Tag Archives: carbohydrates

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 diseasesJournal of Dental Research, 88 (2009): 490-502.

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

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Filed under Carbohydrate, Causes of Diabetes, coronary heart disease, Glycemic Index and Load

High Glycemic Load and Low Grain Fiber Increase Risk of Type 2 Diabetes in Men

Minimally refined grain

Minimally refined grain

A study published in 1997 helped establish the association between glycemic load, dietary fiber, and type 2 diabetes in men.

Methodology

Over 42,000 mostly middle-aged men in the Health Professionals Follow-up Study, without diabetes at baseline, were followed over six years to see if  diet composition was related to onset of type 2 diabetes.  Food intake was determined by a questionnaire.  95% of participants were white.

Results

523 cases of type 2 diabetes developed.  Men with the highest glycemic index eating pattern were 37% more likely to develop diabetes compared to the lowest glycemic index.

Cereal (grain) fiber was inversely related to risk of diabetes.  That is, the higher the intake of grain fiber, the lower the risk of developing diabetes.

The combination of high glycemic load and low cereal fiber yielded the highest rate of diabetes.

Total dietary fiber was not associated with reduced risk of diabetes.

Fiber from fruits and vegetables was not associated with diabetes one way or the other.

As other studies found, total carbohydrate intake was not related to risk of diabetes.

Take-Home Points

These findings may or may not apply to women and non-white ethnic groups.

Grains in a minimally refined form reduced the incidence of diabetes in this population.

Diets with a high glycemic load increase the risk of diabetes, at least in men.

Elsewhere, I’ve reviewed studies indicating that, in women, both high glycemic load and high glycemic index eating increase the risk of type 2 diabetes.  Click here for details.

We must wonder if  established cases of diabetes would respond positively to diets with low glycemic load and grains in a minimally refined form.  Or is it too late?

Steve Parker, M.D.

Reference:  Salmeron, Jorge, et al.  Dietary fiber, glycemic load, and risk of NIDDM in Men.  Diabetes Care, 20 (1997): 545-550

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Filed under Carbohydrate, Causes of Diabetes, Fiber, Glycemic Index and Load

Can Diabetes Be Prevented in Older Adults?

42-15653241A study published yesterday supports the idea that even in older adults, over 65, type 2 diabetes can be prevented in most cases by healthy lifestyle choices.

Researchers examined the participants in the Cardiovascular Health Study – 4,883 men and women over 65 at baseline – over the course of 10 years.  Median age at enrollment was 73.  Participants were followed clinically for 10 years.  New cases of diabetes over 10 years: 337.  Researchers suspected, based on previous studies in younger folks, that a reduced incidence of diabetes onset would be related to:

  • physical activity levels above the median (half of people exercise less than the median, half exercise more)
  • never smoking, or minimal and years ago
  • “healthy diet,” defined as high fiber, low glycemic index foods, lower trans fats, higher polyunsaturated-to-saturated fat ratio
  • low body mass index (not overweight)
  • waist circumference under 92 cm (36.2 inches) for men and 88 cm (34.6 inches) for women
  • low to moderate alcohol use

We’ll call these “lifestyle factors.”  Participants were analyzed to see how well they fit this profile and whether or not they developed diabetes.

Results

The more each of these lifestyle factors characterized a person, the lower the risk of developing diabetes.

High physical activity and healthy diet by themselves reduced risk of diabetes by half.

Study authors estimate that healthy lifestyle choices could prevent eight or nine out of 10 cases of diabetes in older adults.

Take-Home Point

The researchers rightfully point out that their results are associations, not proof that these lifestyle factors prevent diabetes.  Given the totality of the evidence from this and other studies, I would adopt many of the low-risk lifestyle choices if I wanted to avoid diabetes.

Steve Parker, M.D.

Reference:  Mozaffarian, D., et al.  Lifestyle risk factors and new-onset diabetes mellitus in older adultsArchives of Internal Medicine, 169, (2009): 798-807.

Update April 30, 2009:

Research in younger populations has associated the following factors with prevention of type 2 diabetes:

  1. Avoid overweight, or lose weight if you are overweight (body mass index over 25)
  2. Regular physical activity
  3. Don’t start smoking, or quit if you do
  4. Pick the right parents

Some cases of diabetes are related to genetic factors beyond our control.  Having parents or close relatives with diabetes suggests that you may be genetically predisposed.  Genetics is not necessarily destiny, however.

-Steve

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Lipid Overload as the Cause of Type 2 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., writes 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 many readers.  I’m writing this to solidify my own understanding of a new theory.  If you are not interested in physiology, you can quit reading now. 

Still with me? 

Definitions and Physiology

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

The 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. 

Insulin is a protein hormone produced by pancreatic beta cells.  Insulin:

  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 impair 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, 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, would not seem to make much sense.  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 intake if someone is 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, Roger H.  Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention.  Journal of the American Medical Association, 299 (2008): 1185-1187.

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