Monthly Archives: April 2012

Mediterranean Diet Prevents Middle-Age Weight Gain? I Wish…

Several mainstream media sources last year touted the Mediterranean diet as an effective method for prevention of the expected middle-age weight gain. Reuters is one source, for example. Men on the Mediterranean diet gained 2 lb (about a kilogram) less than other men over six years. Mediterranean-dieting women gained weight too, but a whole 0.77 lb (0.35 kg) less than others.

Big whoop.

The media attention was based on a Spanish study of over 10,000 men and women university graduates over the course of six years. Average baseline age was 38. A Mediterranean diet score was calculated based on a food frequency questionnaire given only at the start of the study. Adherence with a Mediterranean-style diet was judged for each individual as either low, medium, or high.

You’d think this research report would tell you how much weight these folks gained on average over six years, and how many pounds less if one followed the Mediterranean diet. Think again. No such luck, which reminds me of one of my favorite aphorisms: “eschew obfuscation.”

I had to do my own calculations based on Table 3. And I still don’t know how much the average person in this cohort gained over six years.

I am a die-hard Mediterranean diet advocate. It’s linked to myriad health benefits. I’d love to believe it prevents middle-age weight gain. But the results of this study are so modest as to be almost nonexistent.

Steve Parker, M.D.

Reference: Beunza, J., Toledo, E., Hu, F., Bes-Rastrollo, M., Serrano-Martinez, M., Sanchez-Villegas, A., Martinez, J., & Martinez-Gonzalez, M. (2010). Adherence to the Mediterranean diet, long-term weight change, and incident overweight or obesity: the Seguimiento Universidad de Navarra (SUN) cohort American Journal of Clinical Nutrition DOI: 10.3945/ajcn.2010.29764

High-Carbohydrate Eating Promotes Heart Disease in Women

Women double their risk of developing coronary heart disease if they have high consumption of carbohydrates, according to research published in the Archives of Internal Medicine.

Men’s hearts, however, didn’t seem to be affected by carb consumption. I mention this crucial sex difference because many experts believe that replacing saturated fat with carbohydrates is a major cause of heart disease. If true, it seems to apply only to women.

(Another nutrition science trend to keep an eye on is the thought that excessive consumption of omega-6 fats contributes to hardening of the arteries, including coronary heart disease. I’m talking about soy oil, safflower oil, corn oil, among others. No doubt, we’re eating a lot more omega-6 now than at the start of the 20th century.)

We’ve known for a while that high-glycemic-index eating was linked to heart disease in women but not men. Glycemic index is a measure of how much effect a carbohydrate-containing food has on blood glucose levels. High-glycemic-index foods raise blood sugar higher and for longer duration in the bloodstream.

High-glycemic-index foods include potatoes and white bread, for example.

The study at hand included over 47,000 Italians who were interrogated via questionnaire as to their food intake, then onset of coronary heart disease—the cause of heart attacks—was measured over the next eight years.

Among the 32,500 women, 158 new cases of coronary heart disease were found.

Researchers doing this sort of study typically compare the people eating the least carbs with those eating the most. The highest quartile of carb consumers and glycemic load had twice the rate of heart disease compared to the lowest quartile.

The Cleave-Yudkin theory of the mid-20th century proposed that excessive amounts of refined carbohydrates cause heart disease and certain other chronic systemic diseases. Gary Taubes has also written extensively about this. The research results at hand support that theory in women, but not in men.

Practical Applications

Do these research results apply to non-Italian women and men? Probably to some, but not all. More research is needed.

Women with a family history coronary heart disease—or other CHD risk factors—might be well-advised to put a limit on total carbs, high-glycemic-index foods, and glycemic load. I’d stay out of that “highest quartile.” Don’t forget: heart disease is the No. 1 killer of women.

See NutritionData’s Glycemic Index page for information you can apply today.

FYI, the Low-Carb Mediterranean Diet and Ketogenic Mediterranean Diet are also low in glycemic index.

Steve Parker, M.D.

Disclaimer: All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status. Always consult your personal physician before making any dietary or exercise changes.

Addendum: Alert reader Nadia Hassan brought to my attention that I had originally written that pasta has a high glycemic index. Citing appropriate references, Nadia convinced me that pasta has a low-to-moderate glycemic index, from around 30 to 60. Its GI also is higher if over-cooked. I corrected my original post.

References:

Sieri, Sabina, et al. Dietary glycemic load and index and risk of coronary heart disease in a large Italian cohort. The EPICOR study. Archives of Internal Medicine, 170 (2010): 640-647.

