Low Carbohydrate Diets Best For Diabetes

Researchers, reporting in the journal Nutrition & Metabolism in July 2005, concluded that low carbohydrate diets compare more favorably, at least over the short term, to traditional low fat for improving glycemic control, insulin sensitivity and dyslipidemia of diabetes with reduction in triglycerides, increase in HDL cholesterol and modification of LDL to a less atherogenic form (i.e. a form where LDL Cholesterol is less likely to deposit in the arteries).

At the time of writing their review these researchers, Surender Arora and Samy McFarlane, were from the Division of Endocrinology, Diabetes and Hypertension, SUNY Downstate Medical Center, and Kings County Hospital Center, Brooklyn, NY.

The following does not represent their complete work and is in part extracted and in part adapted from their review.

A low fat, high carbohydrate diet in combination with regular exercise is the traditional recommendation for treating diabetes. Compliance with these lifestyle modifications is less than satisfactory, however, and a high carbohydrate diet raises postprandial plasma glucose and insulin secretion, thereby increasing risk of cardiovascular disease, hypertension, dyslipidemia, obesity and diabetes.

Moreover, the current epidemic of diabetes and obesity has been, over the past three decades, accompanied by a significant decrease in fat consumption and an increase in carbohydrate consumption. This apparent failure of the traditional diet, from a public health point of view, indicates that alternative dietary approaches are needed.

Because carbohydrate is the major agent that promotes secretion of insulin, some form of carbohydrate restriction is a prima facie [at first sight] candidate for dietary control of diabetes. Evidence from various randomized controlled trials in recent years has convinced us that such diets are safe and effective, at least in short-term. These data show low carbohydrate diets to be comparable or better than traditional low fat high carbohydrate diets for weight reduction, improvement in the dyslipidemia of diabetes and metabolic syndrome as well as control of blood pressure, postprandial glycemia and insulin secretion.

Furthermore, the ability of low carbohydrate diets to reduce triglycerides and to increase HDL cholesterol is of particular importance. Resistance to such strategies has been due, in part, to equating it with the popular Atkins diet. However, there are many variations and room for individual physician planning.

Some form of low carbohydrate diet, in combination with exercise, is a viable option for patients with diabetes. However, the extreme reduction of carbohydrate of popular diets (less than 30 grams per day) cannot be recommended for a diabetic population at this time without further study. On the other hand, the dire objections continually raised in the literature appear to have very little scientific basis. Whereas it is traditional to say that more work needs to be done, the same is true of the assumed standard low fat diets which have an ambiguous [doubtful or uncertain] record at best.

The epidemic of obesity and diabetes in our society over the past three decades has been accompanied by a decline in fat consumption and an apparent attempt to adopt the traditionally recommended low fat diet.

According to the USDA Continuing Survey of Food Intakes by Individuals (CSFII), the absolute amount of fat and saturated fat consumed has decreased during the obesity epidemic although there is a slight increase for women from 1994 to 1995. (J Am Coll Nutr 1999, 18:207-212).

This apparent failure of low fat diets in curbing the obesity pandemic calls into question the effectiveness and long-term usefulness of such dietary recommendation and has led to renewed interest in alternative dietary interventions, notably those recommending reduced carbohydrate intake.

Low fat diets are generally associated with high carbohydrate intake which in turn is associated with several metabolic abnormalities. (Diabetes 1992, 41:1278-1285, Jama 1994, 271:1421-1428). These metabolic abnormalities are more pronounced in the diabetic population, leading to worsening glycemic control, dyslipidemia and increased inflammation to name a few. (Dyslipidemia may be manifested by the total cholesterol, the “bad” LDL cholesterol and the triglyceride concentrations, and a decrease in the “good” HDL cholesterol concentration in the blood).

Traditionally, increased fat intake has been considered as the main cause for excess energy intake and obesity but the trends in food intake during the obesity epidemic do not support this notion. (J Am Coll Nutr 1999, 18:207-212, Jama 1999, 282:1519-1522).

While fat intake has decreased, carbohydrate intake has increased simultaneously. This rise in dietary intake of carbohydrates, and especially highly refined carbohydrate, is a likely culprit in promoting weight gain and obesity. (Nutr Rev 2000, 58:163-169).

In a recent study, significantly greater weight loss was demonstrated with low carbohydrate intervention (less than 10% calories from carbohydrates) despite higher caloric intake (1855 kcal/day) compared to high carbohydrate (60% calories from carbohydrates) with lower caloric intake (1562 kcal/day). (Nutr Metab (Lond) 2004, 1:13).

Two of the low carbohydrate-low fat comparisons were continued for 1 year. (N Engl J Med 2003, 348:2082-2090, 142:403-411, Ann Intern Med 2004, 140:778-785). It is frequently cited that the difference in weight loss between the low carbohydrate diet and low fat diet was not statistically significant after one year but it should be pointed out that in these studies, participants had the freedom to increase the carbohydrate content of the diet over longer duration and it is reasonable to say that as carbohydrate is added back to the diet, its effectiveness wanes.

For example, in the study by Foster and colleagues at the University of Pennsylvania School of Medicine, Philadelphia, the low-carbohydrate diet produced a greater weight loss than did the conventional diet for the first six months, but the differences were not significant at one year. There was no significant difference in the urinary ketone levels between the two study groups after 3 months, suggesting inadequate carbohydrate restriction during the later part of the study which would contribute to the similarity in various parameters between the groups. In addition, the authors of these studies included subjects who had dropped out of the study. This method, justified under the name “intention to treat analysis” obscures the information in the study and has the effect of making the more effective diet look worse. The researchers did concede that adherence was poor and the drop out rate was high in both groups. (N Engl J Med 2003, 348:2082-2090).

In another recent study comparing the effects of four popular diets including a low carbohydrate diet and a low fat diet, there were no significant differences in weight loss in the different groups at the end of 1 year. However, this study also had the shortcomings of the above studies, including small sample size (40 subjects in each group) and poor adherence in all the groups (30-60% dropouts). The low carbohydrate diet group also failed to reach carbohydrate reduction goals of carbohydrate intake of 190 gm/day at 6 months and 12 months as compared to the start of the study of 239 gm/day. Hence, it is not surprising that weight loss was not significantly different in the low carbohydrate diet group. (Jama 2005, 293:43-53).

What is encouraging is that despite such marginal carbohydrate restriction in the low carbohydrate group, this group was able to achieve a modest weight loss that was comparable to the other diet groups, while maintaining a greater improvement in lipid (cholesterol, triglycerides) profile suggesting that even minimal carbohydrate restriction may have beneficial effects in terms of weight loss and might be offered to those at high risk who fail to lose weight with traditional low fat diets.

Diets containing 50-60% calories from carbohydrates have been the standard recommendation for patients with type 2 diabetes and metabolic syndrome. However, evidence from several population groups studies such as the Nurses Health Study and Health Professional Follow-Up Study has linked dietary carbohydrate intake (measured as glycemic load) with risk of type 2 diabetes and cardiovascular disease. (J Nutr Health Aging 2001, 5:132-138, Diabetes Care 2004, 27:538-546).

Compelling evidence from clinical and metabolic studies demonstrate worsening of glycemic control and dyslipidemia in diabetics with high carbohydrate diets whereas low carbohydrate diets may reverse these serious metabolic abnormalities.

Before the discovery of insulin, dietary carbohydrate restriction was the recommended treatment for diabetes management. (J R Soc Health 1997).

To summarize, the effect of a low carbohydrate diet on glycemic control was significantly greater and occurred independent of weight loss in those studies that were able to achieve and maintain adequate carbohydrate restriction. In other studies, the effect on glycemic control was modest and proportional to the weight loss, and at least comparable to that seen with low fat diets.

In conclusion, a low carbohydrate diet is associated with significant improvement in glycemic control and has the potential for reduction in need for exogenous insulin or oral hypoglycemic medications.

For a free resource to help you make healthy food and lifestyle choices for you and your family including topics that will help improve your overall health and sense of well-being related to weight loss, relationships, diet, exercises, nutrition, vitamins, prevention, and more go to Manage Weight Loss Review.

