cure and is the seventh leading cause of death in the United States, according to the Centers for Disease Control and Prevention in Atlanta.

Diabetes has two major subsets. In Type 1 diabetes, most often occurring in children and young adults, the body does not produce insulin and patients must take daily insulin injections to live. Type 1 accounts for about 10 percent of all diabetes cases.

In Type 2 diabetes, the body either doesn't make enough insulin or doesn't properly use it to convert foods. This is the most common form of the disease, comprising about 90 percent of all cases. Weight loss and exercise can control many of these cases.

African-Americans, Hispanic-Americans, American Indians and some Asian Americans and Pacific Islanders are at particularly high risk for Type 2 diabetes. Scientists believe high doses of Vitamin E help diabetics on at least two levels.

First, the vitamin acts as an antioxidant, a kind of chemical shield that protects cells against free radicals - potentially damaging byproducts of the body's metabolism. The U.S. National Institutes of Health in Bethesda, Md., says that free radicals can cause cell damage that may contribute to heart disease and certain cancers. And diabetics have an abnormally large supply of free radicals triggered by the high level of sugars, or glucose, in the blood.

Second, Vitamin E appears to arrest the effects of glucose. Dr. George King, professor of medicine at Harvard Medical School and research director of the Joslin Diabetes Center in Boston, explained that high glucose levels stimulate the development of an enzyme - known as PKC - that is particularly dangerous to diabetics.

"For some reason that isn't clear yet, Vitamin E in high doses not only is an antioxidant but it also inhibits the enzyme PKC. When that is done, you reverse or stop or prevent many of the blood-vessel complications we find in diabetes," said King, one the country's leading Vitamin E researchers.

Damage to nerves, eyes, kidneys and heart appears to be slowed or arrested in diabetics when they take large daily doses of the vitamin, somewhere in the range of 1,000 international units or more. The typical over-the-counter supplement is around 250 to 400 IUs.

Vitamin E "could have dramatic consequences if a larger clinical trial showed that this can be helpful," King added.

Most of the studies showing a benefit have been conducted on small numbers of diabetics, usually under 200 patients. King said large pharmaceutical companies are reluctant to foot the bill for an expensive study with thousands of participants because no single company has a patent on the vitamin.

Likewise, the NIH tends to give vitamin studies low priority "because it's not as sexy as other medical developments," King lamented.

Some of the strongest recent evidence for a benefit to diabetics comes from researchers at the University of Texas Southwestern Medical Center in Dallas, where scientists found that Vitamin E reduced the risk of heart failure in diabetics. Heart disease is one of the most serious side effects of diabetes.

Researchers showed that Vitamin E curtailed the inflammation in blood vessels of the heart. Left unchecked, the swelling of the vessels can lead to heart disease. Researchers studied 75 patients who had Type 2 diabetes. Test subjects received l,200 IUs of Vitamin E daily, and all of the participants experienced a drop-off in inflammation. Dr. Sridevi Devaraj, assistant professor of pathology and a lead researcher on the study, said the results were very encouraging.

"The study showed that Vitamin E significantly decreases micro-vascular complications" in diabetics, he said.

The American Diabetes Association says that some physicians prescribe Vitamin E supplements with a potency of up to 800 IUs per day for diabetes.

Anne Daly, a Springfield, Ill.-based dietitian and spokeswoman for the ADA, says that the vitamin "is pretty low risk and a possible benefit. But it's not a substitute for medicines people might be using (such as insulin injections or other sugar-lowering drugs). It's an adjunct."