Category Archives: Causes of Diabetes

June 21, 2010 · 2:00 AM

Does Lipid Overload Cause Diabetes?

An up-and-coming theory to explain type 2 diabetes suggests that abnormal lipid metabolism, not glucose/sugar metabolism, is the primary metabolic defect.  Roger H. Unger, M.D., wrote about this in the March 12, 2008, issue of the Journal of the American Medical Association.

Early in the writing of this blog entry, I realized it is much too technical for most of my readers.  If you are not interested in physiology, you can quit reading now.  It’s OK  . . . really.  This may be the most boring blog post of mine you have ever read.  I’m writing this to solidify my own understanding of a new theory.

I assure you my prose in The Advanced Mediterranean Diet weight-loss book is not nearly this technical.

Still with me?  [Get out now while you’re still awake!] 

Definitions and Physiology

Diabetes is defined by high blood glucose (sugar) levels. 

ResearchBlogging.orgThe lipid family includes triglycerides (fats and oils), sterols (e.g., cholesterol), and phospholipids (e.g., lecithin, a major cell membrane component).  Fats are almost entirely composed of trigylcerides.  When fats are broken down, fatty acids are produced.  On the other hand, fatty acids can be joined together, along with glycerol, to form triglycerides. 

Glycogen is a storage form of glucose in liver and muscle tissue.  In olden days, some called it “animal starch.” 

Insulin is a protein hormone produced by pancreatic beta cells.  Insulin has multiple actions, not just blood sugar lowering:  

  1. lowers blood glucose levels by driving glucose into cells
  2. inhibits breakdown of glycogen into glucose
  3. inhibits formation of new glucose molecules by the body
  4. stimulates glycogen formation
  5. promotes storage of triglycerides in fat cells (i.e., lipogenesis, fat accumulation)
  6. promotes formation of fatty acids (triglyceride building blocks) by the liver
  7. inhibits breakdown of stored triglycerides
  8. supports protein synthesis 

Fatty acids in muscle tissue block the uptake of glucose from the bloodstream by muscle cells.  Fatty acids in liver tissue impair the ability of insulin to suppress breakdown of glycogen into glucose, and impairs the ability of insulin to suppress production of new glucose molecules.  In other words, an “excessive fatty acid” environment in liver and muscle tissue promotes elevated glucose levels.

Got that?  [This is very difficult material.]  Now on to . . . 

The Lipocentric Theory of Type 2 Diabetes

Type 2 diabetes may be caused by:

  1. Eating too many calories [especially carbohydrates?], leading to…
  2. High insulin levels, leading to…
  3. Stimulation of fat production, leading to…
  4. Increased body fat, leading to…
  5. Deposition of lipids in cells where they don’t belong (that is, not in fat cells), leading to…
  6. Resistance to insulin’s effects on glucose metabolism, leading to…
  7. Lipid accumulation in pancreatic beta cells, damaging them, leading to…
  8. Elevated blood glucose levels, i.e., diabetes.

Perhaps the key to understanding this is to know that “insulin resistance” refers to insulin having less ability to suppress glucose production by the liver, or less ability of various tissues to soak up circulating glucose.  Insulin resistance thereby leads to elevated glucose levels.  But insulin’s effect of “producing fats” (lipogenesis) continues unabated.  Excessive fats, actually fatty acids, accumulate not only in fat cells, but also in liver cells, muscle cells, pancreatic beta cells, and others.  This lipid overload can damage those cells.

If This Theory Is Correct, So What?

Steps #1 and 2 of the lipocentric theory involve excessive caloric intake and high circulating insulin levels, leading to problems down the road.  So overweight people should restrict calories and try to lose at least a modest amount of weight.  Particularly if already having type 2 diabetes or prone to it.   

And what about people with type 2 diabetes who have insulin resistance and have poorly controlled glucose levels?  Most of these have high insulin levels already, contributing to a fat-producing state.  Adding more insulin, by injection, wouldn’t seem to make much sense if there are other alternatives.  The extra insulin would bring glucose levels down, but might also cause lipid overload with associated cellular damage. 

Effective clinical strategies according to Dr. Unger would include 1) caloric restriction, which helps reduce weight, high insulin levels, and fat production, and 2) if #1 fails, add anti-diabetic drugs that reduce caloric intake [exenatide?], that reduce lipid overload [which drug?], or that do both.  

