Advanced Mediterranean Diet

Judging from improvement in hemoglobin A1c, the combination of aerobic and strength training is needed to improve diabetic blood sugar levels.  Both types of exercise—when considered alone—did not improve diabetes control, according to the latest research in the Journal of the American Medical Association.

One type of resistance training

Why is this important?  While the most popular way to control diabetes is drug therapy, we don’t have very little information about the long-term adverse effects of many of these drugs.  Some of my diabetic patients will remember Rezulin (troglitazone), which was pulled from the U.S. market after it was linked to deaths from liver failure.

One of the things that impressed me about Dr. Richard Bernstein’s book, Diabetes Solution, was his strong advocacy of weight training, also known as resistance training and strength training.  Weight lifting is a typical example.

Prior studies had shown exercise-induced  improvements (reductions)  in hemoglobin A1c, a great test for overall diabetes control, in the range of o.66% to 1.0% (absolute change, not relative).  That’s comparable to what we see with many drugs.  Much easier to pop a pill though, huh?

One earlier study showed hemoglobin A1c lowered by 0.4% with resistance training, 0.5% with aerobic training, and 1.0% with combined resistance/aerobic.  But folks doing both aerobic and resistance were exercising 270 minutes a week—39 minutes a day—which was significantly more than the people just doing one type of exercise. [This was the DARE study: Diabetes Aerobic and Resistance Exercise.] 

Investigators at the Pennington Biomedical Research Center in Louisiana wondered which type of exercise would be more effective, comparing the same minutes per week of activity.

Methodology

They randomized 262 sedentary type 2 diabetics to one of four groups: control, aerobic exercise, resistance training 3 days a week, or combined aerobic and resistance training (resistance twice weekly).  All three groups exercised for about 140 minutes a week—just 20 minutes a day, on average—for nine months.  Exercise intensity was 50 to 80% of maximum oxygen consumption (determined by a baseline treadmill stress test).  Nearly all participants were on diabetic drugs; 18% were on insulin.  I think the aerobic group exercised on treadmills.

Participant characteristics:  Women were 64% of the total.  Average age 56. Forty-seven percent were non-white (114 black, 10 Hispanic/other).  Average body mass index was 35.  Average hemoglobin A1c was 7.7%.  Not too many people dropped out of the study before it was over.

Results

No serious adverse event occurred during exercise.  The authors didn’t mention the occurence of hypoglycemia.

The combination training group dropped their hemoglobin A1c average by 0.34% (p = 0.03). The pure resistance and aerobic exercisers didn’t show any improvement over the control group.

The combination group lost 1.6 kg body weight on average compared to the control group.  Pure resistance and aerobic exercisers’ weights didn’t differ from the control group. [Remember, this was not a weight-loss study.]

Comments

The authors write:

The failure of the aerobic group to lose a substantial amount of weight (or fat) has been reported in numerous aerobic exercise trials, which may be due to aerobic training resulting in [higher] energy intake, expenditure compensation, or both.

If you’re trying to lose excess fat weight, resistance training appears to win over aerobic exercise.

Doing either aerobic execise or resistance exercise for an average of 20 minutes a day will not improve hemoglobin A1c levels in most type 2 diabetics.  We can assume blood sugars aren’t lower either.  It takes a combination of both types of exercise to lower hemoglobin A1c.

A hundred and forty minutes of exercise weekly—just 20 minutes a day—is not too much to ask for, if improved health and weight management are the goals.  More would be better.

Over nine months, the control group ended up needing more diabetic drugs.  The combination training group decreased its drug use.

Dr. Bernstein may still by right to stress resistance training over aerobic.  I bet he’d say these folks weren’t exercising enough.  The study at hand suggests that it’s important to do both types of exercise, especially if you’re not going to put much time into it.

The details of the resistance training program are probably important.  You can read the study yourself and decide if participants were on a good regimen.  I’ve little expertise in that area. 

Diabetics taking insulin, sulfonylureas, and meglitinides are at risk for hypoglycemia during exercise. The study authors made little mention of this, so it may be safe to assume it wasn’t a problem. Certified diabetes educators saw participants monthly, which may have nipped the problem in the bud.

