Tag Archives: diabetes

Rosiglitazone Severely Restricted by FDA

MedPageToday reported yesterday on the U.S. Food & Drug Administration’s ruling that the diabetes drug rosiglitazone should be used in new patients only if blood sugars are not controlled with other diabetes drugs, such as pioglitazone.

It sounds as if new users and their doctors may have to jump through some paperwork hoops to get the drug, which is more reason not to prescribe it.

The problem is that scientific studies suggest that rosiglitazone increases the risk of heart attack, heart failure, and death.

Steve Parker, M.D.

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Filed under Diabetes Complications, Drugs for Diabetes

Myth Busted: Alzheimer Dementia NOT Caused By Diabetes

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. 

Brain CT scan

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 epidimiologic. [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.  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. 

ResearchBlogging.orgSenile 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 previously 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. 

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.

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Filed under Carbohydrate, Diabetes Complications

Drug Review: Insulin

Insulin is life-saving for type 1 diabetics.  Many type 2 diabetics will eventually, if not at the outset, need to take insulin for adequate control of blood sugars, which should help prevent diabetes complications.

My comments here are simply a brief review of insulins used by type 2 diabetics.  Anyone taking insulin must work closely with a physician or diabetes nurse educator on proper dosing, injection technique, and recognition and management of hypoglycemia (low blood sugar).

This is NOT an insulin rig! Modern insulin injections barely hurt, if at all.

Insulin’s Mechanism of Action
 

 

 

Insulin is made by the pancreas to keep blood sugars from rising above a fairly strict range: 70-140 mg/dl or 3.89-7.78 mmol/l.  [It has many other actions that I won’t bother to outline here.]  When we eat a meal containing carbohydrates (and proteins to a lesser extent), blood sugar starts to rise as we digest the carbs.  Insulin drives the sugar into our body’s cells for use as immediate energy or conversion to fat as stored energy.  About half of the insulin produced by a healthy body is “basal,” meaning it’s secreted into the bloodstream in a steady, low-volume amount, to keep the liver from making too much sugar (glucose) and controlling fasting sugar levels.  The other half is secreted in to the bloodstream in response to meals.

In type 2 diabetes, the body’s tissues, at first, are resistant to the effect of insulin.  So the pancreas has to secrete more than usual (hyperinsulinism). As the illness progresses, the pancreas cannot keep up with demand for more insulin and starts to “burn out,” producing less insulin.  This is when many type 2 diabetics need to start insulin injections.  [These are generalities; there are exceptions.]

Types of Insulin

Specific names of insulins vary by manufacturer and by country.  By convention, I capitalize only the brand names below, plus NPH and NPL.

We could break them down into two types: human (identical in structure to human insulin) and analogs (minor molecular modifications to the usual human insulin molecule).  But most people don’t care about that.  It’s more helpful to distinguish them by the timing of their action:

  • Rapid acting:  lispro (e.g., Humalog), aspart (e.g., Novolog), glulisine (e.g., Apidra)
  • Short acting:  regular (e.g., Novolin R, Humulin R)
  • Intermediate to long acting:  NPH, glargine (e.g., Lantus), detemir (e.g., Levemir), degludec (e.g., Tresiba), NPL (neutral protamine lispro)

Rapid-acting insulins have onset of action between 5 and 15 minutes, peak effect in 30 to 90 minutes, and duration of action of 2 to 4 hours.

Short-acting “regular insulin” has  onset in 30 minutes, peaks in 2 to 4 hours, and works for 5 to 8 hours.

Intermediate to long-acting insulins start working in 2 hours, don’t have a well-defined peak of action, and may keep working for 20 or more hours (glargine), for 6 to 24 hours (detemir), or 30 to 42 hours (degludec).