Dr. Unger suggests consideration of bariatric surgery, for caloric restriction and cure of diabetes.

Compared with dietary fats and proteins, carbohydrates generally cause higher circulating insulin levels.  And type 2 diabetics taking insulin shots need higher doses for higher intakes of carbohydrate.  So it makes sense to me to consider preferential reduction of carbohydrate consumption if someone’s going to reduce caloric intake.

Dr. Unger and I agree that reduction of excessive food intake and excess body fat is critically important for overweight people with type 2 diabetes.

Steve Parker, M.D.

References: Unger, R. (2008). Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention JAMA: The Journal of the American Medical Association, 299 (10), 1185-1187 DOI: 10.1001/jama.299.10.1185

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June 18, 2010 · 2:00 AM

Sugar-Sweetened Beverages: Bane of Mankind?

Over the last 30 years in the U.S., consumption of sugar-sweetened beverages (SSBs) has increased from3.9% of total calories to 9.2% (in 2001).  In that same time span, the percentage of overweight American adults increased from 47% to 66%.  The obesity percentage rose from15 to 33% of adults. 

[Did the beverages cause the weight gain, or are they just associated?] 

Those are just a few of the many facts shared by the authors of “Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk,” published recently in Circulation.  Sugar-sweetened beverages, by the way, include soft drinks, fruit drinks, energy drinks, and vitamin water drinks. 

ResearchBlogging.orgSounds like an interesting article, doesn’t it?  It’s written by some of the brightest lights in nutritional science, including George Bray and Frank Hu.  Unfortunately, the article is a little too boring and technical for most of my readers.  Here are a few tidbits I enjoyed:

  • Fructose (found in similar amounts in sucrose (table sugar) and high fructose corn syrup) may particularly predispose us to deposit fat in and around our internal abdominal organs (“visceral fat,” which some believe to be more unhealthy than fat  in our buttocks or thighs).
  • Fructose may also lead to fat deposits in cells other than fat cells, potentially interfering with cell function.
  • Fructose may adversely affect lipid metabolism (higher triglyceride levels and lower HDL levels, which could promote heart disease).
  • Fructose raises blood pressure and reduces insulin sensitivity.
  • In the liver, fructose is preferentially converted to lipid, causing high triglyceride levels (associated with heart disease and insulin resistance).  [The authors did not mention the common condition of “fatty liver” (aka hepatic steatosis) in this context.]

Some of the authors conclusions:

  • SSBs are the largest contributor to added-sugar intake in the U.S.
  • SSBs contribute to weight gain.
  • SSBs may cause type 2 diabetes and cardiovascular disease—separate from their effect on obesity—via high glycemic load and increased fructose metabolism, in turn leading to insulin resistance, inflammation, pancreas beta cell impairment, high blood pressure, visceral fat build-up, and adverse effects on blood lipids.

I especially like their final sentence:

For these reasons and because they have little nutritional value, intake of SSBs should be limited, and SSBs should be replaced by healthy alternatives such as water.

Steve Parker, M.D.

Reference: Malik, V., Popkin, B., Bray, G., Despres, J., & Hu, F. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk Circulation, 121 (11), 1356-1364 DOI: 10.1161/CIRCULATIONAHA.109.876185

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April 9, 2010 · 2:00 AM

Prediabetes Ignored Way Too Often

Only half of Americans with prediabetes take steps to avoid progression to diabetes, according to a recent report in the American Journal of Preventive Medicine.

Prediabetes is defined as:

  1. fasting blood sugar between 100 and 125 mg/dl (5.56–6.94 mmol/l) or
  2. blood sugar level 140–199 mg/dl (7.78–11.06 mmol/l) two hours after drinking 75 grams of glucose

Prediabetes is a strong risk factor for development of full-blown diabetes.  It’s also associated with increased risk for cardiovascular disease such as heart attack and stroke.  One of every four adults with prediabetes develops diabetes over the next 3 to 5 years.  The progression can often be prevented by lifestyle modifications such as dietary changes, moderate-intensity exercise, and modest weight loss.  