Barclay, Alan, et al. 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.

Chronic Alcohol May Impair Vision in Diabetics

MedPage Today recently reported that long-term consumption of alcohol may impair vision in diabetics. Drinkers performed less well on vision chart tests than non-drinkers. It’s not a diabetic retinopathy issue.

Beer and distilled spirits were riskier than wine.

The MedPage Today article didn’t comment on the potential health benefits of alcohol consumption. You can bet I’ll keep an eye on this.

Steve Parker, M.D.

Something Fishy

Fish is a major feature of my Ketogenic Mediterranean Diet as well as a healthy component of the traditional Mediterranean diet.

Darya Pino over at Summer Tomato wrote about eating fish: health aspects, which are best to eat, shopping, and sustainability. I recommend it to you, even though I don’t agree with everything. For instance, I think in general the risk of mercury contamination is overblown. (I know that’s little consolation for those few who have suffered mercury poisoning from fish.)

Steve Parker, M.D.

Book Review: Why We Get Fat

Gary Taubes’ latest book is Why We Get Fat: And What To Do About It. I give it five stars per Amazon.com’s ranking system (I love it).

♦ ♦ ♦

At the start of my medical career over two decades ago, many of my overweight patients were convinced they had a hormone problem causing it. I carefully explained that’s rarely the case. As it turns out, I may have been wrong. And the hormone is insulin.

Mr. Taubes wrote this long-awaited book for two reasons: 1) to make the ideas in his 2007 masterpiece (Good Calories, Bad Calories) more accessible to the public, and 2) to speed up the process of changing conventional wisdom on overweight. GCBC was the equivalent of a college-level course on nutrition, genetics, history, politics, science, physiology, and biochemistry. Many nutrition science geeks loved it while recognizing it was too difficult for the average person to digest.

Paradigm Shift

The author hopes to convince us that “We don’t get fat because we overeat; we overeat because we’re getting fat.” We need to think of obesity as a disorder of excess fat accumulation, then ask why the fat tissue isn’t regulated properly. A limited number of hormones and enzymes regulate fat storage; what’s the problem with them?

Mr. Taubes makes a great effort convince you the old “energy balance equation” doesn’t apply to fat storage. You remember the equation: eat too many calories and you get fat, or fail to burn up enough calories with metabolism and exercise, and you get fat. To lose fat, eat less and exercise more. He prefers to call it the “calories-in/calories-out” theory. He admits it has at least a little validity. Problem is, the theory seems to have an awfully high failure rate when applied to weight management over the long run. We’ve operated under that theory for the last half century, but keep getting fatter and fatter. So the theory must be wrong on the face of it, right? Is there a better one?

So, Why DO We Get Fat?

Here is Taubes’s explanation. The hormone in charge of fat strorage is insulin; it works to make us fatter, building fat tissue. If you’ve got too much fat, you must have too much insulin action. And what drives insulin secretion from your pancreas? Dietary carbohydrates, especially refined carbs such as sugars, flour, cereal grains, starchy vegetables (e.g., corn, beans, rice, potatoes), liquid carbs. These are the “fattening carbs.” Dozens of enzymes and hormones are at play either depositing fat into tissue, or mobilizing the fat to be used as energy. It’s an active process going on continously. Any regulatory derangement that favors fat accumulation will CAUSE gluttony (overeating) or sloth (inactivity). So it’s not your fault.

What To Do About It

Cut back on carb consumption to lower your fat-producing insulin levels, and you turn fat accumulation into fat mobilization.

Before you write off Taubes as a fly-by-night crackpot, be aware that he’s received three Science-in-Society Journalism Awards from the National Association of Science Writers. He’s a respected, professional science writer. Having read two of his books, it’s clear to me he’s very intelligent. If he’s got a hidden agenda, it’s well hidden.

One example illustrates how hormones control growth of tissues, including fat tissue. Consider the transformation of a skinny 11-year-old girl into a voluptuous woman of 18. Various hormones make her grow and accumulate fat in the places we now see curves. The hormones make her eat more, and they control the final product. The girl has no choice. Same with our adult fat tissue, but with different hormones. If some derangement is making us grow fatter, it’s going to make us more sedentary (so more energy can be diverted to fat tissue) or make us overeat, or both. We can’t fight it. At not least very well, as you can readily appreciate if look at the people around you at any American shopping mall.