All these times are gross approximations.  Once the insulin is injected into the fat below the skin, it has to be absorbed into the bloodstream and transported to the tissues where it does its magic.  Lots of factors affect this process. For instance, the thicker the fat tissue at the injection site, the slower the absorption.  Absorption tends to be  faster from the abdominal wall, slower from the arms, even slower from the thighs or buttocks.  Absorption can vary from day to day in an individual even when injection site and technique are identical.

As you might have guessed, the short- and rapid-acting insulins are usually injected before a meal in anticipation of blood sugar rising as food is digested.  The intermediate- and long-acting insulins imitate the healthy body’s “basal” insulin.

Manufacturers also supply premixed insulins, combining intermdiate or long-acting insulin with a short- or rapid-acting insulin.  Examples are Humalog 75/25, Humulin 70/30, and Novolog 70/30.

Dose and Selection of Insulin

See your physician or diabetes nurse educator for details.  Many type 2 diabetics get started just with an intermediate or long-acting insulin once or twice daily, with or without diabetes drugs by mouth. Nearly all type 1’s will need a long-acting “basal” insulin (one-third to one-half of their total daily insulin requirement, plus meal-time “bolus” dosing with a rapid-acting insulin. Insulin pumps are a topic for another day.

Side Effects

By far the most common and worrisome is hypoglycemia.

Steve Parker, M.D.

Last update: August 1, 2016

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High Carbohydrate Eating Increases Risk of Diabetes

ResearchBlogging.orgThe American Journal of Clinical Nutrition reported earlier this month that high consumption of carbohydrates, high-glycemic-index eating, and high-glycemic-load eating increases the risk of developing diabetes.  High fiber consumption, on the other hand, seems to protect against diabetes. 

The article abstract doesn’t mention type 1 versus type 2 diabetes, but it’s probably type 2, the most common kind.

The observational reseach was done in the Netherlands, but I bet the findings apply to other populations as well.  Australian researchers had established years ago that high-glycemic-index and high-glycemic-load eating is associated with onset of diabetes, at least in women

Is high carbohydrate consumption putting too much strain on the pancreas, which produces the insulin needed to process the carbs?

Steve Parker, M.D.

Reference:  Sluijs I, van der Schouw YT, van der A DL, Spijkerman AM, Hu FB, Grobbee DE, & Beulens JW (2010). Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) study. The American journal of clinical nutrition PMID: 20685945

1,2,3

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Filed under Carbohydrate, Causes of Diabetes

Documented Health Benefits of the Mediterranean Diet

The enduring popularity of the Mediterranean diet is attributable to three things:

  1. Taste
  2. Variety
  3. Health benefits

 For our purposes today, I use “diet” to refer to the usual food and drink of a person, not a weight-loss program.

The scientist most responsible for the popularity of the diet, Ancel Keys, thought the heart-healthy aspects of the diet related to low saturated fat consumption.  He also thought the lower blood cholesterol levels in Mediterranean populations (at least Italy and Greece) had something to do with it, too.  Dietary saturated fat does tend to raise cholesterol levels, both LDL and HDL.

Even if Keys was wrong about saturated fat and cholesterol levels being positively associated with heart disease, numerous studies (involving eight countries on three continents) strongly suggest that the Mediterranean diet is one of the healthiest around.  See References below for the most recent studies.

Relatively strong evidence supports the Mediterranean diet’s association with:

■ increased lifespan

■ lower rates of cardiovascular disease such as heart attacks and strokes

■ lower rates of cancer (prostate, breast, uterus, colon)

■ lower rates of dementia

■ lower incidence of type 2 diabetes

 

Weaker supporting evidence links the Mediterranean diet with:

■ slowed progression of dementia

■ prevention of cutaneous melanoma

■ lower severity of type 2 diabetes, as judged by diabetic drug usage and fasting blood sugars

■ less risk of developing obesity

■ better blood pressure control in the elderly

■ improved weight loss and weight control in type 2 diabetics

■ improved control of asthma

■  reduced risk of developing diabetes after a heart attack

■ reduced risk of mild cognitive impairment

■  prolonged life of Alzheimer disease patients

■ lower rates and severity of chronic obstructive pulmonary disease

■ lower risk of gastric (stomach) cancer

■ less risk of macular degeneration

■ less Parkinsons disease

■ increased chance of pregnancy in women undergoing fertility treatment

■  reduced prevalence of metabolic syndrome (when supplemented with nuts)

■ lower incidence of asthma and allergy-like symptoms in children of women who followed the Mediterranean diet while pregnant

Did you notice that I used the word “association” in relating the Mediterranean diet to health outcomes?  Association, of course, is not causation. 