Investigators looked at 1,402 adult participants in the 2005-2006 National Health and Nutrition Examination Survey (NHANES) who had fasting blood sugar tests and oral glucose tolerance tests diagnostic of  prediabetes.  

The researchers estimate that 30% (almost one out of every three) of the adult U.S. population had prediabetes in 2005-2006, but only 7% of them (less than one in 10) were aware they had it.

Only half of the prediabetics in this survey reported attempts at preventative lifestyle changes in the prior year.  Only one of every three prediabetics reported hearing about risk reduction advice from their healthcare provider.

People, we’ve got to do better! 

My fellow physicians, we’ve got to do better!

The U.S. Centers for Disease Control and Prevention predicts that one of every three Americans born in 2000 will develop diabetes.  The great majority of this will be type 2 diabetes.  You understand now why James Hirsch, author of Cheating Destiny, calls diabetes America’s leading public health crisis.  I agree.

Steve Parker, M.D.

Reference:  Geiss, Linda S., et al.  Diabetes risk reduction behaviors among U.S. adults with prediabetes.  American Journal of Preventive Medicine, 38 (2010): 403-409.

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February 8, 2010 · 2:00 AM

You Know About Insulin. And Now, the REST of the Story . . .

When we digest carbohydrates, blood sugar rises.  If it goes too high it causes problems.  Everybody knows that insulin lowers blood sugar levels, right?  Less well-known is that regulation of blood sugar is the result of complex interactions of multiple hormones, not just insulin.

[As is my habit, I will use “sugar” and “glucose” interchangeably in this post.] 

Allow me to review the main hormones involved in blood glucose regulation:

1. Insulin is made and stored in pancreas beta cells.  As a meal is digested, blood sugar rises; the pancreas releases insulin to bring blood sugar back down by driving it into cells.

2. Amylin is also made and stored in pancreas beta cells and works to reduce blood sugar levels.  Blood levels of amylin rise and fall in concert with insulin levels.  Amylin slows emptying of the stomach, reduces food consumption, and regulates another hormone—glucagon—after meals.

3. Glucagon is from pancreas alpha cells.  It works to raise blood sugar by promoting the liver’s breakdown of glycogen into glucose, and by promoting the liver’s manufacture of new glucose molecules.

4. Glucagon-like peptide -1 (GLP-1) is produced in small intestine cells and it’s main action is to promote insulin secretion by the pancreas beta cells after absorption of food, which lowers blood sugar levels.  GLP-1 (like amylin) also inhibits emptying of the stomach, inhibits glucagon release, and inhibits appetite, all of which would tend to keep a lid on blood sugar levels. 

5. Gastric inhibitory polypeptide (GIP) promotes secretion of insulin following absorption of food.  GIP is also known as glucose-dependent insulinotropic polypeptide.

You can see that some hormonal mechanisms raise glucose levels; others lower glucose levels.  Homeostasis is all about reaching a happy medium between the two, without wild swings one way or the other.  In healthy people, eating food leads to release of gastrointestinal peptides (GLP-1 and GIP), insulin, and amylin.  The interaction among them keeps blood sugar levels in a fairly level low range.  In diabetes, one or more malfunctions in the system leads to abnormally high blood sugars.

The good news is that scientists have used this knowledge to devise new, effective treatments for diabetes.  Examples are GLP-1 analogues and DPP-4 inhibitors.

Steve Parker, M.D.

PS:   In lab animals, GLP-1 stimulates formation of new pancreas beta cells, so it hold promise in halting the progressive beta cell failure characteristic of type 2 diabetes.

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January 10, 2010 · 2:00 AM

Diabetes + Overweight and Obesity = Diabesity

Mark Hyman, M.D., blogged about diabesity at the Huffington Post December 24, 2009.  He defines diabesity as a problem with glucose regulation associated with overweight and obesity.  The glucose physiology problem ranges from metabolic syndrome to prediabetes to full-blown type 2 diabetes.

“Diabesity” has been in circulation for a few years, but hasn’t caught on yet. 