Extracted and adapted from: Arora SK, McFarlane SI. The case for low carbohydrate diets in diabetes management. Nutrition & Metabolism 2005, 2:16 (14 July 2005). © 2005 Arora and McFarlane; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The electronic version of this article is the complete one and can be found online at: http://www.nutritionandmetabolism.com/content/2/1/16

Heart Health: Saturated Fat Should Not Be Restricted.

Written by Kevin Flatt

Assistant Professor Jeff S. Volek and his colleague Cassandra E Forsythe at the University of Connecticut, reporting in the August 2005 issue of the journal Nutrition & Metabolism, dispel common myths and provide a convincing argument that the restriction of saturated fat is not warranted on a low-carbohydrate diet because of their work showing favorable responses in clinical risk factors for diabetes and cardiovascular disease in low-carbohydrate diets that were rich in saturated fat.

They complimented Drs. Arora and McFarlane on their timely review of low carbohydrate diets in diabetes management, who had concluded that low carbohydrate diets compare more favorably, at least over the short term, to traditional low fat for improving glycemic control, insulin sensitivity and dyslipidemia of diabetes with reduction in triglycerides, increase in HDL cholesterol and modification of LDL to a less atherogenic form (i.e. a form where LDL Cholesterol is less likely to deposit in the arteries). (Nutr Metab (Lond) 2005, 2:16).

One point stressed by Arora and McFarlane was that mono and polyunsaturated fat should be emphasized over saturated fat as a way to achieve caloric balance on a carbohydrate-restricted diet.

Assistant Professor Jeff S. Volek and his colleague at the University of Connecticut, contended that the recommendation to intentionally restrict saturated fat is unwarranted and only serves to contribute to the misleading rhetoric surrounding the health effects of saturated fat.

They believe restriction of saturated fat is not warranted on a low-carbohydrate diet because of their work showing favorable responses in clinical risk factors for diabetes and cardiovascular disease in low-carbohydrate diets that were rich in saturated fat.

In addition, German & Dillard (Am J Clin Nutr 2004, 80:550-559) have reviewed several experimental studies of the effects of saturated fats and the results are found to be variable and there is a general failure to meet the kind of specific predictions that would justify the recommendation to reduce saturated fat in the population. Other critical reviews of the evidence have questioned whether public health recommendations for reducing saturated fat intake are appropriate. (J Clin Epidemiol 1998, 51:443-460, J Am Diet Assoc 2002, 102:1621-1630).

Professor Volek and colleague stated in their article that the critical issues are:

1. The atherogenic (the formation of plaques on the walls of the arteries) potential of saturated fats varies greatly depending on chain length and whether it is present alone or added in foods. Stearic acid is a major saturated fat found in beef, chicken, and pork and has repeatedly been shown not to raise LDL cholesterol levels (Am J Clin Nutr 1994, 60:986S-990S).

Even palmitic acid (a saturated fatty acid that is the major fat in meat and dairy products), the most abundant saturated fatty acid in the diet, does not raise LDL cholesterol in the presence of adequate linoleic acid (a liquid polyunsaturated fatty acid abundant in plant fats and oils; a fatty acid essential for nutrition). (Asia Pac J Clin Nutr 2002, 11 Suppl 7:S401-S407).

2. The effect of saturated fat cannot be assumed to be independent of specific dietary conditions. In particular, hypocaloric (low calorie) or low total fat diets may show different results than deduced from epidemiology (population studies). A recent report showed that for women on a relatively low fat diet, a greater saturated fat intake was associated with a reduced progression of coronary atherosclerosis. (Am J Clin Nutr 2004, 80:1175-1184). An editorial described this as “an American paradox”. (Am J Clin Nutr 2004, 80:1102-1103).

3. Evaluation of the overall health effects of saturated fat requires consideration of markers in addition to LDL-cholesterol. Replacement of carbohydrates with any type of fat, providing the same number of calories, results in decreased triglycerides and increased HDL-cholesterol, the effect on HDL-cholesterol being greater for saturated fat compared to unsaturated fat. (Am J Clin Nutr 1995, 61:1368S-1373S).

Reductions in saturated fat also adversely affect HDL subpopulations by decreasing larger HDL2-cholesterol concentrations. (Am J Clin Nutr 1999, 70:992-1000). Whereas increases in saturated fat increase this anti-atherogenic fraction. (Mayo Clin Proc 2003, 78:1331-1336, Am J Med 2004, 117:398-405).

Furthermore, very low-carbohydrate diets rich in saturated fat increase LDL cholesterol size and conversion from a high risk pattern B to a lower risk pattern A phenotype. (J Nutr 2005, 135:1339-1342).

4. Finally, there is the concern that recommendations to limit saturated fat would lead to their replacement with carbohydrate, which can have undesirable effects (increased triglycerides with decreased HDL cholesterol. (Am J Clin Nutr 1995, 61:1368S-1373S).

The authors concluded that for these reasons, they believe that the recommendation to restrict saturated fat in favor of unsaturated fat on a low-carbohydrate diet is unnecessary and may even diminish some of the beneficial physiological effects associated with carbohydrate restriction. At the very least, the food restriction required to reduce saturated fat will compromise the palatability of the diet and ultimately the acceptance of the approach to diabetes management recommended by Arora and McFarlane. (Nutr Metab (Lond) 2005, 2:16).

Adapted from: Jeff S Volek, Cassandra E Forsythe. The case for not restricting saturated fat on a low carbohydrate diet. Nutrition & Metabolism 2005, 2:21 (31 August 2005). © 2005 Volek and Forsythe, licensee BioMed Central Ltd.
http://www.nutritionandmetabolism.com/content/2/1/21.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Diabetes Management: Saturated Fat Should Not Be Restricted.

Written by Kevin Flatt

Assistant Professor Jeff S. Volek and his colleague Cassandra E Forsythe at the University of Connecticut, reporting in the August 2005 issue of the journal Nutrition & Metabolism, dispel common myths and provide a convincing argument that the restriction of saturated fat is not warranted on a low-carbohydrate diet because of their work showing favorable responses in clinical risk factors for diabetes and cardiovascular disease in low-carbohydrate diets that were rich in saturated fat.

They complimented Drs. Arora and McFarlane on their timely review of low carbohydrate diets in diabetes management, who had concluded that low carbohydrate diets compare more favorably, at least over the short term, to traditional low fat for improving glycemic control, insulin sensitivity and dyslipidemia of diabetes with reduction in triglycerides, increase in HDL cholesterol and modification of LDL to a less atherogenic form (i.e. a form where LDL Cholesterol is less likely to deposit in the arteries). (Nutr Metab (Lond) 2005, 2:16).

One point stressed by Arora and McFarlane was that mono and polyunsaturated fat should be emphasized over saturated fat as a way to achieve caloric balance on a carbohydrate-restricted diet.

Assistant Professor Jeff S. Volek and his colleague at the University of Connecticut, contended that the recommendation to intentionally restrict saturated fat is unwarranted and only serves to contribute to the misleading rhetoric surrounding the health effects of saturated fat.

They believe restriction of saturated fat is not warranted on a low-carbohydrate diet because of their work showing favorable responses in clinical risk factors for diabetes and cardiovascular disease in low-carbohydrate diets that were rich in saturated fat.

In addition, German & Dillard (Am J Clin Nutr 2004, 80:550-559) have reviewed several experimental studies of the effects of saturated fats and the results are found to be variable and there is a general failure to meet the kind of specific predictions that would justify the recommendation to reduce saturated fat in the population. Other critical reviews of the evidence have questioned whether public health recommendations for reducing saturated fat intake are appropriate. (J Clin Epidemiol 1998, 51:443-460, J Am Diet Assoc 2002, 102:1621-1630).

Professor Volek and colleague stated in their article that the critical issues are:

1. The atherogenic (the formation of plaques on the walls of the arteries) potential of saturated fats varies greatly depending on chain length and whether it is present alone or added in foods. Stearic acid is a major saturated fat found in beef, chicken, and pork and has repeatedly been shown not to raise LDL cholesterol levels (Am J Clin Nutr 1994, 60:986S-990S).