The way to prove that a particular diet is healthier is to take 20,000 similar young adults, randomize the individuals  in an interventional study to eat one of two test diets for the next 60 years, monitoring them for the development of various diseases and death.  Make sure they stay on the assigned test diet.  Then you’d have an answer for that population and those two diets.  Then you have to compare the winning diet to yet other diets.  And a study done in Caucasians would not necessarily apply to Asians, Native Americans, Blacks, or Hispanics.

Now you begin to see why scientists tend to rely on observational  rather than interventional diet studies.

I became quite interested in nutrition around the turn of the century as my patients asked me for dietary advice to help them lose weight and control or prevent various diseases.  At that time, the Atkins diet, Mediterranean diet, and Dr. Dean Ornish’s vegetarian program for heart patients were all prevalent.  And you couldn’t pick three programs with more differences!  So I had my work cut out for me. 

After much scientific literature review, I find the Mediterranean diet to be the healthiest for the general population.  People with particular medical problems or ethnicities may do better on another diet.  A low-carb Mediterranean diet should be healthier for type 2 diabetics.  Dan Buettner makes a good argument for plant-based diets in his longevity book, The Blue Zones.  The traditional Mediterranean diet qualifies as plant-based.

What do you consider the overall healthiest diet, and why?

Steve Parker, M.D.

References:

Buckland, Genevieve, et al.  Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort studyAmerican Journal of Clinical Nutrition, December 9, 2009, epub ahead of print.  doi: 10.3945/ajcn.2009.28209

Fortes, C., et al.  A protective effect of the Mediterraenan diet for cutaneous melanoma.  International Journal of Epidmiology, 37 (2008): 1,018-1,029.

Sofi, Francesco, et al.  Adherence to Mediterranean diet and health status: Meta-analysis.  British Medical Journal, 337; a1344.  Published online September 11, 2008.  doi:10.1136/bmj.a1344

Benetou, V., et al.  Conformity to traditional Mediterranean diet and cancer incidence: the Greek EPIC cohort.  British Journal of Cancer, 99 (2008): 191-195.

Mitrou, Panagiota N., et al.  Mediterranean Dietary Pattern and Prediction of All-Cause Mortality in a US Population,  Archives of Internal Medicine, 167 (2007): 2461-2468.

Feart, Catherine, et al.  Adherence to a Mediterranean diet, cognitive decline, and risk of dementia.  Journal of the American Medical Association, 302 (2009): 638-648.

Scarmeas, Nikolaos, et al.  Physical activity, diet, and risk of Alzheimer Disease.  Journal of the American Medical Association, 302 (2009): 627-637.

Scarmeas, Nikolaos, et al.  Mediterranean Diet and Mild Cognitive Impairment.  Archives of Neurology, 66 (2009): 216-225.

Scarmeas, N., et al.  Mediterranean diet and Alzheimer disease mortality.  Neurology, 69 (2007):1,084-1,093.

Fung, Teresa, et al.  Mediterranean diet and incidence of and mortality from coronary heart disease and stroke in women.  Circulation, 119 (2009): 1,093-1,100.

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

Salas-Salvado, Jordi, et al.  Effect of a Mediterranean Diet Supplemented With Nuts on Metabolic Syndrome Status: One-Year Results of the PREDIMED Randomized Trial.  Archives of Internal Medicine, 168 (2008): 2,449-2,458.