What interested me about his blog post was that he advocates the Mediterranean diet as both therapeutic and prophylactic.  To quote Dr. Hyman:

The optimal diet to prevent and treat diabesity includes:

  • Fruits
  • Vegetables
  • Nuts
  • Seeds
  • Beans
  • Whole grains
  • Healthy fats such as olive oil, nuts, avocados, and omega-3 fats
  • Modest amounts of lean animal protein including small wild fish such as salmon or sardines

This is commonly known as a Mediterranean diet.  It is a diet of whole, real, fresh food. It is a diet of food you have to prepare and cook from the raw materials of nature.  And it has broad-ranging benefits for your health.

Food for thought, no doubt. 

Steve Parker, M.D.

Reference:  Hyman, Mark.  The diabesity epidemic part III:  Treating the real causes instead of the symptoms.  The Huffington Post, December 24, 2009

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December 9, 2009 · 2:00 AM

Book Review: Good Calories, Bad Calories

Here’s my  review of good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease, by Gary Taubes, 2007.  I give it five stars on Amazon.com’s five-star system (“I love it”).

♦   ♦   ♦

This brilliant book deserves much wider currency among physicians, dietitians, nutritionists, and obesity researchers.  The epidemic of overweight and obesity over the last 30 years should make us question the reigning theories of obesity treatment and prevention.  Taubes questioned those theories and pursued answers wherever the evidence led.  He shares in GCBC his eye-opening, even radical, well-reasoned findings. 

Ultimately, this tome is an indictment of the reigning scientific community and public nutrition policy-makers of the last four decades.  That explains why, twoyears after publication, this serious, scholarly work has not been reviewed by the New England Journal of Medicine, the Journal of the American Medical Association, the American Journal of Clinical Nutrition , and the Journal of the American Dietetic Association (as of August, 2009).

In Part 1, Taubes examines the scientific evidence for what he calls the fat-cholesterol hypothesis.  More commonly known as the diet-heart hypothesis, it’s the idea that dietary fat (especially saturated fat) and cholesterol clog heart arteries, causing heart attacks.  Taubes finds the evidence unconvincing.  He’s probably right.

Part 2, The Carbohydrate Hypothesis, revives and older theory from the mid-twentieth cenury that is elsewhere called the Cleave-Yudkin carbohydrate theory of dental and chronic systemic disease.  In the carbohydrate theory,  high intake of sugary foods, starches, and refined carbhohyrates leads first to dental disease (cavities, gum inflammation, periodontal disease) then, later, to obesity and type 2 diabetes, coronary heart disease, perhaps even cancer and Alzheimer’s Disease.  These are, collectively, the “diseases of civilization.”

Part 3 tackles obesity and weight regulation.  Taubes writes that “…fattening and obesity are caused by an imbalance—a dysequilibirium—in the hormonal regulation of adipose [fat] tissue and fat metabolism.”  Think of the transformation of a skinny 10-year-old girl into a voluptuous young woman.  It’s not over-eating that leads to curvaceous fat deposits, growth of mammary tissue, and increase in height; it’s hormonal changes beyond her control. 

The primary hormonal regulator of fat storage is insulin, per Taubes.  Elevated insulin levels lead to storage of food energy as fat.  Carbohydrates stimulate insulin secretion and make us fat. 

Although it’s a brilliant book, by no means do I agree with all Taubes’ conclusions.  For instance, if carbohydrates cause heart disease, why is glycemic index only very weakly associated with coronary heart disease in men?  It’s way too early to blame cancer and Alzheimers on carbohydrates.  Primitive cultures may not exhibit many of the diseases of civilization because their members die too young.  Taubes is clearly an advocate of low-carb eating.  Why didn’t he directly address the evidence that fruits, vegetables, and whole grains in the right amounts are healthy?

I have to give Taubes credit for thinking “outside the box.”  His search for answers included reviews of esoteric literature and interviews with scientists in the fields of genetics, athropology, public policy, physiologic psychology, and paleontology, to name a few.

Towards the end of the book, Taubes describes a Mediterranean-style or “prudent” diet that is popular these days.  After five years of research for his book, he says that whether a very low-carb meat diet is healthier than a prudent diet “… is still anybody’s guess.”  It’s hard for me to put aside numerous observational studies associating health benefits with legumes, fruits, vegetables, and wholegrains.  So my “guess” is that the Mediterranean-style diet is healthier.  Perhaps the answer is different for each individual.  Heck, maybe the answer is low-carb Mediterranean.  Both Taubes and I are prepared to accept either result when we have proof-positive data.    

