Tag Archives: diabetes

Is mTORC1 Modulation the Key To Diseases of Civilization?

Was Hippocrates the dude that said something about “make food your medicine”?

Bodo Melnik has an article in DermatoEndocrinology regarding the dietary causes of acne.  He also comments on the role of Western foods in obesity, cancer, diabetes, high blood pressure, and neurodegenerative disorders.  These are our old friends, the “diseases of civilization.”  Melnik mentions the Paleolithic diet favorably.

Melnik says it’s all tied in with mTORC1: mammalian target of rapamycin complex 1.

A snippet:

These new insights into Western diet-mediated mTORC1-hyperactivity provide a rational basis for dietary intervention in acne by attenuating mTORC1 signaling by reducing (1) total energy intake, (2) hyperglycemic carbohydrates, (3) insulinotropic dairy proteins and (4) leucine-rich meat and dairy proteins. The necessary dietary changes are opposed to the evolution of industrialized food and fast food distribution of Westernized countries. An attenuation of mTORC1 signaling is only possible by increasing the consumption of vegetables and fruit, the major components of vegan or Paleolithic diets. The dermatologist bears a tremendous responsibility for his young acne patients who should be advised to modify their dietary habits in order to reduce activating stimuli of mTORC1, not only to improve acne but to prevent the harmful and expensive march to other mTORC1-related chronic diseases later in life.

You sciencey types can read the rest.  Our new friend mTOR also seems to be involved with growth of muscle induced by resistance exercise.

h/t Mangan

Polycystic Ovary Syndrome Linked To Higher Rate of Diabetes and Heart Disease

…details are at MedPageToday. Insulin resistance is tied in somehow. PCOS affects five or 10% of women.

High Normal Blood Sugar Levels Linked To Brain Degeneration

MRI scan of brain

MRI scan of brain

Our bodies keep blood sugar levels in a fairly narrow range.  You might think you’re fine if you’re anywhere within the defined normal range.  Think again.  Australian researchers found that folks with fasting blood sugars toward the upper end of the normal range had more degeneration (atrophy) in parts of the brain called the hippocampus and amygdala, compared to those in the low normal range.  Degeneration in those areas is often manifested as dementia.

The hippocampus is critical for learning and memory formation and retention.  The amygdala is also involved in memory as well as emotion.  The two areas are intimately connected, literally.

How Was the Study Done?

Over 250 study participants aged 60 to 64 years had normal brains at baseline and were free of diabetes and prediabetes.  They were overwhelmingly caucasian.  MRI brain scans were done at baseline and again four years later.  Significant atrophy (shrinkage) was seen in the hippocampus and amygdala over time, with greater atrophy seen in those with higher baseline fasting glucose levels.

Fasting blood sugar was measured only once, at the start, and ranged from 58 to 108 mg/dl (3.2 to 6.0 mmol/l).  (Fasting glucose of 108 would be prediabetes according to the American Diabetes Association, but not by the World Health Organization.)  Participants weren’t tested for deterioration of cognition.

So What?

The results of the study at hand are consistent with others that link higher rates of dementia with diabetes.  Diabetics, even when under treatment, usually have higher average blood sugars than non-diabetics.  The study authors speculate that damage from higher blood sugars may be mediated by inflammation and abnormal blood clotting (prothrombotic factors and platelet activation).

The Mayo Clinic recently reported that diets high in carbohydrates and sugar increase the odds of developing cognitive impairment in the elderly years.

It’s interesting to contemplate whether non-diabetics and diabetics would have less risk of developing dementia if blood sugars could be kept in the lower end of the normal range.  How could you do that?  Possibilities include:

  • avoid sugars and other refined carbohydrates
  • limit all carbohydrates
  • favor low-glycemic-index foods over high
  • regular exercise, which helps maintain insulin sensitivity (insulin is a major blood sugar regulator)
  • avoid overweight and obesity, which helps maintain insulin sensitivity
  • for diabetics: all of the above plus drugs that control blood sugar

Steve Parker, M.D.