Mozaffarian, Dariush, et al.  Incidence of new-onset diabetes and impaired fasting glucose in patients with recent myocardial infarction and the effect of clinical and lifestyle risk factors.  Lancet, 370 (2007) 667-675.

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

Shai, Iris, et al.  Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet.  New England Journal of Medicine, 359 (2008): 229-241.

Martinez-Gonzalez, M.A., et al.  Adherence to Mediterranean diet and risk of developing diabetes: prospective cohort study.  British Medical Journal, BMJ,doi:10.1136/bmj.39561.501007.BE (published online May 29, 2008).

Trichopoulou, Antonia, et al.  Anatomy of health effects of the Mediterranean diet: Greek EPIC prospective cohort studyBritish Medical Journal, 338 (2009): b2337.  DOI: 10.1136/bmj.b2337.

Barros, R., et al.  Adherence to the Mediterranean diet and fresh fruit intake are associated with improved asthma control.  Allergy, vol. 63 (2008): 917-923.

Varraso, Raphaelle, et al.  Prospective study of dietary patterns and chronic obstructive pulmonary disease among US men.  Thorax, vol. 62, (2007): 786-791

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Book Review: Diabetes Solution – The Complete Guide to Achieving Normal Blood Sugars

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.

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Whole Grains Reduce Heart Attacks and Strokes

Whole grain consumption is associated with a 21% reduction in cardiovascular disease when compared to minimal whole grain intake, according to a 2008 review article in Nutrition, Metabolism, and Cardiovascular Disease.   

Coronary heart disease is the No. 1 killer in the developed world.  Stroke is No. 3.  The term “cardiovascular disease” lumps together heart attacks, strokes, high blood pressure,  and generalized atherosclerosis (hardening of the arteries). 

Investigators at Wake Forest University reviewed seven pertinent studies looking at whole grains and cardiovascular disease.  The studies looked at groups of people, determining their baseline food consumption via questionnaire, and noted disease development over time.  These are called “prospective cohort studies.” 

None of these cohorts was composed purely of diabetics.

The people eating greater amounts of whole grain (average of 2.5 servings a day) had 21% lower risk of cardiovascular disease events compared to those who ate an average of 0.2 servings a day.  Disease events included heart disease, strokes, and fatal cardiovascular disease.  The lower risk was similar in degree whether the focus was on heart disease, stroke, or cardiovascular death.

Note that refined grain consumption was not associated with cardiovascular disease events. 

Why does this matter?

The traditional Mediterranean diet is rich in whole grains, which may help explain why the diet is associated with lower rates of cardiovascular disease.  If we look simply at longevity, however, a recent study found no benefit to the cereal grain component of the Mediterranean diet.  Go figure . . . doesn’t add up. 

Readers here know that over the last four months I’ve been reviewing the nutritional science literature that supports the disease-suppression claims for consumption of fruits, vegetables, and legumes.  I’ve been disappointed.  Fruit and vegetable consumption does not lower risk of cancer overall, nor does it prevent heart disease.  I haven’t found any strong evidence that legumes prevent or treat any disease, or have an effect on longevity.  Why all the literature review?  I’ve been deciding which healthy carbohydrates diabetics and prediabetics should add back into their diets after 8–12 weeks of the Ketogenic Mediterranean Diet.

The study at hand is fairly persuasive that whole grain consumption suppresses heart attacks and strokes and cardiovascular death.  [The paleo diet advocates and anti-gluten folks must be disappointed.]  I nominate whole grains as additional healthy carbs, perhaps the healthiest.

But . . .

. . .  for diabetics, there’s a fly in the ointment: the high carbohydrate content of grains often lead to high spikes in blood sugar.  It’s a pity, since diabetics are prone to develop cardiovascular disease and whole grains could counteract that.  We need a prospective cohort study of whole grain consumption in diabetics.  It’ll be done eventually, but I’m not holding my breath.