Steve Parker, M.D.

Church, Timothy, et al.  Effects of aerobic and resistance training on hemoglobin A1c levels in patients with type 2 diabetes.  Journal of the American Medical Association, 304 (2010): 2,253-2,262.  doi:10.1001/jama.2010.1710

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.

A Paleolithic diet lowered blood sugar levels better than a control diet in coronary heart disease patients with elevated blood sugars, according to Swedish researchers reporting in 2007.

About half of patients with coronary heart disease have abnormal glucose (blood sugar) metabolism.  Lindeberg and associates wondered if a Paleolithic diet (aka “Old Stone Age,” “caveman,” or ancestral human diet) would lead to improved blood sugar levels in heart patients, compared to healthy, Mediterranean-style, Western diet.

Methodology

Investigators at the University of Lund found enrolled 38 male heart—average age 61—patients and randomized them to either a paleo diet or a “consensus” (Mediterranean-like) diet to be followed for 12 weeks.  Average weight was 94 kg.  Nine participants dropped out before completing the study, so results are based on 29 participants.  All subjects had either prediabetes or type 2 diabetes (the majority) but none were taking medications to lower blood sugar.  Baseline hemoglobin A1c’s were around 4.8%.  Average fasting blood sugar was 125 mg/dl (6.9 mmol/l); average sugar two hours after 75 g of oral glucose was 160 mg/dl (8.9 mmol/l).

The paleo diet was based on lean meat, fish, fruits, leafy and cruciferous vegetables, root vegetables (potatoes limited to two or fewer medium-sized per day), eggs, and nuts (no grains, rice, dairy products, salt, or refined fats and sugar). 

The Mediterranean-like diet focused on low-fat dairy, whole grains, vegetables, fruits, potatoes, fatty fish, oils and margarines rich in monounsaturated fatty acids and alpha-linolenic acid. 

Both groups were allowed up to one glass of wine daily.

No effort was made to restrict total caloric intake with a goal of weight loss.

Results

Absolute carbohydrate consumption was 43% lower in the paleo group (134 g versus 231 g), and 23% lower in terms of total calorie consumption (40% versus 52%).  Glycemic load was 47% lower in the paleo group (65 versus 122), mostly reflecting lack of cereal grains.

The paleo group ate significantly more nuts, fruit, and vegetables.  The Mediterranean group ate significantly more cereal grains,oil, margarine, and dairy products.

Glucose control improved by 26% in the paleo group compared to 7% in the consensus group.  The improvement was statisically significant only in the paleo group.  The researchers believe the improvement was independent of energy consumption, glycemic load, and dietary carb/protein/fat percentages.

High fruit consumption inthe paleo group (493 g versus 252 g daily) didn’t seem to impair glucose tolerance. 

Hemoglobin A1c’s did not change or differ significantly between the groups.

Neither group showed a change in insulin sensitivity (HOMA-IR method).

Comments

The authors’ bottom line:

In conclusion, we found marked improvement of glucose tolerance in ischemic heart disease patients with increased blood glucose or diabetes after advice to follow a Palaeolithic [sic] diet compared with a healthy Western diet.  The larger improvement of glucose tolerance in the Palaeolithic group was independent of energy intake and macronutrient composition, which suggests that avoiding Western foods is more important than counting calories, fat, carbohydrate or protein.  The study adds to the notion that healthy diets based on whole-grain cereals and low-fat dairy products are only the second best choice in the prevention and treatment of type 2 diabetes.

This was a small study; I consider it a promising pilot.  Results apply to men only, and perhaps only to Swedish men.  I have no reason to think they wouldn’t apply to women, too.  Who knows about other ethnic groups?

This study and the one I mention below are the only two studies I’ve seen that look at the paleo diet as applied to human diabetics.  If you know of others, please mention in the Comments section. 