Even palmitic acid (a saturated fatty acid that is the major fat in meat and dairy products), the most abundant saturated fatty acid in the diet, does not raise LDL cholesterol in the presence of adequate linoleic acid (a liquid polyunsaturated fatty acid abundant in plant fats and oils; a fatty acid essential for nutrition). (Asia Pac J Clin Nutr 2002, 11 Suppl 7:S401-S407).

2. The effect of saturated fat cannot be assumed to be independent of specific dietary conditions. In particular, hypocaloric (low calorie) or low total fat diets may show different results than deduced from epidemiology (population studies). A recent report showed that for women on a relatively low fat diet, a greater saturated fat intake was associated with a reduced progression of coronary atherosclerosis. (Am J Clin Nutr 2004, 80:1175-1184). An editorial described this as “an American paradox”. (Am J Clin Nutr 2004, 80:1102-1103).

3. Evaluation of the overall health effects of saturated fat requires consideration of markers in addition to LDL-cholesterol. Replacement of carbohydrates with any type of fat, providing the same number of calories, results in decreased triglycerides and increased HDL-cholesterol, the effect on HDL-cholesterol being greater for saturated fat compared to unsaturated fat. (Am J Clin Nutr 1995, 61:1368S-1373S).

Reductions in saturated fat also adversely affect HDL subpopulations by decreasing larger HDL2-cholesterol concentrations. (Am J Clin Nutr 1999, 70:992-1000). Whereas increases in saturated fat increase this anti-atherogenic fraction. (Mayo Clin Proc 2003, 78:1331-1336, Am J Med 2004, 117:398-405).

Furthermore, very low-carbohydrate diets rich in saturated fat increase LDL cholesterol size and conversion from a high risk pattern B to a lower risk pattern A phenotype. (J Nutr 2005, 135:1339-1342).

4. Finally, there is the concern that recommendations to limit saturated fat would lead to their replacement with carbohydrate, which can have undesirable effects (increased triglycerides with decreased HDL cholesterol. (Am J Clin Nutr 1995, 61:1368S-1373S).

The authors concluded that for these reasons, they believe that the recommendation to restrict saturated fat in favor of unsaturated fat on a low-carbohydrate diet is unnecessary and may even diminish some of the beneficial physiological effects associated with carbohydrate restriction. At the very least, the food restriction required to reduce saturated fat will compromise the palatability of the diet and ultimately the acceptance of the approach to diabetes management recommended by Arora and McFarlane. (Nutr Metab (Lond) 2005, 2:16).

Adapted from: Jeff S Volek, Cassandra E Forsythe. The case for not restricting saturated fat on a low carbohydrate diet. Nutrition & Metabolism 2005, 2:21 (31 August 2005). © 2005 Volek and Forsythe, licensee BioMed Central Ltd.
http://www.nutritionandmetabolism.com/content/2/1/21.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/2.0 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The Multitude of Health Benefits from Natural Sunlight and Vitamin D

John Cannell, MD, Executive Director of The Vitamin D Council, reports on the Vitamin D Conference in Victoria.

The Vitamin D Conference just finished in Victoria was nothing short of spectacular. On the bus into Victoria, I met a representative from the National Cancer Institute whose job was simple: her bosses at the NIH wanted to know if they should fund the flood of grant requests about vitamin D. Given the quality of the papers presented, I can't imagine her answer was anything but yes.

Dr. Tony Norman and Dr. Roger Bouillon, the conference organizers, had to choose from over 300 submissions from scientists around the world. The venerable Dr. Bouillon did not try to back off his recent widely quoted warning that more than a billion people in the world are vitamin D deficient. Both men did a great job balancing presentations on vitamin D nutrition, vitamin D basic science, and the patentable vitamin D analogs sought by drug companies. Of course, I thought more time should have been devoted to vitamin D nutrition but Dr. Norman pointed out that more time was devoted to vitamin D nutrition than ever before. Like Dr. Norman, I am unable to comment on all the presentations that merited it, or this newsletter would be 50 pages long.

Dr. Barbara Gilchrest, who fired Dr. Michael Holick from one of his professorships several years ago after Holick wrote a book saying God knew what she was doing when she created sunlight, gave the Plenary Lecture. Wisely, Dr. Gilchrest overwhelmed the audience with graphic pictures of invasive skin cancer to support her argument that sunlight is evil. Of course, it's harder to show pictures of invasive colon cancer, breast cancer, prostate cancer, and the 15 other internal cancers caused by sunlight deprivation.

However, Dr. Gilchrest is changing her mind. George Bernard Shaw once said, "Progress is impossible without change; and those who cannot change their minds, cannot change anything." Dr. Gilchrest is changing her mind - not about the evils of sunlight - about vitamin D. She is in the process of admitting that this miraculous substance has benefits beyond bone.

Two years ago, she dismissed any concerns about vitamin D with a "take a multivitamin if you are concerned." Now she believes the Food and Nutrition Board needs to consider raising both the Adequate Intake recommendations (how much one should take every day) as well as the Upper Level (the amount one can take on your own, without being under a doctor's care, and without fear of toxicity). My compliments to Dr. Gilchrest.

Dr. Heike Bischoff-Ferrari did a wonderful job, not just presenting her data that optimal vitamin D blood levels need to be at least 40 ng/ml, but for presenting Dr. Ed Giovannucci's data (who had to cancel for personal reasons). Dr. Bischoff-Ferrari reminded us that periodontal disease in inversely related to vitamin D blood levels. She also reminded us that there is strong scientific evidence that vitamin D improves neuromuscular performance in older people.

Dr. Bischoff-Ferrari then presented Dr. Giovannucci's data that one reduces your risk of all cancers about 17% for every 10 ng/ml of vitamin D in your blood. For cancer of the digestive system, the risk reduction is 43%. His data indicates all Americans should be taking about 2,000 IU per day and some Americans need even more to minimize cancer risk. No one know where the curve flattens out; that is, no one knows how much further cancer reduction one gets from 20, 30, or 40 ng/ml incremental increases in blood levels.

Dr. Robert Heaney presented by video hookup and made his quiet but powerful case that about 75% of American women are vitamin D deficient (levels less than 35 ng/ml), that about 3,000 units a day are needed to bring 95 % of the population out of the deficient range, and that 10,000 units a day is the safe upper limit. (This does not mean you should take 10,000 units per day, it means scientists should be able to study 10,000 unit daily doses without the bureaucratic difficulty they now encounter).

Dr. Kimball, working with Dr. Reinhold Vieth, presented data that children (age 10 -17) only increased their average blood level by 11 ng/ml when given 14,000 units per week for eight weeks and that such dosing was safe.

Dr. Hollis presented evidence in Victoria that levels of at least 40 ng/ml are required to normalize the enzyme kinetics of vitamin D. [When I say vitamin D blood levels, I'm referring to 25(OH)D levels; Bruce is studying actual vitamin D levels (cholecalciferol) as well as 25(OH)D levels]. Dr. Hollis continues giving pregnant and lactating South Carolina women about 4,000 to 6,000 units a day in an ongoing study. We predict easier pregnancies and less depression in the moms - lower prenatal and perinatal mortality, fewer birth defects, fewer infections, less diabetes, less psychiatric illness, less asthma, stronger bones, and higher IQs in the children.

Dr. Hathcock did a great job reviewing the evidence that doses below 10,000 units per day have never been shown to be toxic and that 10,000, not 2,000, units per day should be the Upper Limit. He, like so many others, urged the Food and Nutrition Board to revise their outdated recommendations. Moreover, I understand from knowledgeable people at the conference that the Food and Nutrition Board is planning to do just that!

Dr. Dixon presented fascinating evidence that high vitamin D blood levels prevent sunburn! Of course, it makes sense. When vitamin D levels are low, the skin stays as white as it can to make as much vitamin D as it can, just in case you ignore Dr. Gilchrest's advice. When vitamin D levels are high, the skin rapidly tans to prevent excessive vitamin D skin production. A number of people have emailed me that observation: now that their levels are high, they tan very quickly. I've noticed the same thing.