[Update June 12, 2010: The aforementioned study has been done in white women with type 2 diabetes.  Whole grain and bran consumption do seem to protect them against overall death and cardiovascular death.  The effect is not strong.]

What’s a guy or gal to do with this information now?

Non-diabetics:  Aim to incorporate two or three servings of whole grain daily into your diet if you want to lower your risk of heart disease and stroke. 

Diabetics:  Several options come to mind:

  1. Eat whatever you want and forget about it [not recommended].
  2. Does coronary heart disease runs in your family?  If so, try to incorporate one or two servings of whole grains daily, noting and addressing effects on your blood sugar one and two hours after consumption.  Eating whole grains alone will generally spike blood sugars higher than if you eat them with fats and protein.  Review acceptable blood sugar levels here.
  3. Regardless of family history, try to eat one or two servings of whole grains a day, noting and addressing effects on your blood sugar.  Then decide if it’s worth it.  Do you have to increase your diabetic drug dosages or add a new drug?  Are you tolerating the drugs?  Can you afford them?    
  4. Assess all your risk factors for developing heart disease: smoking, sedentary lifestyle, high blood pressure, age, high LDL cholesterol, family history, etc.  If you have multiple risk factors, see Option #3.  And modify the risk factors under your control.   
  5. Get your personal physician’s advice.    

Steve Parker, M.D.

Extra Credit:  The study authors suggest a number of reasons—and cite pertinent scientific references—how whole grains might reduce heart disease:

  • improved glucose homeostasis (protection against insulin resistance, less rise in blood sugar after ingestion [compared to refined grains], improved insulin sensitivity or beta-cell function)
  • advantageous blood lipid effects (soluble fiber from whole grains [especially oats] reduces LDL cholesterol, lower amounts of the small LDL particles thought to be particularly damaging to arteries, tendency to raise HDL cholesterol and trigylcerides [seen with insulin resistance in the metabolic syndrome])
  • improved function of the endothelial cells lining the arteries (improved vascular reactivity)

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.

Reference: Mellen, P.B, Walsh, T.F., and Herrington, D.M.  Whole grain intake and cardiovascular disease: a meta-analysisNutrition, Metabolism and Cardiovascular Disease, 18 (2008): 283-290.

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Filed under Carbohydrate, coronary heart disease, Diabetes Complications, Grains, ketogenic diet, legumes, Mediterranean Diet, Stroke

My Ketogenic Mediterranean Diet and Low-Carb Eating: Six-Month Summary

I started my Ketogenic Mediterranean Diet on September 1, 2009.  After two months, I stopped compulsive record-keeping and food measurement and made a few other intentional tweaks: fish five times a week instead of seven miminum, more nuts (often two ounces a day—I like nuts and they’re convenient), less salad, more dark chocolate.  Otherwise the last four months have been similar to the initial two months of strict KMD.  My daily digestible carbohydrate intake has probably crept up to 40 g compared to 20-25 g on the strict KMD—this is still considered very low-carb. 

Accomplishments

Starting weight was 170 pounds (77.3 kg) on September 1.   After two months—8.6 weeks—my weight clearly stabilized at 155 lb (70.5 kg).  I lost the 15 lb (6.8 kg) over the first six weeks then just hovered around 155 lb.  So average weekly weight loss over the six weeks was 2.5 pounds.  Also lost a couple inches (5 cm) off my waist.

For the last four months—November through February—I’ve been eating the aforementioned liberalized KMD.  Weight has stayed around 155-157 lb (71 kg).  No calorie counting.  I eat as much as I want, except for carbs.  The experience of the first two months taught me how to eat 20-25 g of carbs in a day; it’s the gauge by which I estimate I’m eating 40 g daily now.

Has It Been Easy?

Yeah, relatively easy.  Two other adults in my house are also eating low-carb, which definitely helps.  Blogging here also helps me maintain compliance.  I promised myself to report everything—the good, the bad, and the ugly—honestly.  Accountability is important. 