The higher fruit consumption of the paleo group didn’t adversely affect glucose control, which is surprising.  Fruit is supposed to raise blood sugar.  At 493 grams a day, men in the paleo group ate almost seven times the average fruit intake of Swedish men (75 g/day).  Perhaps lack of adverse effect on glucose control here reflects that these diabetics and prediabetics were mild cases early in the course of the condition—diabetes tends to worsen over time.

Present day paleo and low-carb advocates share a degree of simpatico, mostly because of carbohydrate restriction—at least to some degree—by paleo dieters.  Both groups favor natural, relatively unprocessed foods.  Note that the average American eats 250-300 g of carbohydrates a day.  Total carb intake in the paleo group was 134 g (40% of calories) versus 231 g (55% of calories) in the Mediterranean-style diet.  Other versions of the paleo diet will yield different numbers, as will individual choices for various fruits and vegetables.  Forty percent of total energy consumption from carbs barely qualifies as low-carb. 

Study participants were mild, diet-controlled diabetics or prediabetics, not representative of the overall diabetic population, most of whom take drugs for it and have much higher hemoglobin A1c’s.

Lindeberg and associates in 2009 published results of a paleo diet versus standard diabetic diet trial in 13 diabetics.  Although a small trial (13 subjects, crossover design), it suggested advantages to the paleo diet in terms of heart disease risk factors and improved hemoglobin A1c.  Most participants were on glucose lowering drugs; none were on insulin.  Glucose levels were under fairly good control at the outset.  Compared to the standard diabetic diet, the Paleo diet yielded lower hemoglobin A1c’s (0.4% lower—absolute difference), lower trigylcerides, lower diastolic blood pressure, lower weight, lower body mass index, lower waist circumference, lower total energy (caloric) intake, and higher HDL cholesterol.  Glucose tolerance was the same for both diets.  Fasting blood sugars tended to decrease more on the Paleo diet, but did not reach statistical significance (p=0.08).

The paleo diet shows promise as a treatment or preventative for prediabetes and type 2 diabetes.  Only time will tell if it’s better than a low-carb Mediterranean diet or other low-carb diets. 

Steve Parker, M.D.

Reference:  Lindeberg, S., et al.  Palaeolithic diet improves glucose tolerance more than a Mediterranean -like diet in individuals with ischemic heart disease.  Diabetologia, 50 (2007): 1,795-1,807.  doi: 10.1007/s00125-007-0716-y

Spanish researchers report that the Mediterranean diet reduced the risk of developing diabetes by 50% in middle-aged and older Spaniards, compared with a low-fat diet. 

Over 400 people participated in a trial comparing two Mediterranean diets and a low-fat diet.  Over the course of four years, 10 or 11% of the Mediterraneans developed type 2 diabetes, compared to 18% of the low-fatters.  One of the Mediterranean diets favored olive oil, the other promoted nut consumption.

We’ve seen previously that the Mediterranean diet prevents diabetes—not all cases, of course—in folks who have had a heart attack.  It also reduced the risk of diabetes in younger, generally healthy people in Spain.

So What?

The study at hand is not ground-breaking.  It expands the body of evidence that the Mediterranean diet is one of the healthiest around.

Learn how to move your diet in a Mediterranean direction at Oldways or the Advanced Mediterranean Diet website.

Steve Parker, M.D.

Reference: Salas-Salvado, J., Bullo, M., Babio, N., Martinez-Gonzalez, M., Ibarrola-Jurado, N., Basora, J., Estruch, R., Covas, M., Corella, D., Aros, F., Ruiz-Gutierrez, V., Ros, E., & , . (2010). Reduction in the Incidence of Type 2-Diabetes with the Mediterranean Diet: Results of the PREDIMED-Reus Nutrition Intervention Randomized Trial Diabetes Care DOI: 10.2337/dc10-1288

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) has been considering this issue recently at her 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 this year 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.  Myth busted.  [I hope that’s not copyrighted by the “Myth Busters” TV show.]

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.

Type 2 diabetes is associated with higher incidence of several cancers: liver, pancreas, uterus, colo-rectal, breast, and bladder.  On a brighter note, diabetics have lower risk of prostate cancer.

