Mediterranean Diet Linked to Brain Preservation

 The Mediterranean diet slowed age-related mental decline in elderly Chicago residents, according to researchers at Rush University Medical Center.  The investigators noted that a Manhattan population following the Mediterranean diet also showed slower mental decline and lower rates of Alzheimers dementia.

Over 3,000 study participants (2,280 blacks, 1,510 whites) were studied for an average of eight years.  Food consumption was determined by questionnaires, and mental function was tested every three years.  Adherence to the Mediterranean diet was judged according to a Mediterranean diet score developed by Panagiotakis, et al.

The greater the adherence to the Greek-style Mediterranean diet, the lower the rate of mental decline over the course of the study.

Mental decline to some extent is a normal part of aging.  If we can avoid it or lessen it’s impact, why not?  A couple ways to do that are regular exercise and the Mediterranean diet.

Would a low-carb Mediterranean diet work just as well or better?  Nobody knows yet.

Steve Parker, M.D.

Reference:  Tangney, Christine, et al. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population.  American Journal of Clinical Nutrition, 2010.  doi 10.3945/ajcn.110.007369

 

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Mediterranean Diet Linked to Less Sudden Cardiac Death in Women

"Trust me. You don't want sudden cardiac death until you're very old!"

A Mediterranean-style diet is one of four factors helping to greatly reduce the risk of sudden cardiac death in women, as reported by Reuters on June 5, 2011. The other factors reducing risk were maintainence of a healthy weight, regular exercise, and not smoking.

The study involved women only, so we don’t know if the research, reported in the Journal of the American Medical Association, applies to men.  I bet it does.

This study confirms many earlier ones linking the Mediterranean diet with longevity and reduced rates of heart disease.

Steve Parker, M.D.

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Introducing Paleo Diabetic, a New Blog

A few of my patients have asked me if the paleo diet and lifestyle would be good for their diabetes.  I’m not sure.  A few pilot studies suggest it would be.  I expect much more published scientific research over the coming decade, in addition to self-experimentation reports by patients.  I’ll be looking into the matter at Paleo Diabetic.

The paleo diet in modern times began gathering steam in 2008.  It’s still not widely known or followed, but the trend is definitely upwards. 

The idea behind the paleo diet—also referred to as the Stone Age or caveman diet—is that optimal health depends on adherence to dietary and lifestyle factors to which we’re genetically adapted.  Our current mix of genes overwhelmingly reflects the Paleolithic era of human cultural development, starting anywhere from 750,000 to 2.5 million years ago, and ending around 10,000 years ago.  It’s also called the Stone Age.

The paleo diet pattern isn’t set in stone.  In general, it includes nuts, vegetables, fruits, fish, meat, and poultry.  It excludes or limits grains, dairy, legumes, sugars other than fruit or honey, industrial seed oils (e.g., from soybean and corn), and modern processed, highly refined foods.  Fresh, natural, and “organic” are preferred.

I’ve already got a few posts up and plan on new ones once or twice weekly.  If you’re interested, please join me at Paleo Diabetic.

Steve Parker, M.D.

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Is Grape Seed Extract as Healthful as Wine?

Patients ask me periodically if grape seed extract provides the same health benefit as judicious red wine.  Nobody knows with certainty.  The health benefits of red wine may be due to resveratrol.  Grape seed extract contains potentially healthy antioxidants called proanthocyanidins,

Many people don’t enjoy wine or other alcohol-containing drinks, and others just shouldn’t drink any alcohol.  Should they take a grape seed extract supplement or drink grape juice as a subsitute?  Again, it’s still unclear.  In 2009 I wrote a about a review article looking at the effect of various non-wine grape products and effects on heart disease risk.

A recent meta-analysis out of the University of Connecticut found improvement in two heart disease risk factors in those who take a grape seed extract supplement:

  • systolic blood pressure lower by 1.54 mmHg
  • heart rate lower by 1.42 beats per minute

No effect was seen on lipids (cholesterol and triglycerides), diastolic blood pressure, and C-reactive protein (a test of systemic inflammation).

Granted, these are tiny effects.  It’s unknown whether they, or other unknown effects of grape seed extract, would translate into clinical benefits such as fewer heart attacks and strokes, and longer lifespans.