Staying with the program may be easier for me than for others because I am heavily invested in it, psychologically and time-wise. 

It’s also been helpful for me to participate at two low-carb online communities: LowCarbFriends and Active Low-Carber Forums.  We support each other.  Thanks, guys.

I took diet holidays twice, for three days at both Thanksgiving and Christmas.  Gained three to five pounds (1.8 kg) each time on high-carb eating, but lost it over the next week by returning to the strict KMD.

Any Surprises?

Induction flu.  I’d never heard of it before.  Occurs typically on days 2–5 of very low-carb dieting: achiness and fatigue.  Others also experience headaches and dizziness, and it may last 1–2 weeks.

Rapid weight gain during my diet holidays (aka cheat days).  I was not gorging.  I figure the weight was mostly new glycogen in liver and muscle.  And water.

Eating fish more than once a day is a lot of fish!  Quickly boring, even unappetizing.  But that’s just me.  I need to be a more creative.  Most of my fish lately has been canned tuna.

Assuming that the Daily Values of various nutrients recommended by the U.S. Food and Drug Administration are valid, the KMD foods come up short in many vitamins and minerals.  I bet this is an issue (a problem?) with many, if not most, very low-carb diets if supplements aren’t used.  Those Daily Values are debatable, of course.  For instance, Gary Taubes argues that you don’t need much vitamin C if eating few carbs.  My nocturnal leg cramps and constipation were proof enough for me that I needed at least some supplements.  The recommended KMD supplements remedy the DailyValue shortfall in vitamins and minerals.  Dr. Richard K. Bernstein has a 30-gram carbohydrate diet for his diabetic patients and himself, as outlined in his Diabetes Solution book: no supplements are required.  

As time passes, I worry less about getting enough of various micronutrients.   I feel fine.  I’m still taking the recommended KMD supplements (5 pills a day) plus sugar-free Metamucil.   

I never had hunger that I couldn’t satisfy within the guidelines of the diet. 

No major trouble with cravings or longing for carbs.  I’ve gone six months now without whole grain bread, oatmeal, pizza, and pasta—very unusual for me.  I’d be OK never eating them again.  What I do miss are sweet, often fat-laced, carbohydrates: pie, cookies, cinnamon rolls, candy bars, cake, ice cream.  I doubt that desire will ever disappear, although it does for some who eat very low-carb.   

I counted calories only during the first two months of this experiment.  Remember, fats and proteins are unlimited.  Nevertheless, I ate fewer calories than my baseline intake.   This calorie reduction is a well-documented effect of very low-carb diets.  Fats and proteins are more satiating than carbohydrates.  It’s possible I’ve limited total calories subconsciously. 

[An interesting experiment would be to try to gain weight by over-eating fats and proteins while keeping total digestible carbs under 30 g/day.  Has it been done already?]

What’s Next?

I’d like to answer some intriguing questions.

Why did my weight loss stop where it did, at 155 lb (70.5 kg)? 

If I’d started the KMD at 270 lb (123 kg) instead of 170 lb (77.3 kg), would my weight loss have stopped at 255 lb (116 kg), 210 lb (95.5 kg) or 155 lb (70.5 kg)? 

Will two people, 300 lb each (136 kg), end up at the same final weight when following the program religiously?  Probably not, but why not?    

Six months ago, I believed many scientific studies supported the idea that a higher intake of carbohydrates is healthier, long-term, than the very low-carb Ketogenic Mediterranean Diet and other very low-carb diets.  Studies seemed to support higher carbohydrate intake in the form of traditional fruits, vegetables, legumes, and whole grains.  After reviewing the scientific literature over the last few months, I’m not so sure that higher carb consumption is necessary or beneficial for long-term health and longevity.  The evidence is weak.  Nearly all the pertinent studies are observational or epidemiologic—not the most rigorous science. 