That’s about all we know for sure, according to a report from an expert panel convened by the American Diabetes Association and the American Cancer Society and published recently in CA: A Cancer Journal for Clinicians.

The report is focused on type 2 diabetes simply because 95% of all worldwide cases of diabetes are type 2; we have much more data.  [Type 1 diabetes, you may recall, has onset much earlier  in life and is fatal if not treated with insulin injections.  The type 1 pancreas produces no insulin.]

This report is a good summary of all we know about the cancer/diabetes connection in 2010.  What we don’t know far outweighs what we do know.

Does optimal treatment of diabetes reduce cancer risk?  Do particular diabetic medications raise or lower the risk of cancer?  If an overweight diabetic loses excess weight, does the risk of cancer diminish?  Sorry . . . we don’t know.

In men, 25% of all invasive cancers in the U.S. will be prostate cancer.  In women, breast cancer is the leader, comprising 26% of all cancers.  [Common skin cancers are rarely invasive or fatal and are not included in these statistics.  Melanoma, on the other hand, is invasive.]

The lifetime probability of an individual developing invasive cancer in the U.S. is about 4 in 10 (40%).  A little higher in men (45%), a little lower in women (38%).  The American Cancer Society projected 565,650 deaths from cancer in 2008.  If we look at deaths of people under 85, cancer kills more people than heart disease.

The traditional Mediterranean diet is associated with less risk of prostate, breast, colon, and uterus cancer.  Two of these, you’ll note, are seen at higher rates in diabetics.

Lack of regular exercise is associated with higher cancer rates. 

If I were a type 2 diabetic wanting to reduce my risk of cancer, I’d be sure to exercise regularly, keep my body mass index under 30 (if not lower), consider a Mediterranean-style diet, and ask my doctor to monitor for onset of cancer.

Steve Parker, M.D., author of The Advanced Mediterranean Diet

Reference: Giovannucci, E., Harlan, D., Archer, M., Bergenstal, R., Gapstur, S., Habel, L., Pollak, M., Regensteiner, J., & Yee, D. (2010). Diabetes and Cancer: A Consensus Report CA: A Cancer Journal for Clinicians DOI: 10.3322/caac.20078

Here’s my review of Dr. Bernstein’s Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars, published in 2007.  Per Amazon.com’s rating scale, I give it five stars (I love it).

♦   ♦   ♦ 

Dr. Richard K. Bernstein gives away thousands of dollars’ worth of medical advice in this masterpiece, Diabetes Solution.  It’s a summation of his entire medical career and a gift to the diabetes community.

The book starts off with some incredible testimonials: reversal of diabetic nerve damage, eye damage, and erectile dysfunction.  They’re a bit off-putting to a skeptic like me, like an infomercial.  Dr. Bernstein is either lying about these or he’s not; I believe him.  His strongest testimonial is his own.  He’s been a type 1 diabetic most of his life, having acquired the disease at a time when most type 1’s never saw 55 candles on a birthday cake.  He’s in his mid-70s now and still working vigorously.

I only found one obvious error and assume it’s a misprint. He writes that 95% of people born today in the U.S. will eventually develop diabetes.  That’s preposterous.  The U.S. Centers for Disease Control predicts that one in three born in 2000 will be diagnosed.

Dr. Bernstein delivers lots of facts that I can neither confirm nor refute.  He’s a full-time diabetologist; I am not.

“Put down the bread and no one will get hurt!”

The central problem in type 1 diabetes is that, due to a lack of insulin,  ingested carbohydrates lead to spikes (elevations) in blood sugar.  The sugar elevations themselves are toxic.  The usual insulin injections are not good imitators of a healthy pancreas gland. So Dr. Bernstein is an advocate of low-carb eating (about 30 g daily compared to the usual American 250-300 g).  He says the available insulins CAN handle the glucose produced by a high-protein meal.