Taubes doesn’t base his opinions on late-breaking scientific results.  Instead, his research findings mostly span from 1930 to 1980, especially 1940-1960.  Once the fat-cholesterol (diet-heart) hypothesis took root around 1960 and blossomed in the 1970s, these data were ignored by the entrenched academics and policy-makers of the day. 

To be fair, I’ve got to mention this is not light reading.  A majority of people never read another book after they graduate high school.  Of those who do, many (like me) will have to look up the definition of “tautology,” “solecism,” etc. 

I was taught in medical school years ago that “a calorie is a calorie is a calorie.”  Meaning: if you want to lose excess weight, it doesn’t matter if you cut calories from fat, protein, or carbohydrates.  I really wonder about that now.

Steve Parker, M.D 

Additional Reading

Bray, George A.  Viewpoint: Good Calories, Bad Calories by Gary Taubes.  Obesity Reviews, 9 (2008): 251-263.

Taubes, Gary.  Letter to Editor: Response to Dr. George Bray’s review of Good Calories, Bad Calories.  Obesity Reviews, 10 (2008): 96-98.

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December 7, 2009 · 2:00 AM

Are Fructose and High Fructose Corn Syrup Bad for Us?

Table sugar (sucrose) is a combination of glucose and fructose

Darya Pino earlier this month posted at her Summer Tomato blog a video regarding high fructose corn syrup.  The speaker in the video is pediatric endocrinologist Robert Lustig, M.D., of the University of California—San Francisco.
In the U.S. between 1970 and 1990, consumption of high fructose corn syrup increased over 1000%.  During those two decades, the incidence of overweight and obesity nearly doubled.  Many wonder if this is more than just coincidental. Most of this fructose is in soft drinks.  Soft drink consumption per person in 1942 was two servings per week.  In 2000, consumption was two servings per day.  Of course, these drinks typically have few nutrients other than sugars.
I wrote about fructose possibly being “the new trans fat” almost two years ago.

Dr. Lustig is convinced that high fructose corn syrup (HFCS) is a chronic toxin, at least in the amounts many of us eat, and the cause of our current epidemic of childhood and adult obesity and overweight.  Even if this idea is not new to you, you may be interested to hear the biochemistry and physiology behind his position.  If you didn’t enjoy college lectures or are not a food science geek, you probably won’t be able to sit through this 1.5-hour video. 

I enjoyed the heck out of it!  Made me feel like I was back in college again.  Few of my professors were as good as Dr. Lustig at lecturing. 

Here are a few of his other major points:

  • HFCS was invented in Japan in the 1960s, then introduced to U.S. markets in 1975
  • sucrose and fructose are both poisons
  • in the U.S. we eat 63 pounds (28.6 kg) of HFCS and 141 pounds (64.1 kg) of sugar per year [he didn’t define “sugar” in this context]
  • he praises Yudkins book, Pure, White, and Deadly [I’ve written about the Cleave-Yudkin carbohydrate theory of chronic disease]
  • the triglyceride/HDL ratio predicts heart disease much better than does LDL cholesterol
  • chronic high fructose intake causes the metabolic syndrome [does he think it’s the only cause?]
  • only the liver can metabolize fructose, in contrast to every other tissue and organ that can use glucose as an energy supply
  • high fructose consumption increases the risk of gout and high blood pressure
  • fructose interferes with production of our body’s production of nitrous oxide—a natural circulatory dilator—leading to higher blood pressures
  • fructose increases de novo lipogenesis—in other words, it creates body fat
  • fructose interferes with natural chemical messengers that tell your brain you’ve had enough food and it’s time to stop eating
  • high fructose intake reduces LDL particle size, potentially increasing the future risk of cardiovascular disease such as heart attacks [small, dense LDL cholesterol is more damaging to your arteries that large, fluffy LDL]

So What? 

You don’t need polititians to reduce your consumption of sugary soft drinks and high fructose corn syrup—do it yourself starting today.  Read food labels—HFCS is everywhere.  I’ve found it in sausage! 

The food industry greatly reduced use of trans fats in response to consumer concerns, before the polititians ever dabbled in it.  HFCS can go the same route.  Consumption of soft drinks, sports drinks, and other sugary beverages—the major sources of HFCS—is up to you.