Reference:  Cherbuin, Nicolas, et al.  Higher normal fasting plasma glucose is associated with hippocampal atrophy: The PATH Study.  Neurology, September 4, 2012, vol. 79, No. 10, pp: 1,010-1,026.  doi:10.1212/WNL.0b013e31826846de

Dietitians Weigh In On Mediterranean Diet for Diabetes

An eating pattern similar to the traditional Mediterranean diet can be integrated with existing national guidelines for the management of diabetes, blood pressure, and cholesterol. Existing data suggest that the Mediterranean diet has health benefits, including improved glycemic control and reduced cardiovascular risk, and may offer benefits to diabetes patients and clinicians alike in terms of palatability, ease of explanation and use, and promotion of improved health.

Olive oil and vinegar

Olive oil and vinegar

This excerpt is from an article by three dietitians writing in Diabetes Spectrum in 2009.  Click through for details if interested.

—Steve

Reference:  doi: 10.2337/diaspect.24.1.36 Diabetes Spectrum January 1, 2011 vol. 24 no. 1 36-40

How Many Diabetic Diets Are There?

Elizabeth Woolley reviews most of them at her About.com column on type 2 diabetes. I don’t endorse everything there; just thought you might be interested.

I still see doctors at the hospital order “ADA diet” (American Diabetes Association) for their patients with diabetes.

There is no ADA diet.

-Steve

Nuts: What’s Not to Love?

MPj04031620000[1]Nut consumption is strongly linked to reduced coronary heart disease, with less rigorous evidence for several other health benefits, according to the American Journal of Clinical Nutrition.

This is why I’ve included nuts as integral components of the Ketogenic Mediterranean Diet and the Advanced Mediterranean Diet.

Regular nut consumption is associated with health benefits in observational studies of various populations, within which are people eating few nuts and others eating nuts frequently. Health outcomes of the two groups are compared over time. Frequent and long-term nut consumption is linked to:

  • reduced coronary heart disease (heart attacks, for example)
  • reduced risk of diabetes in women (in men, who knows?)
  • less gallstone disease in both sexes
  • lower body weight and lower risk of obesity and weight gain

The heart-protective dose of nuts is three to five 1-ounce servings a week.

Steve Parker, M.D.

Reference: Sabaté, Joan and Ang, Yen. Nuts and health outcomes: New epidemiologic evidence. American Journal of Clinical Nutrition, 89 (2009): 1,643S-1,648S.

Glycemic Index and Chronic Disease Risk (Mostly in Women)

I’ve written about glycemic index (GI), glycemic load (GL), and glycemic diets in preparation for today’s post.

The concept of glycemic index was introduced by Jenkins et al in 1981 at the University of Toronto.

Studies investigating the association between disease risk and GI/GL have been inconsistent. By “inconsistent,” I mean some studies have made an association in one direction or the other, and other studies have not. Diseases possibly associated with high-glycemic diets have included diabetes, cardiovascular disease, cancer, gallbladder disease, and eye disease.

“Diet” in this post refers to a habitual way of eating, not a weight loss program.

Researchers with the University of Sydney (Sydney, Australia) identified the best-designed published research reports investigating the relationship between certain chronic diseases and glycemic index and load. The studied diseases were type 2 diabetes, coronary heart disease, stroke, breast cancer, colorectal cancer, pancreatic cancer, endometrial cancer, ovarian cancer, gallbladder disease, and eye disease.

Methodology

Literature databases were searched for articles published between 1981 and March, 2007. The researchers found 37 studies that enrolled 1,950,198 participants ranging in age from 24 to 76, with BMI’s averaging 23.5 to 29. These were human prospective cohort studies with a final outcome being occurrence of a chronic disease (not its risk factors). Twenty-five of the studies were conducted in the U.S., five in Canada, five Europe, and two in Australia. Ninety percent of participants were women [for reasons not discussed]. Food frequency questionnaires were used in nearly all the studies. Individual studies generated between 4 to 20 years of follow-up, and 40,129 new cases of target diseases were identified.