Bottom Line

Grape seed extract and other non-wine grape products may be as beneficial as red wine in prolonging lifespan and preventing heart disease.  But we have much stronger evidence in favor of red wine and other alcohol-containing drinks.

Steve Parker, M.D.

 Reference:  Feringa, H.H.H, et al. The Effect of Grape Seed Extract on Cardiovascular Risk Markers: A Meta-Analysis of Randomized Controlled TrialsJournal of the American Dietetic Association, 111 (2011): 1,173-1,181.

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A Good Night On-Call

 

At the hospital last night, I admitted an elderly heart patient with chest pain.  I asked if he’d ever heard of the Mediterranean diet.  He answered, “What’s that? Does it mean you only eat those kinds of people?”

Steve Parker, M.D.

PS: In the course of our conversation, he worked in five other one-line jokes. What a blessing.

PPS:  Q: Why did the cannibal eat the trapeze artist?

A: He wanted a balanced meal.

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The Holy Grail of Diabetes Treatment: Preserving Beta Cell Function

 A Nobel Prize in Medicine belongs to whoever (whomever?) figures out how to reliably and affordably protect and preserve beta cell function starting early in the course of type 2 diabetes.  Or type 1 diabetes, for that matter.

Dietary carbohydrates lead to secretion of insulin into the bloodstream by the pancreas’s beta cells.  The insulin limits and reverses the rise in blood sugar that results from digestion of carbohydrates.  If blood sugar rises too high, it damages our bodies. 

Type 2 diabetes is a disorder of carbohydrate metabolism.  Insulin from the beta cells isn’t doing its job adequately because tissues that should be taking up bloodstream sugar are resistant to insulin’s effect of driving sugar into the cells.  The beta cells pump out increasing amounts of insulin, trying to overcome the resistance of the tissues.  Eventually the beta cells become exhausted or “burned out,” reflected in diminished beta cell mass.  This situation has usually been present for years before type 2 diabetes is formally diagnosed.  This scenario is a leading theory of the development of type 2 diabetes.

Type 2 diabetes is considered by most physicians to be a progressive illness, requiring more and more drugs to control as the years pass.  That’s because the beta cells are dying off or otherwise becoming totally nonfunctional.  Once they’re gone, it’s hard (impossible?) to get them back.  If diabetes could be diagnosed early on, we’d find healthier beta cells to work with.  Perhaps we could strengthen or protect them.  This is what beta cell preservation is all about.  Keep them working as nature intended, avoiding the expense and risks of drug therapy.

So I was excited to find an article entitled “Effects of exenatide on measures of beta cell function after three years in metformin-treated patients with type 2 diabetes.”  Exenatide is sold in the U.S. as Byetta.  It’s a GLP-1 analogue.  

European researchers studied 36 type 2 diabetics for three years.  All were taking metformin.  Sixteen of them also took exenatide, whereas 20 also took insulin glargine (e.g., Lantus in the U.S.). 

What Did They Find?

Both groups achieved similar levels of blood sugar control after three years.  Exanatide users lost 5.7  kg (12.5 lb) while glargine users gained 2.1 kg (4.6 lb). 

After three years of drug use, the subjects were told to stop exenatide and glargine while continuing metformin. After four weeks off-drug:

  • insulin sensitivity improved significantly in the exenatide group while glargine had no effect
  • first-phase insulin secretion improved by a small amount in the exenatide group

However, 12 weeks after stopping the study drugs, hemoglobin A1c and fasting blood sugars returned to pretreatment levels in both groups.  (Hemoglobin A1c is a blood test of overall diabetes control over the preceeding three months.)   

Final Thoughts

You have to wonder if the improved insulin sensitivity in the exenatide group simply reflects their weight loss as compared to the weight gain in the insulin glargine group.  Improved insulin sensitivity is good, any way you can get it. 

ResearchBlogging.orgWhen measured 12 weeks after stopping the study drugs, hemoglobin A1c and fasting blood sugar levels were no better than baseline levels three years earlier.  Very disappointing.  If exanatide or glargine preserved beta cell function, you’d want to see better post-treatment numbers.  The search for beta cell preservation continues.

Steve Parker, M.D.