This’N’That

Taubes’s writing is clear and persuasive. He doesn’t beat you over the head with his conclusions. He lays out a logical series of facts and potential connections and explanations, helping you eventually see things his way. If insulin controls fat storage by building and maintaining fat tissue, and if carboydrates drive insulin secretion, then the way to reduce overweight and obesity is carbohydrate-restricted eating, especially avoiding the fattening carbohydrates. I’m sure that’s true for many folks, perhaps even a majority.

If you’re overweight and skeptical about this approach, you could try out a very-low-carb diet for a couple weeks or a month at little expense and risk (but not zero risk). If Mr. Taubes and I are right, there’s a good chance you’ll lose weight. At the back of the book is a university-affiliated low-carb eating plan.

If cutting carb consumption is so critical for long-term weight control, why is it that so many different diets—with no focus on carb restriction—seem to work, if only for the short run? Taubes suggests it’s because nearly all diets reduce carb consumption to some degree, including the fattening carbs. If you reduce your total daily calories by 500, for example, many of those calories will be from carbs. Simply deciding to “eat healthy” works for some people: stopping soda pop, candy bars, cookies, desserts, beer, etc. That cuts a lot of fattening carbs right there.

Losing excess weight or controlling weight by avoiding carbohydrates was the conventional wisdom prior to 1960, as documented by Mr. Taubes. Low-carb diets for obesity date back almost 200 years. The author attributes many of his ideas to German internist Gustav von Bergmann (1908).

Taubes discusses the Paleolithic diet, mentioning that the average paleo diet derived about a third of total calories from carbohdyrates (compared to the standard American diet’s 55% of calories from carb). My prior literature review found 40-45% of paleo diet calories from carbohydrate. I’m not sure who’s right.

Minor Bone of Contention RE: Coronary Heart Disease

Mr. Taubes provides numerous scientific references to back his assertions. I checked out one in particular because it didn’t sound right. Some background first.

Reducing our total fat and saturated fat consumption over the last 40 years was supposed to lower our LDL cholesterol, thereby reducing the burden of coronary heart disease, which causes heart attacks. Instead, we’ve experienced the obesity epidemic as those fats were replaced by carbohydrates. Taubes mentions a 2009 medical journal article by Kuklina et al, in which Taubes says Kuklina points out the number of heart attacks has not decreased as we’ve made these diet changes. Kuklina et al don’t say that. In fact, age-standardized heart attack rates have decreased in the U.S. during the last decade.

Furthermore, autopsy data document a reduced prevalence of anatomic coronary heart disease in people aged 20-59 from 1979 to 1994, but no change in prevalence for those over 60. The incidence of coronary heart disease decreased in the U.S. from 1971 to 1998 (the latest reliable data). Death rates from heart disease and stroke have been decreasing steadily over the last 40 years in the U.S.; coronary heart disease death rates are down by 50%. I do agree with Taubes that we shouldn’t credit those improvements to reduced total and saturated fat consumption. [Reduced trans fat consumption may play a role, but that’s off-topic.]

I think Mr. Taubes would like to believe that coronary artery disease is either more severe or unchanged in the last few decades because of low-fat, high-carb eating. That would fit nicely with some of his theories, but it’s not the case. Coronary artery disease is better now thanks to a variety of factors, but probably not diet (setting aside the trans-fat issue).

Going Forward

Low-carb dieting was vilified over the last half century partly out of concern that the accompanying high fat consumption would cause premature heart attacks, strokes, and death. We know now that total dietary fat and saturated fat have little to do with coronary heart disease and atherosclerosis (hardening of the arteries), which sets the stage for a resurgence of low-carb eating.

I advocate Mediterranean-style eating as the healthiest, in general. It’s linked with prolonged life and lower risk of heart disease, stroke, dementia, diabetes, and cancer. On the other hand, obesity is a strong risk factor for premature death and development of heart disease, stroke, diabetes, and cancer. If consistent low-carb eating cures the obesity, is it healthier than the Mediterranean diet? Maybe so. Would a combination of low-carb and Mediterranean be better? Maybe so. I’m certain Mr. Taubes would welcome a decades-long interventional study comparing low-carb with the Mediterranean diet. But that’s probably not going to happen in our lifetimes.

Gary Taubes rejects the calories-in/calories-out theory of overweight that hasn’t done a very good job for us over the last 40 years. Taubes’s alternative ideas deserve serious consideration.

Steve Parker, M.D.

References:

Coronary heart disease autopsy data: American Journal of Medicine, 110 (2001): 267-273.

Reduced heart attacks: Circulation, 12 (2010): 1,322-1,328.