On the other hand, I still can’t help feeling that the recommended eating styles of people like Monica Reinagel, Darya Pino, and Holly Hickman may be healthier than the KMD over the long run, at least for people free of diabetes and prediabetes.  What features unify those three?  Food that is minimally processed, fresh, locally produced when able, including a variety of fruits, vegetables, nuts, whole grains, and legumes. 

It seems that the human body is marvelously designed to survive, even thrive, with multiple ways of eating—but not all ways.   

The strongest evidence for higher carb consumption supports whole grains as a preventative for heart disease (coronary artery disease).  But the effect is modest. 

The argument against higher carb consumption is simple for people with diabetes and prediabetes: carbs raise blood sugar levels, sometimes to an unhealthy degree.  

I don’t see much role for highly processed, refined carbohydrates except as a cheap source of energy (calories).

What’s next for me is to formalize an opinion on which carbs, if any, and in what amount, to add back into the diet of those who have lost weight with the Ketogenic Mediterranean Diet.  The answer will probably be different for two groups:

  1. those who have diabetes, prediabetes, or metabolic syndrome
  2. healthy people who just need to control weight

The goal is to maximize health and longevity without tipping over into excessive carb intake that leads to overweight and obesity with associated illnesses.  

The traditional Mediterranean diet—long associated with health and longevity—is rich in carbohydrates.  The Ketogenic Mediterranean Diet—much lower in carbs—has great potential to help with loss of excess weight and control of blood sugar levels.  Does the KMD incorporate enough of the healthy components of the Mediterranean diet?  We may never know for sure.

Steve Parker, M.D.

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Filed under ketogenic diet, My KMD Experience

Grains and Legumes: Any Effect on Heart Disease and Stroke?

Several scientific studies published in the first five years of this century suggest that whole grain consumption protects agains coronary heart disease and possibly other types of cardiovascular disease, such as stroke. 

Note that researchers in this field, especially outside the U.S., use the term “cereal” to mean “a grass such as wheat, oats, or corn, the starchy grains of which are used as food.”  They also refer frequently to glycemic index and glycemic load, spelled “glycaemic” outside the U.S.  Most of the pertinent studies are observational (aka epidmiologic): groups of people were surveyed on food consumption, then rates of diseases were associated with various food types and amounts.  “Association” is not proof of causation. 

Here are highlights from a 2006 review article in the European Journal of Clinical Nutrition

The researchers concluded that a relationship between whole grain intake and coronary heart disease is seen with at least a 20% and perhaps a 40% reduction in risk for those who eat whole grain food habitually vs those who eat them rarely.

Whole grain products have strong antioxidant activity and contain phytoestrogens, but there is insufficient evidence to determine whether this is beneficial in coronary heart disease prevention.

Countering the positive evidence for whole grain and legume intake has been the Nurses Health Study in 2000 that showed women who were overweight or obese consuming a high glycaemic load (GL) diet doubled their relative risk of coronary heart disease compared with those consuming a low GL diet.

The intake of high GI carbohydrates (from both grain and non-grain sources) in large amounts is associatied with an increased risk of heart disease in overweight and obese women even when fiber intake is high but this requires further confirmation in normal-weight women.

Promotion of carbohydrate foods should befocused on whole grain cereals because these have proven to be associatied with health benefits.

Whether adding bran to refined carbohydrate foods can improve the situation is also not clear, and it was found that added bran lowered heart disease risk in men by 30%.

Recommendation:  Carbohydrate-rich foods should be whole grain and if theyare not, then the lowest GI product available should be consumed.

My Comments

This journal article focuses on whole grains rather than legumes, and promotes whole grains more than legumes.  For people with diabetes, this may be a bit of a problem since grains—whole or not—generally have a higher glycemic index than legumes, which may have adverse effects on blood sugar control.  Keep in mind that highly refined grain products, like white bread, have a higher glycemic index than whole grain versions.