Dr. B reminds us that insulin is the main fat-building hormone, which is one reason diabetics gain weight when they start insulin, and why type 2 diabetics with insulin resistance (and high blood insulin levels) are overweight and have trouble losing weight.  You can have resistance to insulin’s blood sugar lowering action yet no resistance to its fat-building (fat-storing) action.  Insulin also stimulates hunger, so insulin-resistant diabetics are often hungry.

“Carbohydrate counting” is a popular method for determining a dose of injected insulin.  Dr. B says the gram counts on most foods are only a rough estimate—far too rough.  He minimizes the error by minimizing the input (ingested carbs).  From his days as an engineer, he notes “small inputs, small mistakes.”

Dr. B also cites problems with the absorption of injected insulin.  Absorption is variable: the larger the dose, the greater the variability.  So don’t eat a lot of carbs that require a large insulin dose.  For adult type 1 diabetics, his recommended rapid-acting insulins doses are usually three to five units.  If a dose larger than seven units is needed, split it into different sites.

He recommends diabetics aim for normal glucoses (90 mg/dl or less) almost all the time, and hemoglobin A1c of 5% or less.  This is extremely tight control, tighter than any expert panel recommends.  He says this is the best way to avoid the serious complications of diabetes. 

Here’s a smattering of “facts” in the book that made an impact on me, a physician practicing internal medicine for over two decades.  I want to remember them, incorporate into my practice, or research further to confirm:

• Hemoglobin A1c of 5% equals an average blood sugar of 100 mg/dl (5.56 mmol/l).  For each one % higher, average glucose is 40 mg/dl (2.22  mmol/l) higher.
• He’s against any drugs that overstimulate (“burn out”) the remaining pancreas function in type 2 diabetics: sulfonylureas, meglitinides, “phenylalanine derivatives”.  Pancreas-provoking agents cause hypoglycemia and destroy beta cell function.
• The insulin sensitizers are metformin and thiazolidinediones.  He likes these.
• Blood sugar normalization in type 2 diabetes and early-stage type 1 can help restore beta cell function.
• He often speaks of preserving beta cell function.
• He believes in “insulin-mimetic agents” like alpha lipoic acid (especially R-ALA, and take biotin with either form) and evening primrose oil.  These  are no substitute for insulin injections but allow for lower insulin doses.  ALA and evening primrose oil don’t promote fat storage like insulin does.
• He says many cardiologists take ALA for its antioxidant properties [news to me]
• He says rosiglitazone works within two hours [news to me] but later admits it may take 12 weeks to see maximal benefit
• One of his goals is to preserve beta cell function if at all possible
• He prefers rosiglitazone over pioglitazone due to fewer drug interactions
• “Americans are fat largely because of sugar, starches, and other high-carbohydrate foods.”
• He’s convinced that people who crave carbohydrates have inherited the problem, which also predisposes to insulin resistance and type 2 diabetes.  Low-carb diets decrease the cravings for many, in his experience.
• In small amounts, alcohol is relatively harmless: dry wine, beer, spirits.  Very few doctors have the courage to say this.
• If you’re in a restaurant, you can use urine sugar test strips and saliva to test for presence of sugar or flour in food
• A rule of thumb: one gram of carbohydrate will raise blood sugar about 5 mg/dl (0.28  mmol/l) or less for most diabetic adults weighing 140 lb (64  kg) and about 2.5 mg/dl (0.139 mmol/l) in a 280-pounder (127  kg).  This must refer to type 1 diabetics or a type 2 with little residual pancreas beta cell function; variable degrees of insulin resistance and beta cell reserve in many type 2s would make this formula unreliable.
• Be wary of maltodextrin in Splenda: it does raise blood sugar.
• Much new to me in his section on artificial sweeteners.  Be wary of them.
• He avoids all grains, breads, crackers, barley, oats, rice, and pasta.
• Most diet sodas are OK.
• Coffees with 1-2 tsp milk is OK.  Cream is OK.
• He eats NO fruit and recommends against it.
• He avoids beets, corn, potatoes, and beans. A slice of tomato in one cup of salad is OK.  A small amount of onion is OK.
• String beans and snow peas are OK.
• Cooked vegetables tend to raise blood sugar more rapidly than raw.
• Use “Equal” aspartame tabs as a sweetener.  Don’t use “powdered” Splenda.
• Avoid nuts: too easy to overeat.
• For desert: sugar-free Jell-O Brand Gelatin.
• Yogurt?  Plain, whole milk, unsweetened.  Flavor with cinnamon, Da Vinci syrups, baking flavor extracts, stevia or Equal.
• Avoid balsamic vinegar.
• Need fiber?  Bran crackers or soybean products.
• “Ideally, your blood sugar should be the same after eating as it was before.”  85 mg/dl (4.72  mmol/l) is his usual goal.  If blood sugar rises by more than 10 mg/dl (0.56 mmol/l) after a meal, either the meal has to be changed or medication changed.
• Protein is a source of glucose: keep protein amounts at meals constant from day to day, especially if taking glucose-lowering drugs.
• The lowest-carb meal of the day should be breakafast.  Why?  Dawn phenomenon.
• He promotes strenuous, prolonged exercise, especially weight training (extensive discussion and instruction in book).
• Many diabetics on insulin need dose adjustments in 1/2 and 1/4 unit increments [news to me: if I ordered 4 and 1/4 units of insulin at the hospital, the nurses would laugh].
• Typical rapid-acting insulin doses for his adult type 1 patients are 3-5 units.  The “industrial doses” of insulin seen or recommended by many physicians reflect diets too high in carbohydrate.
• He says Lantus only acts for nine hours (nighttime injection) or 18 hours (AM injection).
• He doesn’t like mixed insulins (e.g., 70/30).
• Humalog and Novolog are more potent than regular insulin, so the dose is about 2/3 of the regular insulin dose
• “Only a few of the 20 available [home glucose monitoring] machines are suitably accurate for our purposes.”  “None are suitably accurate or precise above 200 mg/dl [11.11 mmol/l].”
• Vitamin C in doses over 250 mg interferes with fingertip glucose monitors.  Later he says doses over 500 mg cause falsely low readings.
• He prefers regular insulin (45 minutes before meal) over Novolog and Humalog, because of its five-hour duration of action.
• Insulin users need to check glucose levels hourly while driving.
• His personal basal insulin is 3 units Lantus twice daily.
• He urges use of glucose (e.g., Dextrotabs) to correct hypoglycemia.
• He says hypoglycemia is rare on his regimen.
• He has an entire chapter on gastroparesis.