Dr. Marie Demay presented her basic science research that vitamin D is involved in hair follicles. I loved her talk although she's a scientist and I'm a psychiatrist so I didn't understand much of what she said. However, I've always thought that vitamin D will really take off once science shows it's involved in any of three things: sex, athletic performance, or hair growth. In Victoria, we saw evidence for neuromuscular (athletic) performance and hair growth.

Dr. Cedric Garland recounted how, 26 years ago, he and his brother Frank first thought about the relationship between vitamin D and colon cancer. The brothers, together with colleague Ed Gorham, were the first to provide epidemiological evidence that vitamin D deficiency is involved in numerous cancers. Their seminal 1980 paper is going to be reprinted, a well-deserved honour. (Int J Epidemiol. 1980 Sep;9(3):227-31).

Dr. Thadhani and his group from Harvard reviewed their recent discovery that calcitriol and similar drugs increase survival in patients with renal failure. He also presented evidence that renal failure patients have profound deficiencies of both calcitriol and vitamin D and their vitamin D deficiency is not corrected by giving calcitriol or its analogs, which is the current practice.

Of course, Dr. Robert Modlin stole the show when he reported on his research just published in Science that vitamin D may be, in effect, a powerful antibiotic. For the first time, the UCLA group showed that when researchers add vitamin D to African American blood, their blood makes more of the natural antibiotics that humans rely on the fight infection.

Dr. Adrian Martineau, from the Imperial College in London, followed Modlin and showed vitamin D helped fight tuberculosis, probably from increasing these same natural antibiotics. Science has discovered more than 200 of these naturally occurring antimicrobial peptides; they are especially prevalent in the upper and lower respiratory tract; at least one inactivates the influenza virus. Let's not forget that two other groups have also recently shown the antibiotic potential of vitamin D. (Science. 2006 Mar 24;311(5768):1770-3, J Immunol. 2004 Sep 1;173(5):2909-12, FASEB J. 2005 Jul;19(9):1067-77, J Virol. 1986 Dec;60(3):1068-74).

Dr. Lu presented evidence that the vitamin D content of fish is much less than previously thought, including mackerel. Salmon is OK but the vitamin D almost disappears when the salmon is fried.

Dr. Hardin, from Columbia University, presented evidence that blood levels above 50 ng/ml should help patients with lupus. A group from the University of Manchester presented the mechanism by which vitamin D should reduce arteriosclerosis.

A group from the University of Chicago presented evidence that vitamin D should not only prevent colon cancer, but help treat it as well. Dr. Robert Scragg of the University of Auckland presented evidence that ethnic differences in vitamin D levels explain a significant proportion of the reason African Americans are more hypertensive than whites. The group from San Diego presented evidence that vitamin D deficiency is intimately involved in breast, colon, and ovarian cancer.

A group from the University of Manitoba presented evidence that one-month-old infants tolerate 2,000 units of vitamin a day for three months quite well without any evidence of adverse effects. A group from Wake Forest University demonstrated that higher vitamin D levels were associated with better neuromuscular (athletic) performance in older Americans (should help younger Americans too).

A group from the University of Amsterdam showed that the increased risk of falling from vitamin D deficiency is much worse in people with a common genetic variation of the vitamin D receptor. Dr. Chen presented evidence that plain old vitamin D should prevent prostate cancer.

Dr. Barsony, of Georgetown University, presented evidence that low blood sodium is a risk factor for vitamin D deficiency and that such deficiencies may not be able to be corrected until the low blood sodium is corrected. Dr. Barsony really thought outside the box to discover this potentially very important clinical finding.

Dr. Godar presented evidence that young Americans, not just older Americans, are not getting much vitamin D from sunlight. Dr. Taylor showed evidence that a significant number of young children have a previously undetected form of vitamin D in their blood. (Sunlight triggers the creation of a number of different versions of vitamin D in the skin, that's why it's risky to avoid the sun and only depend on oral vitamin D.) Dr. Patel and a group from the University of Manchester announced evidence that vitamin D deficiency may be involved in inflammatory polyarthritis.

Dr. Grant was involved in six presentations; the most interesting was his replication of a 1937 finding that squamous cell skin cancer reduces one's risk for a number of internal cancers. That's why I used to be so happy when my dermatologist found a squamous cell cancer on my skin. However, now that I maintain my level at about 60 ng/ml, he hasn't been able to find any new ones.

Dr. Bulmer and his group from the Royal Victoria Infirmatory produced evidence that vitamin D may play a role in allowing fertilized ova to implant in the uterus and thus enhance fertility. Dr. Reichrath presented evidence that transplant recipients are at a high risk for vitamin D deficiency and that 50,000 units once a month may be the most practical way of ensuring sufficiency.

Dr. Selby from the University of Manchester found the same problem in patients with chronic pancreatitis. A group from the University of Tennessee found the same problem in African Americans with heart failure. A group from Norway confirmed that cancer patients do better if they are diagnosed when vitamin D levels are the highest.

Finally, the Australian group headed by Dr. Darryl Eyles and Dr. John McGrath continue to present their convincing evidence (confirmed at this meeting by Dr. Abreu and a group from France) that profound maternal vitamin D deficiency in mammals causes permanent brain damage in their offspring. The racial implication of their work is overwhelming because most of the women in the USA who are profoundly deficient are African American. Are African Americans more likely to be born brain damaged than whites? Would pennies worth of vitamin D improve the disparate prenatal, perinatal, and postnatal outcome in African Americans? The sad fact is that McGrath's and Eyles' work will continue to be ignored because our society has no way to rationally discuss, assimilate, or act on such racially charged scientific discoveries.

John Cannell, MD.
The Vitamin D Council.

Make sure you’re taking D3. If the label says vitamin D2, then it’s not the good kind of vitamin D. Vitamin D has to be taken with fat. Taking a vitamin D pill with orange juice isn’t going to work, it won’t absorb.

Try to get brand-name recommendations. Sadly, many doctors haven’t learned about supplements in medical school, so your doctor may not be able to advise you on that. To find the best brands, do your homework. Either get names of products from people you trust, or go on the Internet and look these supplements up.

Dr. Michael Holick, a leading vitamin D researcher who serves as director of the general clinical research center at Boston University Medical Center, said it’s difficult to get enough vitamin D from food, noting that you’d have to eat a 3½-ounce serving of fish like salmon, mackerel or sardines “almost every day just to begin to satisfy your requirement.”

The NIH agrees. It can be difficult to obtain enough vitamin D from natural food sources. For many people, consuming vitamin D fortified foods and adequate sunlight exposure are essential for maintaining a healthy vitamin D status. In some groups, dietary supplements may be needed to meet the daily need for vitamin D.

Prevent Diabetes Problems: Keep Your Feet Healthy.

Written by Kevin Flatt

High blood glucose from diabetes causes two problems that can damage your feet:

Nerve damage. One problem is damage to nerves in your legs and feet. With damaged nerves, you might not feel pain, heat, or cold in your legs and feet. A sore or cut on your foot may get worse because you do not know it is there. This lack of feeling is caused by nerve damage, also called diabetic neuropathy. It can lead to a large sore or infection.

Poor blood flow. The second problem happens when not enough blood flows to your legs and feet. Poor blood flow makes it hard for a sore or infection to heal. This problem is called peripheral vascular disease. Smoking when you have diabetes makes blood flow problems much worse.

These two problems can work together to cause a foot problem. For example, you get a blister from shoes that do not fit. You do not feel the pain from the blister because you have nerve damage in your foot. Next, the blister gets infected. If blood glucose is high, the extra glucose feeds the germs. Germs grow and the infection gets worse. Poor blood flow to your legs and feet can slow down healing. Once in a while a bad infection never heals. The infection might cause gangrene.

To keep gangrene from spreading, a doctor may have to amputation a toe, foot, or part of a leg.

Taking care of your feet.

Wash your feet in warm water every day. Make sure the water is not too hot by testing the temperature with your elbow. Do not soak your feet. Dry your feet well, especially between your toes.