Did you notice that the abstract doesn’t recommend a specific amount of whole grains for the general population?  My educated guess would be one or two servings a day. 

Grains are high in carbohydrate, so anyone on a low-carb diet may have to cut carbs elsewhere. 

Diabetes predisoses to development of coronary heart disease.  Whole grains seem to help prevent heart disease, yet may adversely affect glucose control, contributing to diabetic complications.  It’s a quandary.  “Caught between the horns of a dilemma,” you might say.  So, what should a diabetic do with this information in 2010, while we await additional research results?

Several options come to mind:

  1. Eat whatever you want and forget about it.
  2. Note whether coronary heart disease runs in your family.  If so, try to incorporate one or two servings of whole grains daily, noting and addressing effects on your blood sugar.
  3. Try to eat one or two servings of whole grains a day, noting and addressing effects on your blood sugar.  Then decide if it’s worth it.  Is there any effect?  Do you have to increase your diabetic drug dosages or add a new drug?  Are you tolerating the drugs?    
  4. Assess all your risk factors for developing heart disease: smoking, sedentary lifestyle, high blood pressure, age, high LDL cholesterol, family history, etc.  If you have multiple risk factors, see Option #3.  And modify the risk factors under your control.   
  5. Get your personal physician’s advice.    

Before you stress out over this, be aware that we don’t really know whether a diabetic who doesn’t eat grains will have a longer healthier life by starting a daily whole grain habit.  Maybe . . . maybe not.  The study hasn’t been done.    

Steve Parker, M.D.

References:

Flight, I. and Clifton, P.  Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literatureEuropean Journal of Clinical Nutrition, 60 (2006): 1,145-1,159.

Malik, V. and Hu, Frank.  Dietary prevention of atherosclerosis: go with whole grainsAmerican Journal of Clinical Nutrition, 85 (2007): 1,444-1,445.

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Filed under Carbohydrate, coronary heart disease, Diabetes Complications, Grains, legumes, Stroke

Do Beans and Peas Affect Glucose Control in Diabetics?

Beans and peas improve control of blood sugar in diabetics and others, according to a recent report from Canadian researchers.  The effect is modest.

Dietary pulses are dried leguminous seeds, including beans, chickpeas, lentils, and peas.  Pulses fed to healthy volunteers have a very low glycemic index, meaning they don’t cause much of a rise in blood sugar compared to other carbohydrates.  They are loaded with fiber and are more slowly digested than foods such as cereals.   

Investigators examined 41 clinical trials (1,674 participants) on the effects of beans and peas on blood glucose control, whether used alone or as part of low-glycemic-index or high-fiber diets.  Eleven trials looked at the effect of beans and peas alone, with the experimental “dose” averging 1oo g per day (about half a cup).  The article doesn’t specify whether the weight of the pulse was the dry weight or the prepared weight.  I will assume prepared.

Pulse given alone or as part of a high-fiber or low-glycemic index diet improved markers of glucose control, such as fasting blood sugar and hemoglobin A1c.  The absolute improvement in HgbA1c was around 0.5%.  Effects in healthy non-diabetics were less dramatic or non-existent.

My Comments

This study was very difficult  for me to digest.  The researchers lumped together studies on diabetics  and non-diabetics, using various doses and types of pulses.  No wonder they found “significant interstudy heterogeneity.” 

Cardiovascular disease is common in diabetics.  I’m aware of at least one study linking legume consumption with lower rates of cardiovascular disease.  I was hoping this study would answer for me whether I should recommend legumes such as peas and beans for my type 2 diabetics.  Beans and peas do represent a low glycemic load, which is good.  But I think I’ll have to keep looking for better-designed studies.

Steve Parker, M.D. 

Reference:  Sievenpiper, J.L., et al.  Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetesDiabetologia, 52 (2009): 1,479-1,495.  doi: 10.1007/s00125-009-1395-7

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Filed under Carbohydrate, Fiber, Prevention of T2 Diabetes