Associations between GI, GL, and risk of developing a chronic disease were measured as rate ratios comparing the highest with the lowest quantiles. For example, GI and GL were measured in the study population. The population was then divided into four groups (quartiles), reflecting lowest GI/GL to medium to highest GI/GL diets. The lowest GI/GL quartile was compared with the highest quartile to see if disease occurrence was different between the groups. Some studies broke the populations into tertiles, quintiles, deciles, etc.

Findings

Comparing the highest with the lowest quantiles, studies with a high GI or GL independently

  • increased the risk of type 2 diabetes by 27 (GL) or 40% (GI)
  • increased the risk of coronary heart disease by 25% (GI)
  • increased the risk of gallbladder disease by 26% (GI) or 41% (GL) (gallstones and biliary colic, I assume, but the authors don’t specify)
  • increased the risk of breast cancer by 8% (GI)
  • increased risk of all studied diseases (11) combined by 14% (GI) or 9% (GL)

Overall, high GI was more strongly associated with chronic disease than was high GL

So low-GI diets may offer greater protection against disease than low-GL diets.

Comments from the Researchers

They speculate that low-GI diets may be more protective than low-GL because the latter can include low-carb foods such as cheese and meat, and low-GI, high-carb foods. Both eating styles will reduce glucose levels after meals while having very different effects in other areas such as pancreas beta cell function, free fatty acid levels, triglyceride levels, and effects on satiety.

High GI and high GL diets, independently of known confounders, modestly increase the risk of chronic lifestyle-related diseases, with more pronounced effects for type 2 diabetes, coronary heart disease, and gallbladder disease.

Direct quotes:

. . . 90% of participants were female; therefore, the findings may not be generalizable to men.

There are plausible mechanism linking the development of certain chronic diseases with high-GI diets. Specifically, 2 major pathways have been proposed to explain the association with type 2 diabetes risk. First the same amount of carbohydrate from high-GI food produces higher blood glucose concentrations and a greater demand for insulin. The chronically increased insulin demand may eventually result in pancreatic beta cell failure, and, as a consequence, impaired glucose tolerance. Second, there is evidence that high-GI diets may directly increase insulin resistance through their effect on glycemia, free fatty acids, and counter-regulatory hormone secretion. High glucose and insulin concentrations are associated with increased risk profiles for cardiovascular disease, including decreased concentrations of HDL cholesterol, increased glycosylated protein, oxidative status, hemostatic variables, and poor endothelial function

Low-GI and/or low-GL diets are independently associated with a reduced risk of certain chronic diseases. In diabetes and heart disease, the protection is comparable with that seen for whole grain and high fiber intakes. The findings support the hypothesis that higher postprandial glycemia is a universal mechanism for disease progression.

My Comments

Studies like this tend to accentuate the differences in eating styles since they compare the highest with the lowest post-prandial (after meal) glucose levels. Most people are closer to the middle of the pack, so a person there has potentially less to gain by moving to a low-GI diet. But still some to gain, on average, particularly in regards to avoiding type 2 diabetes and coronary heart disease.

(To be fair, many population-based studies use this same quantile technique. It increases the odds of finding a statistically significant difference.)

Only two of the 37 studies examined coronary heart disease, the cause of heart attacks. One study was the massive Nurses’ Health Study database with 75,521 women. The other was the Zutphen (Netherlands) Elderly Study which examined men 64 and older. Here’s the primary conclusion of the Zutphen authors verbatim:

Our findings do not support the hypothesis that a high-glycemic index diet unfavorably affects metabolic risk factors or increases risk for CHD [coronary heart disease] in elderly men without a history of diabetes or CHD.

So there’s nothing in the meta-analysis at hand to suggest that high-GI/GL diets promote heart disease in males in the general population.