Look at your feet every day to check for cuts, sores, blisters, redness, calluses, or other problems. Checking every day is even more important if you have nerve damage or poor blood flow. If you cannot bend over or pull your feet up to check them, use a mirror. If you cannot see well, ask someone else to check your feet.

If your skin is dry, rub lotion on your feet after you wash and dry them. Do not put lotion between your toes

File corns and calluses gently with an emery board or pumice stone. Do this after your bath or shower.

Cut your toenails once a week or when needed. Cut toenails when they are soft from washing. Cut them to the shape of the toe and not too short. File the edges with an emery board.

Always wear shoes or slippers to protect your feet from injuries.

Always wear socks or stockings to avoid blisters. Do not wear socks or knee-high stockings that are too tight below your knee.

Wear shoes that fit well. Shop for shoes at the end of the day when your feet are bigger. Break in shoes slowly. Wear them 1 to 2 hours each day for the first 1 to 2 weeks.

Before putting your shoes on, feel the insides to make sure they have no sharp edges or objects that might injure your feet.

Tell your doctor right away about any foot problems.

Ask your doctor to look at your feet at each diabetes checkup. To make sure your doctor checks your feet, take off your shoes and socks before your doctor comes into the room.

Ask your doctor to check how well the nerves in your feet sense feeling.

Ask your doctor to check how well blood is flowing to your legs and feet.

Ask your doctor to show you the best way to trim your toenails. Ask what lotion or cream to use on your legs and feet.

If you cannot cut your toenails or you have a foot problem, ask your doctor to send you to a foot doctor (podiatrist).

Make sure you wear shoes that fit well. Special shoes can be made to fit softly around your sore feet or feet that have changed shape. These special shoes help protect your feet. Medicare and other health insurance programs may pay for special shoes. Talk to your doctor about how and where to get them.

Extracted and adapted from: The National Diabetes Information Clearinghouse (NDIC), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). NIH Publication No. 06-4282. March 2006. This publication is not copyrighted.

The Dangers of Diabetes Patients Not Understanding Disease Risks

Written by Kevin Flatt

Diabetic neuropathy is the medical term for damage to the nervous system from diabetes. Having high blood glucose for many years can damage the blood vessels that bring oxygen to some nerves. High blood glucose can also hurt the covering on the nerves. In people with diabetes, damaged nerves may stop sending messages. Or they may send messages too slowly or at the wrong times.

The majority of people with diabetes have never heard of diabetic neuropathy - nerve damage that causes pain, numbness, or tingling in the feet and hands - researchers report.

Study author Dr. Aaron I. Vinik of the Strelitz Diabetes Research Institute in Norfolk, Virginia, told Reuters Health that the numbers are spectacular. People with neuropathy are at increased risk of foot injury and even amputation, because injuries can go unnoticed due to lack of sensation and then develop into ulcers or lesions that become infected. Even without serious injuries, diabetics with neuropathy can become hypersensitive to even the lightest touch, so that wearing socks or touching bed sheets, for example, can be very painful.

According to the American Diabetes Association, which commissioned the study, an estimated 50 percent of diabetics develop neuropathy. However, 56 percent of the people who were having symptoms had never heard of diabetic neuropathy. Nearly 1 in 7 diabetics with symptoms of neuropathy who had mentioned their symptoms to their doctors said that their doctors had not mentioned anything about a potential cause. (www.nlm.nih.gov 1/5/2005).

Peripheral nerves go to the arms, hands, legs, and feet.

Damage to these nerves can make your arms, hands, legs, or feet feel numb. Also, you might not be able to feel pain, heat, or cold when you should. You may feel shooting pains or burning or tingling, like “pins and needles.” These feelings are often worse at night. They can make it hard to sleep. Most of the time these feelings are on both sides of your body, like in both of your feet. But they can be on just one side.

Autonomic nerves help you know your blood glucose is low.

Some people take diabetes medicines that can accidentally make their blood glucose too low. Damage to the autonomic nerves can make it hard for them to feel the symptoms of hypoglycemia, also called low blood glucose. This kind of damage is more likely to happen if you have had diabetes for a long time. It can also happen if your blood glucose has been too low very often.

Autonomic nerves go from your spinal cord to your lungs, heart, stomach, intestines, bladder, and sex organs.

Damage to these nerves can make food pass through the digestive system too slowly or too quickly. Nerve problems can cause nausea (feeling sick to your stomach), vomiting, constipation, or diarrhea. Nerve damage to your stomach is called gastroparesis. When nerves to the stomach are damaged, the muscles of the stomach do not work well and food may stay in the stomach too long. Gastroparesis makes it hard to keep blood glucose under control.


Other possible consequences of damage to the autonomic nerves:

Erectile dysfunction or impotence. Many men who have had diabetes for many years experience it. In the case of a woman this damage can prevent a woman’s vagina from getting wet when she wants to have sex. A woman might also have less feeling around her vagina.

Might make your heart beat faster or at different speeds.

Nerves leading to the bladder can make it hard to know when you should go to the bathroom. The damage can also make it hard to feel when your bladder is empty. Both problems can cause you to hold urine for too long, which can lead to bladder infections. Another problem can be leaking drops of urine accidentally.

Nerves to the blood vessels that keep your blood pressure steady. Damage to these nerves makes your blood move too slowly to keep your blood pressure steady when you change position. When you go from lying down to standing up or when you exercise a lot, the sudden changes in blood pressure can make you dizzy.

Cranial nerves go from your brain to your eyes, mouth, ears, and other parts of your head.

Damage to these nerves usually happens in one eye, causing double vision. This problem happens all of a sudden and usually lasts for a short time.

Damage to these nerves usually happens on only one side of the face. This nerve damage causes that side of the face to hang lower or sag. Usually the lower eyelid and lips sag. This problem is called Bell’s palsy. It happens all of a sudden and tends to correct itself.

How do I know if I have nerve damage?

If you have one or more of the problems mentioned above, you may have some nerve damage from diabetes. Tell your doctor about the problem. Ask your doctor what you can do to make the problem better and to stop it from getting worse.

This article was in part adapted from: The National Diabetes Information Clearinghouse (NDIC) NIH Publication No. 06–4284, March 2006. This publication is not copyrighted.

Smoking and Lung Damage and Emphysema - The Vitamin A Link

Written by Kevin Flatt

Vitamin A is required to protect the cells that line the airways (and other cells) from infection and the harmful effects of carcinogens (cancer causing substances). It is these cells first line of defence and functions as a barrier against infection and maintains their integrity and function.

Please note I do not advocate or support smoking. However, as many people find it very difficult to quit, any information that may help prevent damage caused by smoking should be presented.

In 1991 researchers T.E. Edes and colleagues reporting in the journal Nutrition and Cancer hypothesized that depletion of vitamin A can be induced by exposure to carcinogens (cancer causing substances) such as benzopyrene found in cigarette smoke.

The study was designed to determine if benzopyrene exposure depletes tissue vitamin A and whether beta-carotene might prevent the depletion. Rats were fed a diet containing benzopyrene supplemented with or without beta-carotene.

The authors noted there was a decline in tissue retinol (vitamin A) in the liver and small intestine by two weeks, with a 30% decline by four weeks. But, in the case of the rats fed beta-carotene, there was no effect of benzopyrene on tissue vitamin A levels. A note of interest is that the benzopyrene had no effect on serum (blood) vitamin A levels in both groups of rats during four weeks.

The authors concluded that a high intake of beta-carotene prevented the vitamin A depletion effect of benzopyrene exposure. They went on to say, “Further studies appear warranted to determine whether some of the adverse effects of environmental carcinogens, as found in cigarette smoke, charcoal-broiled meats, and industrial wastes, might be alleviated by dietary intervention.” (Nutrition and Cancer. 1991;15(2):159-66.).

In 1993 Edes and a colleague at the Harry S. Truman Memorial Veterans Affairs Hospital, Columbia, Missouri, reported in a review that exposure to benzopyrene, a carcinogen (cancer causing substance) promotes vitamin A depletion in exposed tissues.

They noted that the effect is apparent while on a vitamin A sufficient diet but significantly, without a decline in serum (blood) Vitamin A. In other words, benzopyrene depleted vitamin A even when the diet was adequate in the vitamin, and this depletion is not apparent in blood tests.