Reduced incidence of coronary heart disease: www.UpToDate.com, topic: “Epidemiology of Coronary Heart Disease,” accessed December 11, 2010.

Death rates for coronary heart disease: Journal of the American Medical Association, 294 (2005): 1,255-1,259.

Disclosure: I don’t know Gary Taubes. I requested from the publisher and received a free advance review copy of the book. Otherwise I received nothing of value for this review.

Disclaimer: All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status. Always consult your personal physician before making any dietary or exercise changes.

Update April 22, 2013:

As mentioned above, WWGF was based on Taubes’ 2007 book, Good Calories, Bad Calories. You may be interested in a highly critical review of GCBC by Seth at The Science of Nutrition.

Vitamins Slow Rate of Brain Shrinkage in Elderly

A cocktail of three common B vitamins slowed the rate of brain shrinkage over two years in elderly patients with mild cognitive impairment, according to researchers at the University of Oxford.

As a hospitalist, I see 10 or 20 brain scans every week. A healthy 40-year-old brain nicely fills out the allotted space in the skull. Most 70-year-old brains have an obvious degree of shrinkage. Those with the most shrinkage typically have worse mental functioning, often diagnosed clinically as dementia, or its precursor, mild cognitive impairment (MCI).

The medical term for brain shrinkage is brain atrophy. It reflects loss of brain cells or decrease in brain cell size. I see A LOT of atrophied brains and impaired mental functioning—aka cognition—in the elderly.

Not everybody with atrophy has mental impairment; healthy brains slowly atrophy with age. Alzheimer’s disease patients atrophy quickly; MCI patients atrophy at an intermediate rate. MCI patients converting over the years to Alzheimer’s show a faster rate of atrophy.

Mild cognitive impairment affects 14 to 18% of those over age 70 (five million in the U.S.). Half of these convert to Alzheimer’s disease or another dementia within five years. We desperately need a way to prevent or slow that conversion.

That’s why I was excited to see a research report in which brain atrophy was slowed with three simple daily vitamins: folic acid 0.8 mg, B12 0.5 mg, and B6 20 mg. The investigators will report later on whether the vitamins helped prevent mental decline.

These three vitamins are involved in homocysteine metabolism; they decrease blood levels of homocysteine. Read elsewhere if you want the boring details.

Methodology

Oxford area participants were at least 70 years of age and had mild cognitive impairment but not dementia. Blood homocysteine levels were drawn periodically. Participants were randomized to take either placebo (83 subjects) or the daily vitamins (85 subjects) for two years. MRI scans were done periodically to determine brain volume. Tests of mental functioning were done periodically. More subjects were in the study at the outset but some dropped out and others didn’t have technically adequate MRI scans.

Results

After adjustment for age, the annual rate of brain atrophy was 30% less in the vitamin group compared to placebo.

For the placebo group, the rate of brain atrophy was clearly related to baseline homocysteine levels: higher homocysteine, faster atrophy.

Although the study was not powered to detect an effect of treatment on cognition (findings to be reported separately), in a post hoc analysis, we noted that final cognitive test scores were correlated to the rate of atrophy.

Atrophy appears to be a major determinant of cognitive decline in this population.

There were no significant safety issues and no differences in adverse events between the groups.

The vitamin group lowered homocysteine levels by 32% compared to placebo.

Reduction in brain shrinkage rate was best in those with a higher baseline homocysteine level (over 13 micromol/L); those with the lowest baseline levels (<9.5 micromol/L) showed no effect of vitamin therapy. [In the U.S., 13% of those over 60 have concentrations over 13 micromol/L, whereas the median is 10 micromol/L.]

Comments

Although this is small study, I’m excited about the future clinical implications. The results need to be replicated. I can’t wait to hear from this group regarding the details of mental functioning tests. If preservation of brain function or other practical benefits don’t accompany a slower rate of atrophy , it’s no use taking the vitamins.

A 2008 study found no clinical benefit with a similar vitamin mix in Alzheimer’s patients with mild to moderate disease. In other words, the rate of mental decline was no different than the placebo group. Average homocysteine level was 9.16 micromole/L and fell by 30% during the 18-month-long study. Even those with the highest homocysteine levels showed no benefit. Perhaps B vitamins need to be started much earlier in the disease process to be effective.

The time may come where we screen all 60-year-olds for above-average homocysteine levels, starting them on the vitamin cocktail.