However, the recent Canadian study in Archives of Internal Medicine found strong evidence linking CHD with high-glycemic index diets. Although not mentioned in the text of that article, Table 3 on page 664 shows that the association is much stonger in women than in men. Relative risk for women on a high-glycemic index/load diet was 1.5 (95% confidence interval = 1.29-1.71), and for men the relative risk was 1.06 (95% confidence interval = 0.91-1.20). See reference below.

Nine of the 37 studies examined the occurrence of type 2 diabetes. Only one of these studied men only – 42,759 men: the abstract is not available online and the Sydney group does not mention if high-GI or high-GL was positively associated with onset of diabetes in this cohort. Two of the diabetes studies included both men and women, but the abstracts don’t break down the findings by sex. (I’m trying to deduce if the major overall findings of this meta-analysis apply to men or not.)

I don’t know anybody willing to change their diet just to avoid the risk of gallstones. It’s only after they develop symptomatic gallstones that they ask me what they can do about them. The usual answer is surgery.

The report is well-done and seems free of commercial bias, even though several of the researchers are authors or co-authors of popular books on low-GI eating.

Steve Parker, M.D.

References:

Barclay, Alan W.; Petocz, Peter; McMillan-Price, Joanna; Flood, Victoria M.; Prvan, Tania; Mitchell, Paul; and Brand-Miller, Jennie C. Glycemic index, glycemic load, and chronic disease risk – a meta-analysis of observational studies [of mostly women]. American Journal of Clinical Nutrition, 87 (2008): 627-637.

Brand-Miller, Jennie, et al. “The New Glucose Revolution: The Authoritative Guide to the Glycemic Index – The Dietary Solution for Lifelong Health.” Da Capo Press, 2006.

Mente, Andrew, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine, 169 (2009): 659-669.

Dental Problems and Chronic Systemic Disease: A Carbohydrate Connection?

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.

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.

Low-Carb Mediterranean Diet Beats Low-Fat For Recent-Onset Type 2 Diabetes

A low-carbohydrate Mediterranean diet dramatically reduced the need for diabetic drug therapy, compared to a low-fat American Heart Association diet. The Italian researchers also report that the Mediterranean dieters also lost more weight over the first two years of the study.

Investigators suggest that the benefit of the Mediterranean-style diet is due to greater weight loss, olive oil (monunsaturated fats increase insulin sensitivity), and increased adiponectin levels.

The American Diabetes Association recommends both low-carbohydrate and low-fat diets for overweight diabetics. The investigators wondered which of the two might be better, as judged by the need to institute drug therapy in newly diagnosed people with diabetes.

Methodology

Newly diagnosed type 2 diabetics who had never been treated with diabetes drugs were recruited into the study, which was done in Naples, Italy. At the outset, the 215 study participants were 30 to 75 years of age, had body mass index over 25 (average 29.5), had average hemoglobin A1c levels of 7.73, and average glucose levels of 170 mg/dl.

Participants were randomly assigned to one of two diets:

  1. Low-carb Mediterranean diet (“MED diet”, hereafter): rich in vegetables and whole grains, low in red meat (replaced with poultry and fish), no more than 50% of calories from complex carbohydrates, no less than 30% of calories from fat (main source of added fat was 30 to 50 g of olive oil daily). [No mention of fruits. BTW, the traditional Mediterranean diet derives 50-60% of energy from carbohydrates.]
  2. Low-fat diet based on American Heart Association guidelines: rich in whole grains, restricted additional fats/sweets/high-fat snacks, no more than 30% of calories from fat, no more than 10% of calories from saturated fats.

Both diet groups were instructed to limit daily energy intake to 1500 (women) or 1800 (men) calories.

All participants were advised to increase physical activity, mainly walking for at least 30 minutes a day.

Drug therapy was initiated when hemoglobin A1c levels persisted above 7% despite diet and exercise.

The study lasted four years.

Results

By the end of 18 months, twice as many low-fat dieters required diabetes drug therapy compared to the MED dieters—24% versus 12%.

By the end of four years, seven of every 10 low-fat dieters were on drug therapy compared to four of every 10 MED dieters.