Reviewing the studies to date they observed that although these studies involved dietary intake of benzopyrene, it would be realistic to surmise cigarette smoke exposure “would have a similar effect in the lungs and perhaps stomach and bladder.”

ScienceDaily reported on July 28, 2004 that while studying the relationship between vitamin A, lung inflammation, and emphysema, Richard Baybutt, associate professor of human nutrition at Kansas State University, made a surprising discovery: a link between vitamin A and emphysema in smokers. He found that a common carcinogen in cigarette smoke, benzo(a)pyrene, induces vitamin A deficiency.

In his initial research, Baybutt took just weaned male rats and divided them into two groups, one of which was exposed to cigarette smoke, and the other to air. In the rats exposed to cigarette smoke, levels of vitamin A dropped significantly in direct correlation with their development of emphysema.

The ScienceDaily article quoted Baybutt: “When the lung content of vitamin A was low, the score of emphysema was high,” he said. “So, the hypothesis is that smokers develop emphysema because of a vitamin A deficiency.”

In the second study, both groups of rats were exposed to cigarette smoke, but one group was given a diet rich in vitamin A. Among those rats receiving the vitamin A-rich foods, emphysema was effectively reduced.

Baybutt believes vitamin A’s protective effects may help explain why some smokers do not develop emphysema.

The ScienceDaily report further quoted Baybutt: “There are a lot of people who live to be 90 years old and are smokers,” he said. “Why? Probably because of their diet…The implications are that those who start smoking at an early age are more likely to become vitamin A deficient and develop complications associated with cancer and emphysema. And if they have a poor diet, forget it.”

In this study published in The Journal of Nutrition, Ting Li, Richard Baybutt and colleagues stated: “We showed previously that vitamin A deficiency per se causes emphysema. Benzo(a)pyrene, a constituent in cigarette smoke, induces vitamin A depletion when administered to rats; therefore, we tested the hypothesis that cigarette smoke induces vitamin A depletion, which is associated with the development of emphysema.”

They noted that Vitamin A levels decreased significantly in serum, lung and liver of smoke-treated rats. The researchers’ conclusion: Exposure to cigarette smoke induces vitamin A depletion in rats, which is associated with the development of emphysema. (The Journal of Nutrition August 1, 2003; 133(8): 2629 - 2634.)

It is worth noting that marijuana smoke contains more of the cancer causing substance (and vitamin A depleting) chemical benzopyrene than tobacco smoke. An average marijuana cigarette contains 30 nanograms of this carcinogen, compared to 21 nanograms in an average tobacco cigarette. (Marijuana and Health, National Academy of Sciences, Institute of Medicine report, 1982.)

Once again, let me reiterate that I am in no way promoting smoking! If any damage can be prevented in those who cannot quit and those around them, then the information may help save lives and government costs – not to mention the trauma suffered by families of people with emphysema. Also note that benzopyrene is not exclusive to cigarettes.

Smoking is not the only source of benzopyrene

Benzopyrene is found in coal tar (coal tar may be found in shampoos and hair dyes), in automobile exhaust fumes (especially from diesel engines), tobacco smoke, and in charbroiled food. Recent studies have revealed that levels of benzopyrene in burnt toast are significantly higher than once thought, although it is unproven whether burnt toast is itself carcinogenic.

A 2001 National Cancer Institute study found levels of benzopyrene to be significantly higher in foods that were cooked well-done on the barbecue, particularly steaks, chicken with skin, and hamburgers. Japanese scientists showed that cooked beef contains mutagens, chemicals that are capable of altering the chemical structure of DNA.

Related articles:

Smoking - Vitamin A and Emphysema


References

Journal of Nutrition (Vols. 130 and 133).

McCullough, F. et al. The effect of vitamin A on epithelial integrity. Proceedings of the Nutrition Society. 1999; volume 58: pages 289-293.

Edes TE, Gysbers DG, Buckley CS, Thornton WH Jr. Exposure to the carcinogen benzopyrene depletes tissue vitamin A: beta-carotene prevents depletion. Nutr Cancer. 1991;15(2):159-66.

Edes TE, Gysbers DS. Carcinogen-induced tissue vitamin A depletion. Potential protective advantages of beta-carotene. Ann N Y Acad Sci. 1993 May 28;686:203-11; discussion 211-2. Review.

Wikipedia, the free encyclopedia.

Copyright 2007 Kevin Flatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Cinnamon lowers cholesterol and triglycerides

Written by Kevin Flatt

Cinnamon has been demonstrated to improve blood sugar, triglycerides, LDL (bad) cholesterol, and total cholesterol in a number of studies. Although these studies have involved volunteers with type 2 diabetes, the focus of this article is on the effects of cinnamon on cholesterol and triglycerides.

Researchers have sought out nutrients that can simultaneously improve glucose metabolism and lipid levels (cholesterol, triglycerides). Cinnamon has proved to be such a dual-action agent.

Agricultural Research Service chemist Richard A. Anderson and co-workers at the Beltsville (Maryland) Human Nutrition Research Center, analyzed plants and spices used in folk medicine and found that a few spices (especially cinnamon) made fat cells much more responsive to insulin, the hormone that regulates sugar metabolism (the process in which cells convert glucose to energy) and thus controls the level of glucose in the blood. (Judy McBride, Agricultural Research July 2000).

“If you can improve insulin function the cholesterol goes down, triglycerides go down, glucose goes down, and all this goes towards the alleviation of type 2 diabetes,” said Richard A. Anderson, a research chemist with the nutrient requirements and functions laboratory at the U.S. Department of Agriculture in Beltsville, Md. (HealthDay News 5/4/06).

Dr. Anderson’s personal 60-point decline in total cholesterol occurred only after he switched from sprinkling cinnamon on his breakfast cereal to taking it in a capsule. Saliva contains a chemical harmful to cinnamon rendering it ineffective. (Medical News Today 9/4/2006).

A study, published in the December 2003 issue of Diabetes Care, demonstrated that in people with type 2 diabetes, consuming as little as 1 gram of cinnamon per day was found to reduce blood sugar, triglycerides, LDL (bad) cholesterol, and total cholesterol. One gram is the equivalent of about a half a teaspoon.

The study was conducted in Pakistan and was organised by Alam Khan, a postdoctoral fellow in Dr. Anderson’s lab. Sixty volunteers (30 men and 30 women) with type 2 diabetes were divided into six groups. The first three groups consumed 1, 3, or 6 grams of cinnamon daily for 40 days, while the other three groups consumed equivalent numbers of placebo capsules (sugar pills).

In the groups taking cinnamon, it lowered blood levels of fats and “bad” cholesterol, which are also partly controlled by insulin. Triglycerides were lowered by 23-30%, LDL cholesterol 7-27% and total cholesterol 12-26% depending on the dose (i.e. 1, 3, or 6 grams per day). No significant changes were seen in those groups receiving a placebo (sugar pill). LDL cholesterol and total cholesterol levels continued to decline throughout the following 20 days after cinnamon use was stopped. (Diabetes Care. 2003 Dec;26(12):3215-8).

Only a little cinnamon was necessary, said Anderson, who helped conduct the study. He calls its medicinal properties the most significant nutritional discovery in 25 years. “I don’t know of anything else,” he said, other than drugs, “that can change glucose, triglycerides and cholesterol levels nearly so much.” (Medical News Today 30/1/2004).

A study conducted in Korea and published in the October 2006 issue of the Journal of Ethnopharmacology demonstrated that cinnamon extract fed to diabetic rats in different dosages (50, 100, 150 and 200 mg per kg) for 6 weeks blood insulin levels and HDL (good) cholesterol levels were significantly higher. Triglycerides and total cholesterol were also significantly lower. (Journal of Ethnopharmacology 2006 Mar 8;104(1-2):119-23. Epub 2005 Oct 5).