Steve Parker, M.D.

PS: The Advanced Mediterranean Diet and Ketogenic Mediterranean Diet are naturally low in fructose.

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October 20, 2009 · 6:54 PM

Fish Consumption Linked to Type 2 Diabetes

CB064567A recent study suggests that fish intake may modestly increase the risk of developing type 2 diabetes. 

Harvard researchers examined the dietary habits of over 195,000 study participants over the course of at least 14 years.  Increasing consumption of fish and long-chain omega-3 fatty acids (mostly from fish) was linked to a higher onset of type 2 diabetes—up to 24% higher comparing the lowest with the highest consumers.

Implications

This is a preliminary research finding and requires validation by other studies.  The study authors write:

Given the beneficial effects of LCFA [long-chain fatty acids] intake on many cardiovascular disease risk factors, the clinical relevance of this relation and its possible mechanisms require further investigation.

At this point, I believe that the benefits of reasonable omega-3 fatty acid and fish consumption outweight the possible risk of developing type 2 diabetes.

Steve Parker, M.D.

References: Kaushik, M., et al.  Long-chain omega-3 atty acids, fish intake, and the risk of type 2 diabetes mellitus.  American Journal of Clinical Nutrition, 90 (2009): 613-620.

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August 5, 2009 · 4:45 AM

Dental Problems and Systemic Chronic Disease: A Carbohydrate Connection?

Perfect health on a carnivorous, low-carb diet

Perfect health on a carnivorous, low-carb diet

Dentists are considering a return to an old theory that dietary carbohydrates first cause dental diseases, then certain systemic chronic diseases, according to a review in the June 1, 2009, Journal of Dental Research. 

We’ve known for years that some dental and systemic diseases are associated with each other, both for individuals and populations.  For example, gingivitis and periodontal disease are associated with type 2 diabetes and coronary heart disease.  The exact nature of that association is not clear.  In the 1990s it seemed that infections – chlamydia, for example – might be the unifying link, but this has not been supported by subsequent research.     

The article is written by Dr. Philippe P. Hujoel, who has been active in dental research for decades and is affiliated with the University of Washington (Seattle).  He is no bomb-throwing, crazed, radical. 

The “old theory” to which I referred is the Cleave-Yudkin idea from the 1960s and ’70s that excessive intake of fermentable carbohydrates, in the absence of good dental care, leads both to certain dental diseases – caries (cavities), periodontal disease, certain oral cancers, and leukoplakia – and to some common systemic chronic non-communicable diseases such as coronary heart disease, type 2 diabetes, some cancers, and dementia.  In other words, dietary carbohydrates cause both dental and systemic diseases – not all cases of those diseases, of course, but some.   

Dr. Hujoel does not define “fermentable” carbohydrates in the article.  My American Heritage Dictionary defines fermentation as:

  1. the anaerobic conversion of sugar to carbon dioxide and alcohol by yeast
  2. any of a group of chemical reactions induced by living or nonliving ferments that split complex organic compunds into relatively simple substances

As reported in David Mendosa’s blog at MyDiabetesCentral.com, Dr. Hujoel said, “Non-fermentable carbohydrates are fibers.”  Dr. Hujoel also shared some personal tidbits there. 

In the context of excessive carbohydrate intake, the article frequently mentions sugar, refined carbs, and high-glycemic-index carbs.  Dental effects of excessive carb intake can appear within weeks or months, whereas the sysemtic effects may take decades. 

Hujoel compares and contrasts Ancel Keys’ Diet-Heart/Lipid Hypothesis with the Cleave-Yudkin Carbohydrate Theory.  In Dr. Hujoel’s view, the latest research data favor the Carbohydrate Theory as an explanation of many cases of the aforementioned dental and systemic chronic diseases.  If correct, the theory has important implications for prevention of dental and systemic diseases: namely, dietary carbohydrate restriction.

Adherents of the paleo diet and low-carb diets will love this article; it supports their choices.

I agree with Dr. Hujoel that we need a long-term prospective trial of serious low-carb eating versus the standard American high-carb diet.  Take 20,000 people, randomize them to one of the two diets, follow their dental and systemic health over 15-30 years, then compare the two groups.  Problem is, I’m not sure it can be done.  It’s hard enough for most people to follow a low-carb diet for four months.  And I’m asking for 30 years?!   