One caveat, however. Ten years ago doctors were quite excited about preventing heart disease events (e.g., heart attacks, cardiac deaths) and strokes in people with high homocysteine levels. We knew that high levels were associated with cardiac events and strokes, and we knew the B vitamins would lower the blood levels. We learned a couple years ago that B vitamin therapy actually didn’t help heart patients or those at high risk for heart disease. Nor do the vitamins prevent strokes. (If you’re a heart patient still taking Foltx, ask your cardiologist if it’s OK to stop it now.)

Steve Parker, M.D.

References:

Smith, A., Smith, S., de Jager, C., Whitbread, P., Johnston, C., Agacinski, G., Oulhaj, A., Bradley, K., Jacoby, R., & Refsum, H. (2010). Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial PLoS ONE, 5 (9) DOI: 10.1371/journal.pone.0012244

Aisen, P.S., et al. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: A randomized controlled trial. Journal of the American Medical Association, 300 (2008): 1,774-1,783.

Low-Carb Diets Killing People?

Animal-based low-carb diets are linked to higher death rates, according to a study in the Annals of Internal Medicine. On the other hand, a vegetable-based low-carb diet was associated with a lower mortality rate, especially from cardiovascular disease.

As always, “association is not causation.”

Since I created the Low-Carb Mediterranean Diet, it’s just a matter of time before someone asks me, “Haven’t you heard that low-carb diets cause premature death?” So I figured I’d better take a close look at the new research by Fung and associates.

It’s pretty weak and unconvincing. I have little to add to the cautious editorial by William Yancy, Matthew Maciejewski, and Kevin Schulman published in the same issue of Annals.

The study at hand was observational over many years, using data from the massive Nurses’ Health Study and Health Professionals’ Follow-up Study. To find the putative differences in mortality, the researchers had to compare the participants eating the most extreme diets. The 80% of study participants eating in between the extremes were neutral in terms of death rates.

They report that “…the overall low-carbohydrate diet score was only weakly associated with all-cause mortality.” Furthermore,

These results suggest that the health effects of a low-carbohydrate diet may depend on the type of protein and fat, and a diet that includes mostly vegetable sources of protein and fat is preferable to a diet with mostly animal sources of protein and fat.

In case you’re wondering, all these low-carb diets derived between 35 and 42% of energy (total calories) from carbohydrate, with an average of 37%. Anecdotally, many committed low-carbers chronically derive 20% of calories from carbohydrate (100 g of carb out of 2,000 calories/day). The average American eats 250 g of carb daily, 50-60% of total calories.

Yancy et al point out that “Fung and coworkers did not show a clear dose-response relationship in that there was not a clear progression of risk moving up or down the diet deciles.” If animal proteins and fats are lethal, you’d expect to see some dose-response relationship, with more deaths as animal consumption gradually increases over the deciles.

The Fung study is suggestive but certainly not definitive. Anyone predisposed to dietary caution who wants to eat lower-carb might benefit from eating fewer animal sources of protein and fat, and more vegetable sources. Fung leaves it entirely up to you to figure out how to do that. Compared to an animal-based low-carb diet, the healthier low-carb diet must subsitute more low-carb vegetables and higher-fat plants like nuts, seeds, seed oils and olive oil, and avocadoes, for example. What are higher-protein plants? Legumes?

You can see how much protein and fat are in your favorite vegetables at the USDA Nutrient Database.

The gist of Fung’s study dovetails with the health benefits linked to low-meat diets such as traditional Mediterranean and DASH. On the other hand, if an animal-based low-carb diet helps keep a bad excess weight problem under control, it too may by healthier than the standard American diet.

See the Yancy editorial for a much more detailed and cogent analysis. As is so often the case, “additional studies are needed.”

Steve Parker, M.D.

Reference: Fung, Teresa, et al. Low-carbohydrate diets and all-cause and cause specific mortality: Two cohort studies. Annals of Internal Medicine, 153 (2010): 289-298.

“But Doc, I’m Too Heavy to Exercise!”

I’ve written elsewhere about the death-defying aspect of exercise and myriad other health benefits of regular physical activity.

Very heavy folks potentially have more to gain in terms of health and longevity compared to skinny people. So it’s a cruel irony that the heavier you are, the harder it is exercise. At some point even light exercise becomes impossible.

Average-height women tipping the scales at about 280 pounds (127 kg) and men at 360 pounds (164 kg) aren’t going to be able to jog around the block, much less run a marathon. These weights are 100 percent over ideal or healthy levels. An actual “exercise program” probably won’t be possible until some weight is lost simply through very-low-carb eating, calorie restriction, or bariatric surgery. The initial exercise goal for you may just be to get moving through activities of daily living and perhaps brief walks and calisthenics while sitting in a chair.