Anderson has cautioned, however, that consumers should not simply start dousing their food with cinnamon [at high doses]. He noted, for example, that cinnamon in powder form is rendered ineffective by contact with saliva, and its lack of solubility in water can result in an unwanted build up of the spice in the body. “But I certainly think there are things people can do,” he added. “We recommend you add cinnamon to your coffee before you grind it, as this eliminates, in essence, the toxic components of cinnamon. Or you can use cinnamon sticks to make tea in hot water, which does the same thing. Or you can buy the cinnamon capsules in the store with the water-soluble extract in the equivalent of 1/4 to 1/2 teaspoons twice a day.” (HealthDay News 5/4/06).

Remember that Dr. Anderson’s personal 60-point decline in total cholesterol occurred only after he switched from sprinkling cinnamon on his breakfast cereal to taking it in a capsule. Saliva contains a chemical harmful to cinnamon rendering it ineffective.

References

Khan A, Safdar M, Ali Khan MM, Khattak KN, Anderson RA. Cinnamon improves glucose and lipids of people with type 2 diabetes. Diabetes Care. 2003 Dec;26(12):3215-8.

Kim SH, Hyun SH, Choung SY. Anti-diabetic effect of cinnamon extract on blood glucose in db/db mice. J Ethnopharmacol. 2006 Mar 8;104(1-2):119-23. Epub 2005 Oct 5.


Copyright 2007 Kevin Flatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Diabetes: Cloves improve insulin function, lowers glucose

By Kevin Flatt

One of two studies presented at the Experimental Biology 2006 meeting, in San Francisco, demonstrated that extracts of cloves were found to improve the function of insulin and to lower glucose, total cholesterol, LDL and triglycerides in people with type 2 diabetes.

Earlier studies had shown these positive effects in laboratory studies; the study presented at Experimental Biology provides the first evidence of these beneficial effects in humans taking the equivalent of one to two cloves per day. Dr. Alam Khan, Agricultural University, Peshawar, Pakistan, a former postdoctoral student and Fulbright Fellow in the Anderson laboratory, reports the first study of the effect of cloves on insulin function in humans. (Medical News Today 9/4/2006).

The clove study involved 36 men and women diagnosed with type 2 diabetes. Three groups of patients consumed either one, two or three grams of cloves for 30 days in capsule form, while a fourth consumed none of the spice. At the end of the study, regardless of the amount of cloves consumed, all those who ingested cloves showed a drop in glucose, triglycerides and LDL (“bad”) cholesterol levels. Blood levels of HDL (“good”) cholesterol were not affected among the clove eaters. Those who did not ingest cloves experienced no changes. (HealthDay News 5/4/2006).

Dr. Khan says the finding that intake of 1 to 3 grams of cloves per day lowered risk factors of diabetes without changing HDL [cholesterol] concentration suggest strongly that cloves are beneficial for people with type 2 diabetes. (Medical News Today 9/4/2006).

“The people who would benefit the most are those who have impairments in their blood sugar,” said Anderson. “These are the 40 million people with metabolic syndrome who are pre-diabetic, people with type 2 diabetes, and even the severely diabetic and the severely overweight - although they may not benefit as much because the impairments in their insulin are much, much worse.” (HealthDay News 5/4/2006).

Co-authors of the study in addition to Dr. Khan and Dr. Anderson are Dr. Syed Saceed Qadir, Agricultural University, Peshawar, Pakistan, and Dr. Khan Nawaz Khattak, HMC, Hayatabad, Peshawar, Pakistan. The research was supported by the Higher Education Commission of Pakistan.

“This abstract extends this work to humans and demonstrates that consumption of as little as 1 g of cloves by people with type 2 diabetes leads to improvements in blood sugar, insulin, cholesterol, and triglycerides,” Anderson commented. “The major contribution of this study is that it demonstrated that consumption of cloves may be important in the alleviation of diabetes and cardiovascular diseases in humans.” (Medscape Medical News April 4, 2006).

Cloves contains significant amounts of an active component called eugenol, which has made it the subject of numerous health studies, including studies on the prevention of toxicity from environmental pollutants like carbon tetrachloride, digestive tract cancers, and joint inflammation. Clove also contains a variety of flavonoids, including kaempferol and rhamnetin, which also contribute to clove’s anti-inflammatory (and antioxidant) properties. Cloves are an excellent source of manganese, a very good source of dietary fiber, vitamin C and omega-3 fatty acids and a good source of calcium and magnesium. (WHF The George Mateljan Foundation).

Indian researchers, reporting in the journal Prostaglandins, Leukotrienes, and Essential Fatty Acids in 2000, compared the antioxidant properties of seven spice extracts (garlic, ginger, onion, mint, cloves, cinnamon and pepper). They found the highest antioxidant activities in cloves, followed by cinnamon, pepper, ginger, garlic, mint and onion. The antioxidant activity of these spice extracts were retained even after boiling for 30 min at 100 degrees C, indicating that the active components are not destroyed by heat. (Prostaglandins, Leukotrienes, and Essential Fatty Acids 2000 Feb;62(2):107-10).

References

http://www.medicalnewstoday.com

http://www.healthday.com

Shobana S, Naidu KA. Antioxidant activity of selected Indian spices. Prostaglandins Leukot Essent Fatty Acids. 2000 Feb;62(2):107-10.

http://www.whfoods.com

Copyright 2007 Kevin Flatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.

Vitamin D protects against prostate cancer & increases survival rates

Written by Kevin Flatt

Natural Sunlight Helps Prevent Prostate Cancer and Increases Survival. The fat-soluble vitamins A and D have both been found to affect the growth of prostate cancer in preclinical experiments. Of the two, vitamin D has been the focus of greater attention in recent years, and there are indications that it may be useful both in the prevention and treatment of prostate cancer. (Semin Urol Oncol. 1999 May;17(2):77-84).

“…the cells treated with Vitamin D fared much better. And while the vitamin protects healthy cells, Rebecca Mason’s experiments are showing that Vitamin D has the opposite effect on cancer cells. It kills them.” - Professor Michael Holick.

It was reported on 18 Sep 2005 that sunshine may protect against prostate cancer. The findings appear in the June issue of Cancer Research. “It’s a pretty impressive finding,” Gary G. Schwartz, one of the researchers in the study, told WebMD. “Men with high solar exposure had their risk of prostate cancer cut in half. This leaves us with even greater confidence that vitamin D deficiency really does increase a man’s risk of prostate cancer.” Unlike other vitamins, a person’s main source of vitamin D isn’t food; it’s sunshine. The body makes its own vitamin D, but only when it’s exposed to the sun. (http://www.cbsnews.com/stories/2005/06/15/health/webmd/main.shtml).

Reduced risk of advanced prostate cancer was associated with high sun exposure determined by reflectometry and high occupational outdoor activity. (Cancer Res. 2005 Jun 15;65(12):5470-9).

Back in 1992, Hanchette and Schwartz analyzed American prostate cancer deaths in relation to sunlight and discovered a negative correlation, a very significant association. That is, they found that men who received more sunlight were less likely to die from prostate cancer. (Cancer. 1992 Dec 15;70(12):2861-9).

In the same year, Schwartz discovered that death rates from prostate cancer were correlated with death rates from multiple sclerosis, another disease know to be associated with lack of sunlight. Again, he proposed that lack of vitamin D may a causative factor in both diseases. (Neuroepidemiology. 1992;11(4-6):244-54).

In 2000, Ahonen and colleagues conducted a careful study of calcidiol levels in young men and followed them for the development of prostate cancer. (Calcitriol is the active form of vitamin D, the form made in optimal quantities by your body when your vitamin D blood levels are ideal). He found a relationship between low vitamin D blood levels and prostate cancer. Ahonen found young men with calcidiol levels below 40 nm/L (16 ng/ml) were three times more likely to develop prostate cancer than were men with higher levels. Just as important, he found these men were six times more likely to develop invasive cancers. This finding implied a treatment effect for vitamin D as the prevention of invasiveness is a key goal of treatment. (Cancer Causes Control. 2000 Oct;11(9):847-52).