Dr. Hujoel writes:

Possibly, when it comes to fermentable carbohydrates, teeth would then become to the medical and dental professionals what they have always been for paleoanthropologists: “extremely informative about age, sex, diet, health.”

Dr. Hujoel mentioned a review of six studies that showed a 30% reduction in gingivitis score by following a diet moderately reduced in carbs.  He mentions the aphorism: “no carbohydrates, no caries.”  Anyone prone to dental caries or ongoing periodontal disease should do further research to see if switching to low-carb eating might improve the situation. 

Don’t be surprised if your dentist isn’t very familiar with the concept.  Has he ever mentioned it to you?

Steve Parker, M.D.,

Author of The Advanced Mediterranean Diet

Reference:  Hujoel, P.  Dietary carbohydrates and dental-systemic diseases.  Journal of Dental Research, 88 (2009): 490-502.

Mendosa, David.  Our dental alarm bell.  MyDiabetesCentral.com, July 12, 2009.

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June 22, 2009 · 2:00 AM

Do Vitamin D and Calcium Supplements Cut Risk of Diabetes?

Cliffs of Dover: Pure White Calcium Carbonate

Cliffs of Dover: Pure White Calcium Carbonate

Several studies have associated vitamin D and calcium intake with lower risk of developing type 2 diabetes.  After reading that the Institute of Medicine in 2010 will probably increase the recommended amounts of vitamin D for every one, I decided to review the literature pertinent to diabetes.

Over the last 10 years, studies have associated low blood levels of vitamin D with a higher risk of cardiovascular disease, death, type 2 diabetes, some cancers, infections, autoimmune diseases, frequent falls in the elderly, and dementia.

The Institute of Medicine (in the U.S.) currently recommends 200 IU (international units) per day for people under 50, 400 IU for people 50-70, with an upper intake level of 2,000 IU per day.  I assume those amounts refer to a combination of food (or supplements) and the vitamin D your skin makes (but how do we know that?). 

The new recommendation is expected to be around 1,000-2,000 IU per day.  It’s quite difficult to get close to that just with food.  With adequate sun exposure, we can make some vitamin D.  But the dermatologists have scared us out of the sun with horror stories of skin cancer.  I’ve seen some tragic cases in my own patients.  Skin covered with sunscreen doesn’t make vitamin D.  It can be difficult to get enough sun exposure, especially at higher latitudes in winter

I reviewed scientific articles pertinent to tyepe 2 diabetes via PubMed and list the best ones for you below.   The evidence in favor of using vitamin D and calcium supplements to prevent diabetes is weak, but may be correct. 

I found nothing to suggest that high vitamin D and calcium intake (whether food or supplements) helps control established cases of diabetes. 

Take-Home Points 

If you want to prevent type 2 diabetes with supplements, 1000 IU of vitamin D and 800-1000 mg of elemental calcium daily might help.  The evidence is not strong.  It might help; it might not.  But it’s unlikely to hurt.  Check with your personal physician first.  More studies are needed.  Calcium supplements are routinely recommended by expert nutrition panels for people over 60 to prevent osteoporosis.  The vitamin D supplement may be healthy in other ways.

Who, in particular, might want to prevent type 2 diabetes?  People with . . .

I’m sufficiently convinced about the nondiabetic vitamin D benefits that I’m going to start taking 1,000 IU per day.

Steve Parker, M.D.,

References:

Pittas, Anastassios, et al.  The effects of calcium and vitamin D supplementatinon on blood glucose and markers of inflammatin in nondiabetic adults.  Diabetes Care, 30 (2007): 980-9896.

Chowdhurry, T.A., et al.  Vitamin D and type 2 diabetes: Is there a link?  Primary Care Diabetes, April 21, 2009 (Epub ahead of print).

Pittas, Anastassios, et al.  Vitamin D and calcium intake in relation to type 2 diabetes in women.  Diabetes Care, 29 (2006): 650-656.

Knept, P., et al.  Serum vitamin D and subsequent occurrence of type 2 diabetes.  Epidemiology, 19 (2008): 666-671.

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