The MED dieters lost 2 kg (4.4 lb) more weight by the end of one year, compared to the low-fat group. The groups were no different in net weight loss when measured at four years: down 3–4 kg (7–9 lb).

Compared to the low-fat group, the MED diet cohort achieved significantly lower levels of fasting glucose and hemoglobin A1c throughout the four years.

The MED diet group saw greater increases in insulin sensitivity, i.e., they had less insulin resistance.

The MED group had significantly greater increases in HDL cholesterol and decreases in trigylcerides throughout the study. Total cholesterol decreased more in the MED dieters, but after the first two years the difference from the low-fat group was not significantly different.

Comments

The MED diet here includes “no more than 50% of calories from complex carbohydrates.” The authors don’t define complex carbs. Simple carbohydrates are monosaccharides and disaccharides. Complex carbs are oligosaccharides and polysaccharides. Another definition of complex carbs is “fruits, vegetables, and whole grains,” which I think is definition of complex carbs applicable to this study.

The editors of the Annals of Internal Medicine conclude that:

A low-carbohydrate, Mediterranean-style diet seems to be preferable to a low-fat diet for glycemic control in patients with newly diagnosed type 2 diabetes.

I’m sure the American Diabetes Association will take heed of this study when they next revise their diet guidelines. If I were newly diagnosed with type 2 diabetes, I wouldn’t wait until then.

This study dovetails nicely with others that show prevention of type 2 diabetes with the Mediterranean diet, reversal of metabolic syndrome—a risk factor for diabetes—with the Mediterranean diet (supplemented with nuts), and prevention of type 2 diabetes and pre-diabetes in people who have had a heart attack.

Studies like these support my Low-Carb Mediterranean Diet.

For general information on Mediterranean eating, visit Oldways.

Steve Parker, M.D.

Reference: Esposito, Katherine, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes. Annals of Internal Medicine, 151 (2009): 306-314.

Does Diabetes Cause Dementia?

Contrary to popular belief among the experts, type 2 diabetes is not one of the causes of Alzeimer dementia. They may indeed be associated with each other, but that’s not causation.

An oft-repeated theory from Gary Taubes 2007 masterpiece, Good Calories, Bad Calories, is that many of the chronic diseases of modern civilization, including Alzheimer disease, are caused by abnormal blood sugar and insulin metabolism. Especially high insulin levels induced by a diet rich in refined carbohydrates. If that’s the case, you’d expect to see a high prevalence of Alzheimer disease in older type 2 diabetics.

Dr. Emily Deans (psychiatrist) looked at this issue last year at her great Evolutionary Psychiatry blog.

The brains of Alzheimer patients, under a microscope, are characterized by many senile plaques (aka neuritic plaques) and neurofibrillary tangles. That’s the gold standard for diagnosis. Nevertheless, brain biopsies are rarely done to diagnose Alzheimer disease in living patients, and even autopsies after death are rare. The diagnosis usually is clinical, based on ruling out other illnesses, etc.

Nearly all the studies associating diabetes with Alzheimers disease (and other dementias) are observational or epidemiologic. (The exception is the Honolulu-Asia Aging Study.) Establishing an association is helpful in generating theories, but establishing causation is the goal. At least five studies confirm an association.

Neurology in 2011 reported findings of Japanese researchers who examined the brains of 135 people who died between 1998 and 2003. They lived in Hisayama, a town with an incredibly high autopsy rate of 74%. These people before death had undergone an oral glucose tolerance test. Their insulin resistance was calculated on the basis of fasting glucose and fasting insulin (HOMA-IR). None of them showed signs of dementia at the time of study enrollment in 1988.

What Did They Find?

Twenty-one of the 135 subjects developed Alzheimer-type dementia. The investigators don’t say if the diagnosis was based on the brain examination, or just a clinical diagnosis without a brain biopsy or autopsy. How this got beyond the article reviewers is beyond me. [If I’m missing something, let me know in the comments section below.] It must be a clinical diagnosis because if you don’t act demented, it doesn’t matter how many senile plaques and neurofibrillary tangles you have in your brain.