In 2001, Luscombe and colleagues at the School of Medicine in North Straffordshire Hospital in England published three studies linking ultraviolet exposure and skin type to the development of prostate cancer. They found that cumulative outdoor sun exposure, outdoor occupations and skin type was associated with reduced risk of advanced stage tumours. They also found that childhood sunburns dramatically reduced the risk of developing prostate cancer, probably because those with fair skin are more likely to burn but also find it easier to make vitamin D in their skin. Furthermore, they found that people who have difficulty making a skin pigment called melanin (a natural sun screen) are much less likely to develop prostate cancer. (Br J Cancer. 2001 Nov 16;85(10):1504-9 and Carcinogenesis. 2001 Sep;22(9):1343-7 and Lancet. 2001 Aug 25;):641-2).

In 2003, Chen and Holick at Boston University School of Medicine called for the use of vitamin D in prostate cancer. After reviewing most of the research on the subject, the authors concluded, "adequate exposure to sunlight or oral supplementation might provide a simple way to increase synthesis of calcitriol in the prostate and, therefore, decrease the risk of prostate cancer." They added, “adequate vitamin D nutrition should be maintained, not only for bone health in men and women, but because it might decrease the risk of prostate cancer and mitigate metastatic disease should it develop.” (Trends Endocrinol Metab. 2003 Nov;14(9):423-30).

In 2003, Bodiwala and colleagues in England studied sun exposure and skin type and again found that men who sunbathed or otherwise exposed themselves to sunlight were less likely to develop prostate cancer. They also identified men with various combinations of skin type and reduced sun exposure, which were up to 13 times more likely to develop prostate cancer. Those with fair skin seemed to obtain equal protection with less sun exposure that the other skin types, probably because those with fair skin find it easier to make vitamin D in their skin. (Cancer Lett. 2003 Oct 28;200(2):141-8 and Carcinogenesis. 2003 Apr;24(4):711-7 and Cancer Lett. 2003 Mar 31;192(2):145-9).

In 2004 researchers in Norway showed that patients diagnosed with prostate cancer in the summer and autumn, when vitamin D levels are the highest, have a significantly better prognosis than patients diagnosed in the winter or spring. The authors concluded that their “study supports the hypothesis that vitamin D may influence cancer specific mortality in a beneficial way. A possible mechanism to explain our results might be a combined action of vitamin D and cancer treatment that amplifies the treatment effect. In confirmed, in addition to traditional cancer treatment, vitamin D would be of particular importance in the primary prevention of deaths from cancer.” (Cancer Causes Control. 2004 Mar;15(2):149-58).

Medical News Today reported on 18 Sep 2005 that Scientists reporting in the journal Photochemisty and Photobiology estimated that about 50,000-63,000 annual cancer deaths in the U.S. (10% of all cancer deaths) could be prevented if all Americans had sufficient vitamin D. These findings are based on data in the Atlas of Cancer Mortality Rates for the United States, , (cancer.gov/atlasplus/type.html), but are also supported by a number of recent reports that vitamin D plays a very important role in increasing survival once cancer is discovered. These deaths greatly outnumber the annual number of deaths from melanoma (8000) and skin cancer (2000). (Medical News Today 18 Sep 2005).

Leading vitamin D researchers are suggesting that the optimum adult level seems to be 4,000 daily units which is 20 times the government level for those 50 and under. The government says 2,000 is the limit for all ages before side-effects result. The researchers disagree and say amounts considerably above 2,000 units may be warranted when considering the multitude of potential benefits. (CBN News 10/1/2007).

Make sure you’re taking D3. If the label says vitamin D2, then it’s not the good kind of vitamin D. So often, you see orange juice or foods that say they’re vitamin D fortified. But many times, those are fortified with D2. Vitamin D has to be taken with fat. Taking a vitamin D pill with orange juice isn’t going to work, it won’t absorb.

Try to get brand-name recommendations. Sadly, many doctors haven’t learned about supplements in medical school, so your doctor may not be able to advise you on that. To find the best brands, do your homework. Either get names of products from people you trust, or go on the Internet and look these supplements up.

Typically, dieticians say the best source of vitamins is through the foods we eat, rather than supplements. But Judy Carr, a registered dietician and certified diabetes educator says the best food sources of vitamin D aren’t necessarily the foods we love. In December, after reading a little more about the vitamin, Carr asked her doctor to include a vitamin D analysis with her routine blood work. She was surprised when her results came back showing her levels were on the low end of normal. “I’m thinking if that’s me, because I don’t have a horrible diet, I can’t imagine what the general population’s is,” Carr says. (Denver Post 14/2/2007).

Dr. Michael Holick, a leading vitamin D researcher who serves as director of the general clinical research center at Boston University Medical Center, said it’s difficult to get enough vitamin D from food, noting that you’d have to eat a 3½-ounce serving of fish like salmon, mackerel or sardines “almost every day just to begin to satisfy your requirement.”

The NIH agrees. It can be difficult to obtain enough vitamin D from natural food sources. For many people, consuming vitamin D fortified foods and adequate sunlight exposure are essential for maintaining a healthy vitamin D status. In some groups, dietary supplements may be needed to meet the daily need for vitamin D.

A tablespoon of cod-liver oil contains more than 1,300 IUs. Salmon (360 IUs for 3.5 ounces), sardines (250 IUs for 13/4 ounces) and fortified milk (about 100 IUs per serving) are also good sources.

No matter what cancer you have, or are trying to prevent, the real question is should cancer patients be left vitamin D deficient? Many experts will tell you that vitamin D should not be taken for breast cancer or prostate cancer until well controlled scientific studies prove it helps. The problem with that approach is two-fold. First, you may die waiting for the studies to be conducted and two, it misses the point. The point is this: women with breast cancer should not allow themselves to be vitamin D deficient and neither should their doctors. (vitamindcouncil.com).

Finally, I’ve always thought that it’s pretty significant that the parts of the body least exposed to the sun are more likely to experience a malignant melanoma.

But a new look at 528 melanoma victims over five years also found that increased sun exposure led to increased survivability, according to the study led by Marianne Berwick of the department of internal medicine at the University of New Mexico. “It’s totally counterintuitive, and we’re trying to investigate it,” said Berwick, who is doing a similar study of 3,700 melanoma patients worldwide. “It’s really strange, because sunburn seems to be one of the factors associated with improved survival.” (The Baltimore Sun 2/2/2005).

Related articles:
Cancer (General) Articles and News

The Multitude of Health Benefits from Natural Sunlight and Vitamin D

References

Konety BR, Johnson CS, Trump DL, Getzenberg RH. Vitamin D in the prevention and treatment of prostate cancer. Semin Urol Oncol. 1999 May;17(2):77-84

http://www.abc.net.au/catalyst/stories/s.htm

John EM, Schwartz GG, Koo J, Van Den Berg D, Ingles SA. Sun exposure, vitamin D receptor gene polymorphisms, and risk of advanced prostate cancer. Cancer Res. 2005 Jun 15;65(12):5470-9.

Hanchette CL, Schwartz GG. Geographic patterns of prostate cancer mortality. Evidence for a protective effect of ultraviolet radiation. Cancer. 1992 Dec 15;70(12):2861-9.

Schwartz GG. Multiple sclerosis and prostate cancer: what do their similar geographies suggest? Neuroepidemiology. 1992;11(4-6):244-54.

Ahonen MH, Tenkanen L, Teppo L, Hakama M, Tuohimaa P. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels (Finland). Cancer Causes Control. 2000 Oct;11(9):847-52.

http://vitamindcouncil.com

Luscombe CJ, French ME, Liu S, Saxby MF, Jones PW, Fryer AA, Strange RC. Prostate cancer risk: associations with ultraviolet radiation, tyrosinase and melanocortin-1 receptor genotypes. Br J Cancer. 2001 Nov 16;85(10):1504-9.

Luscombe CJ, French ME, Liu S, Saxby MF, Jones PW, Fryer AA, Strange RC. Outcome in prostate cancer associations with skin type and polymorphism in pigmentation-related genes. Carcinogenesis. 2001 Sep;22(9):1343-7.

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Copyright 2007 KevinFlatt. Disclaimer: The information contained in this article is presented for information purposes only and is in no way intended to replace professional medical care or attention by a qualified practitioner. It cannot and should not be used as a basis for diagnosis or choice of treatment.