Dr. Bernstein’s recommended eating program in a nutshell:

• Some similarities to the Atkins diet, which he never mentions.
• No simple sugars or “fast-acting” carbs like bread and potatoes, because even type 2s have impaired or nonexistent phase 1 insulin response.
• Limit carbs to an amount that will work with your injected insulin or your remaining phase 2 insulin response, if any.
• “Stop eating when you no longer feel hungry, not when you’re stuffed.”
• Follow a predetermined meal plan (each meal: same grams of carb and ounces of protein)
• Six g (or less) of carbs at breakfast, 12 g (or less) at lunch and evening meal.  So his patients count carb grams and protein ounces.
• Supplements are not required IF glucoses are controlled and eating a variety of veggies.  Otherwise you may need B-complex or multivitamin/multimineral supplement.
• Recipes are provided.

His has four basic drug treatment plans, tailored to the individual.  They are outlined in the book.  Dr. B provides detailed notes on what he does with his personal patients.

Overall impressions:

• Too complicated for most, and they won’t give up higher carb consumption.  It requires a high degree of committment and discipline.  In fact, I’ve never had a patient tell me they were on the Bernstein program.
• If I had type 1 diabetes, I might well follow his plan or the Low-Carb Mediterranean Diet, NOT the high-carb diet recommended by the ADA and many dietitians.
• And if I had type 2 diabetes?  Low-Carb Mediterranean Diet first, Diabetes Solution as second choice.
• If one can get his hemoglobins A1c down to 5% with other methods, would that be just as good?  Dr. B would argue that all other methods have blood sugar swings that are too wide.
• Many new ideas and techniques here, at least to me.
• He pretty much reveals his entire program here, which is priceless.
• I’m not sure this plan will work unless the patient’s treating physician is on-board.
• His personal testimony and breadth of knowledge are very persuasive. 