Senile plaques, but not neurofibrillary tangles, were more common in those with higher levels of blood sugar (as measured two hours after the 75 g oral glucose dose), higher fasting insulin, and higher insulin resistance. People with the APOE epsilon-4 gene were at even higher risk for developing senile plaques.

The researchers did not report whether the subjects in this study had been diagnosed during life with diabetes or not. One can only hope those data will be published in another paper. Why make us wait?

Average fasting glucose of all subjects was 106 mg/dl (5.9 mmol/l); average two-hour glucose after the oral glucose load was 149 mg/dl (8.3 mmol/l). By American Association of Clinical Endocrinologists criteria, these are prediabetic levels. Mysteriously, the authors fail to mention or discuss this. [I don’t know if AACE criteria apply to Japanese.] Some of these Japanese subjects probably had diabetes, some had prediabetes, others had normal glucose and insulin metabolism.

As with all good research papers, the authors compare their findings with similar published studies. They found one autopsy study that tended to agree with their findings (Honolulu) and three others that don’t (see references below). In fact, one of the three indicated that diabetes seems to protect against the abnormal brain tissue characteristic of Alzheimer disease.

Botton Line

Type 2 diabetes doesn’t seem to be a cause of Alzheimer disease, if autopsy findings and clinical features are the diagnostic criteria for the disease.

If we assume that type 2 diabetics have higher than normal blood sugar levels and higher insulin levels for several years, then hyperglycemia and hyperinsulinemia don’t cause or contribute to Alzheimer dementia.

Type 2 diabetes is, however, linked with impaired cognitive performance, at least according to many of the scientific articles I read in preparation for this post. So type 2 diabetics aren’t in the clear yet. It’s entirely possible that high blood sugar and /or insulin levels cause or contribute to that. (Any volunteers to do the literature review? Best search term may be “mild cognitive impairment.”)

Type 2 diabetes is associated with Alzheimer disease, but we have no proof that diabetes is a cause of Alzheimers. Nor do we have evidence that high blood sugar and insulin levels cause Alzheimer disease.

Alzheimer disease is a major scourge on our society. I’d love to think that carbohydrate-restricted eating would help keep blood sugar and insulin levels lower and thereby lessen the devastation of the disease. Maybe it does, but I’d like to see more convincing evidence. It’ll be years before we have a definitive answer.

For now, we have evidence that the Mediterranean diet seems to 1) protect againstAlzheimers and other dementias, 2) prevent some cases of type 2 diabetes, and 3) reduce the need for diabetic medications in diabetics.

For more information on practical application of the Mediterranean diet, visit Oldways and the Advanced Mediterranean Diet website.

Steve Parker, M.D.

References:

Matsuzaki T, Sasaki K, Tanizaki Y, Hata J, Fujimi K, Matsui Y, Sekita A, Suzuki SO, Kanba S, Kiyohara Y, & Iwaki T (2010). Insulin resistance is associated with the pathology of Alzheimer disease: the Hisayama study. Neurology, 75 (9), 764-70 PMID: 20739649

Heitner, J., et al. “Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects: a retrospective postmortem immunocytochemical and histofluorescent study.” Neurology, 49 (1997): 1306-1311. Autopsy study, No. of subjects not in abstract. They looked for senile plaques and neurofibrillary tangles, etc. The title says it all.

Beeri, M.S., et al. “Type 2 diabetes is NEGATIVELY [emphasis added] associated with Alzheimer’s disease neuropathology.” J. Gerontol A. Biol Sci. Med. Sci. 60 (2005): 471-475. 385 autopsies. The title again says it all.

Arvanitakis, Z., et al. “Diabetes is related to cerebral infarction but NOT [emphasis added] to Alzheimers disease pathology in older persons.” Neurology, 67 (2006): 1960-1965. Autopsy study of 233 Catholic clergy, about 50:50 women:men.