“I’ll get started after I finish this cigarette.”

Markedly obese people who aren’t up to the aforementioned extreme weights can usually tolerate a low-intensity physical activity program. At 50 percent over ideal weight, an average-height woman of 210 pounds (95 kg) is carrying 70 excess pounds (32 kg) of fat. Her male counter-part lugs around 90 pounds (41 kg) of unnecessary fat. This weight burden causes dramatic breathlessness and fatigue upon exertion, and makes the joints and muscles more susceptible to aching and injury.

If you’re skinny, just imagine trying to walk or run a mile carrying a standard five-gallon (19 liter) water cooler bottle, which weighs only 43 pounds (19.5 kg) when full. The burden of excess fat makes it quite difficult to exercise.

If you’re markedly obese, several tricks will enhance your exercise success. I want you to avoid injury, frustration, and burn out. Start with light activity for only 10 or 15 minutes, gradually increase session length (e.g., by two to four minutes every two to four weeks) and increase exercise intensity only after several months. Your joints and muscles may appreciate easy, low-impact exercises such as stationary cycling, walking, swimming, and pool calisthenics/water aerobics.

You may also benefit from the advice of a personal fitness trainer arranged through a health club, gym, or YMCA/YWCA. Check out several health clubs before you join. Some of them are primarily meat markets for beautiful slender yuppies. You may feel more comfortable in a gym that welcomes and caters to overweight people. Hospitals are increasingly developing fitness centers with obese orthopedic, heart, and diabetic patients in mind.

Steve Parker, M.D.

Ketogenic Diet for Alzheimers Disease?

Ketogenic diets have seen a resurgence in the last two decades as a treatment for childhood epilepsy, particularly difficult-to-control cases not responding to drug therapy. It works, even in adults. That’s why some brain experts are wondering if ketogenic diets might be helpful in other brain disorders, such as Alzheimer’s disease and Parkinson’s disease.

I’ll save you some time and just give you the conclusion of a 2006 scientific article I read: maybe, but it’s way too soon to tell.

The article is called “Neuroprotective and disease-modifying effects of the ketogenic diet,” from researchers at the National Institutes of Health’s National Institue of Neruological Disorders and Stroke. Sounds promising doesn’t it?

The article goes into detail about how the ketogenic diet might be good for brain health. Dr. Emily Deans would be very interested in that, but most of my readers not. Two-and-a-half pages on non-human animal studies, too.

What is this “Ketogenic diet” used for epilepsy?

The most common ketogenic diet for childhood epilepsy is the one developed by Wilder in 1921. It was a popular treatment for epilepsy in the 1920s and 1930s. Fats provide 80 to 90% of the calories in the diet, with sufficient protein for growth, and minimal carbohydrates. Since carbs are in short supply, the body is forced to use fats as an energy source, which generates ketone bodies—acetoacetate, acetone, beta-hydroxybutyrate, largely from the liver.

So what?

Not much. This article may have been written to stimulate future research, and I hope it does. I just searched PubMed for “ketogenic diet AND Alzheimer” and came up with nothing new since 2006.

Could the Ketogenic Mediterranean Diet prevent or alleviate Alzheimer’s disease? At this point, just flip a coin.

Steve Parker, M.D.

Reference: Gasior M, Rogawski MA, & Hartman AL (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioural pharmacology, 17 (5-6), 431-9 PMID: 16940764

Prevalence Figures for Diabetes and Prediabetes

In January of 2011, the U.S. Centers for Disease Control and Prevention released the latest estimates for prevalence of diabetes and prediabetes. The situation is worse than it was in 2008, the last figures available.

  • Nearly 27% of American adults age 65 or older have diabetes (overwhelmingly type 2)
  • Half of Americans 65 and older have prediabetes
  • 11% of U.S. adults (nearly 26 million) have diabetes (overwhelmingly type 2)
  • 35% of adults (79 million) have prediabetes, and most of those affected don’t know it

The CDC estimates that one of every three U.S. adults could have diabetes by 2050 if present trends continue.

The press release from the CDC mentions that physical activity and avoidance of overweight will prevent some cases of diabetes. I believe that limiting consumption of refined carbohydrates like sugar and flour would also help.

Those who already have diabetes and prediabetes should consider carbohydrate-restricted Mediterranean-style eating, as in Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet.

Steve Parker, M.D.