Steve Parker, M.D.

Disclosure:  I was given nothing of value by Dr. Bernstein or his publisher in return for this review.

A low-carbohydrate Mediterranean diet improved HDL cholesterol levels and glucose control better than either the standard Mediterranean diet or American Diabetes Association diet, according to Israeli researchers reporting earlier this year.

Background

Prior studies suggest that diets rich in monounsaturated fatty acids (olive oil, for example) elevate HDL cholesterol and reduce LDL cholestrol and triglycerides in type 2 diabetics.

Low-carb diets improve blood sugar levels and reduce excess body weight in type 2 diabetics, leading to the ADA’s allowance in 2008 of a low-carbohydrate diet as an alternative to standard diabetic diets.

Many—probably most—type 2 diabetics have insulin resistance:  the body’s cells that can remove sugar from the bloodstream are not very sensitive to the effect of insulin driving insulin into those cells.  They “resist” insulin’s effect.  Consumption of monounsaturated fatty acids  improves insulin sensitivity.  In other words, insulin is better able to push blood sugar into cells, removing it from the bloodstream.

Previous studies have shown that both low-carb diets and the Mediterranean diet reduce after-meal elevations in blood sugar, which likely lowers levels of triglycerides and LDL cholesterol.

How Was the Study Done?

The goal was to compare effects of three diets in overweight type 2 diabetics in Israel over the course of one year.  Study participants totalled 259.  Average age was 56, average weight 86 kg (189 lb), average hemoglobin A1c 8.3%, and average fasting plasma glucose (sugar) was 10.3 mmol/L (185 mg/dl).  [Many diabetics in the U.S. fit this profile.]  People taking insulin were excluded from the study, as were those with proliferative diabetic retinopathy—no reasons given. 

Participants were randomly assigned to one of three diets, so there were about 85 in each group.  [Over the course of one year, people dropped out of the study for various reasons, leaving each group with about 60 subjects.] 

Here are the diets:

• 2003 ADA (American Diabetes Association) diet:  50-55% of total caloric intake from carbohydrate (mixed glycemic index carbs), 30%  from fat, 20% from protein
• Traditional Mediterranean (TM):  50-55% low-glycemic-index carbs, 30% fat—high in monounsaturated fat, 15-20% protein
• Low-carb Mediterranean (LCM) :  35% low-glycemic-index carbs, 45% fat—high in monounsaturated fat, 15-20% protein

Patients were followed-up by the same dietitian every two weeks for one year.  All were advised to do aerobic exercise for 30-45 minutes at least three days a week.

Olive oil is traditionally the predominant form of fat in the Mediterranean diet and is a particularly rich source of monounsaturated fat.  At no point in this report was olive oil mentioned, nor any other source of monounsaturated fat.  Until I hear otherwise, I will assume that olive oil was the major source of monounsaturated fat in the TM and LCM diets. 

 All diets were designed to provide 20 calories per kilogram of body weight. 

In all three diets, saturated fat provided 7% of total calories.  Monounsaturated fatty acids provided 23% of total calories in the LCM, and  10% in the other two diets.  Polyunsaturated fatty acids provided 15% of calories in the LCM, and 12% in the other two diets.  The ADA diet provided 15 grams of fiber, the TM had 30 g, and the LCM had 45 g.

Adherence to the assigned diet was assessed with a “food frequency questionnaire” administered at six months.

What Did the Researchers Find?

Average reported energy intake was similar in all three groups: 2,222 calories per day.

Monounsaturated fat intake differences were statistically significant: 14.6, 12.8, and 12.6% for the LCM, TM, and ADA diets, respectively.  Polyunsaturated fat intake differences were statistically significant: 12.9, 11.5, and 11.2% for the LCM, TM, and ADA diets, respectively.

Percentage of energy from carbs was highest for the ADA diet (45.4%), intermediate for the TM diet (45.2%), and lowest for the LCM diet (41.9%).

At the end of 12 months, all three groups lost about the same amount of weight (8-9 kg or 18-20 lb), body mass index, and waist circumference.

Hemoglobin A1c fell in all three groups, but was significantly greater for the LCM group than for the ADA diet (6.3% absolute value vs 6.7%).

Triglycerides fell in all three groups, but was significantly greater for the LCM diet compared to the ADA diet.

The LCM group achieved a significant increase (12%) in HDL cholesterol compared to the ADA diet, but not different from the TM group.

LDL cholesterol fell in all three groups, and the LCM group’s drop (25%) was clearly superior to that of the ADA diet (14%) but about the same as the TM diet (21%).

Conclusions of the Investigators

We found that an intensive community-based dietary intervention reduced cardiovascular risk factors in overweight patients with [type 2 diabetes] for all three diets.  The LCM group had improved cardiovascular risk factors compared to either the ADA or the TM groups.

Only the LCM improved HDL levels and was superior to both the ADA and TM in improving glycaemic control.

It would appear that the low carbohydrate Mediterranean diet should be recommended for overweight diabetic patients.

My Comments

There’s no way the average diabetic could replicate this low-carb Mediterranean diet without working closely with a dietitian or nutritionist.

Any superiority of this low-carb Mediterranean diet may have as much to do with the increased monounsaturated fat intake as with the reduced carb consumption.  Monounsaturated fatty acid consumption is thought to improve insulin sensitivity. 

NutritionData’s Nutrient Search Tool can give you a list of foods high in monounsaturated fat.

The Mediterranean diet and low-carb diets independently have been shown to lower after-meal glucose levels, which probably lowers LDL cholesterol and triglycerides.

I’m disappointed the dietitians were not able to achieve a lower level of carbohydrate consumption in the low-carb Mediterranean diet group.  I suspect if they had, improvements in glucose control and lipids would have been even better.  But proof awaits another day.

We saw last year an article in the Annals of Internal Medicine that showed a dramatic reduction in the need for glucose-lowering drugs in type 2 diabetics following a different low-carb Mediterranean diet over four years, compared to a low-fat American Heart Association diet.  These two studies convince me a low-carb Mediterranean diet has real life-preserving and life-enhancing potential. 

Diabetics looking for a low-carb Mediterranean diet today have several options:

• design their own
• consult a dietitian or nutritionist
• use the Low-Carb Mediterranean Diet available free at the Diabetic Mediterranean Diet

If you’re aware of any other low-carb, explicitly Mediterranean-style diets, please share in the Comments section or e-mail me.

Steve Parker, M.D. 

References:

Elhayany, A., Lustman, A., Abel, R., Attal-Singer, J., & Vinker, S. (2010). A low carbohydrate Mediterranean diet improves cardiovascular risk factors and diabetes control among overweight patients with type 2 diabetes mellitus: a 1-year prospective randomized intervention study Diabetes, Obesity and Metabolism, 12 (3), 204-209 DOI: 10.1111/j.1463-1326.2009.01151.x 

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.

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! 

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.

The traditional Mediterranean diet has long been associated with longer lifespans and lower rates of chronic diseases: heart disease, strokes, dementia, and cancer (breast, prostate, lung, uterus).  Recent research has expanded the benefit list.

I ran across a good summary of the health benefits of Mediterranean-style eating at Medical News Today, published online May 6, 2009.  An excerpt:

The following health benefits have been observed by people who have a Mediterranean diet:

• Longer lifespan
• Lower risk of dying at any age
• Lower risk of dying from heart disease
• Lower risk of dying from cancer
• Lower risk of developing Type 2 diabetes
• Lower risk of hypertension (high blood pressure)
• Lower risk of raised cholesterol levels
• Lower risk of becoming obese
• Lower risk of developing Alzheimer’s disease

Not mentioned above is the lower risk of Parkinson’s Disease and chronic obstructive pulmonary disease.  You’ll also find a fair description of the traditional Mediterranean diet.

Steve Parker, M.D.