Reference: Bunck, M., Corner, A., Eliasson, B., Heine, R., Shaginian, R., Taskinen, M., Smith, U., Yki-Jarvinen, H., & Diamant, M. (2011). Effects of Exenatide on Measures of Beta-Cell Function After 3 Years in Metformin-Treated Patients With Type 2 Diabetes Diabetes Care, 34 (9), 2041-2047 DOI: 10.2337/dc11-0291

PS: In case it matters to you, this study was funded at least partially by Amylin Pharmaceuticals and Eli Lilly and Company.

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Insulin Resistance, Lipotoxicity, Type 2 Diabetes, and Atherosclerosis

This will bore most readers.

I just want to mention a scientific review article from 2009 that reviews insulin activity (down to a molecular level) in the context of type 2 diabetes, atherosclerosis, and insulin resistance.  Towards the end it starts sounding like an informercial for thiazolidinedione drugs

The author makes a great case for the dangers of hyperinsulinemia.

Good reference overall.

R. A. DeFronzo wrote “Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009.”   Diabetologia, 2010 (53); 1,270-1,287.  doi: 10.1007/s00125-010-1684-1

Steve Parker, M.D.

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Low-Carb Diet Reduces Weight AND Increases Adiponectin

Compared to a low-fat diet, a very-low-carb diet yielded better fat loss and improved adiponectin levels, according to researchers at the University of Cincinnati.  Read on to find out why this matters.

Adiponectin is a hormone-like protein secreted by fat cells. But the fatter you are, the less adiponectin you have in your bloodstream.  This hormone has several effects:

    • it’s anti-inflammatory
    • high levels of one form of it (a high molecular weight oligomer) are linked to lower rates of diabetes
    • low circulating levels are associatedwith athersclerosis (hardening of the arteries), high blood pressure, and impaired function of cells lining our arteries
    • it sensitizes the liver and muscles to insulin, which helps keep blood sugars under control

    In summary, it’s a good thing to have around.  Low levels are linked to illnesses.  Overweight and obesity tend to lower your levels of adiponectin.  If you’re overweight and have low levels of adiponectin, you should be healthier if you can raise your levels.  How do you do that?  Lose weight.

U. of Cincinnati investigators wanted to know if a very-low-carb diet would increase adiponectin levels better than a common low-fat weight loss diet.  They randomized 81 obese women to follow either a low-fat diet (American Heart Association Step 1) or a very-low-carbohydrate diet based on the Atkins diet.  Women followed the diets for either four or six months.

Findings

Both groups lost weight, but the very-low-carb group lost more: 9.1 kg loss for very-low-carb vs 4.97  for the low-fat group.

The very-low-carb group lost more body fat: 5.45 kg vs 2.62 kg.  (Fat loss was determined by DEXA scan.)

Adiponectin increased in the VLC group but not the LF group.

Discussion

We can’t tell from this article if adiponectin results would be the same in men.  The authors didn’t mention.

ResearchBlogging.orgIn fairness, the authors cite another similar study that found equal degrees of weight loss and adiponectin increase in both low-fat and low-carb groups.  It was a year-long intervention and average weight loss was 13.5% for both groups, a greater degree of weight loss than in the study at hand, in which the very-low-carb group lost 10% of body weight and the low-fat group lost 5.4%.  So you can probably increase your leptin with a low-fat diet if you lose enough excess weight.

Would the Ketogenic Mediterranean Diet work just as well as the very-low carb diet used in this study?  I suspect so, but don’t have the $500,000 it would take to do the research.  Care to donate?

Steve Parker, M.D.

Reference:
Summer, S., Brehm, B., Benoit, S., & D’Alessio, D. (2011). Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet Obesity DOI: 10.1038/oby.2011.60

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Which Of Three Low-Carb Diets Reduces Future Risk of Diabetes?

Men eating low-carb diets featuring protein and fats from sources other than red and processed meats may reduce risk of developing type 2 diabetes later, compared to other types of low-carb diets.  The same Boston-based researchers previously looked for a similar association in women and found none.

The article in American Journal of Clinical Nutrition seems to me unusually complicated, like the first sentence of this post.  It was frustrating to read, searching for but not finding much useful for clinical practice.  How low-carb were these diets?  Thirty-seven to 43% of energy from carbs in the most dedicated dieters, compared to 50-60% in the standard American diet.

After wading through most of this article, I came away with the impression the authors were just data-mining a huge database, to add one more item to their CVs (curriculum vitae).  This article is a confusing mess, or maybe I’m just stupid. I regret wasting an hour on it.

Steve Parker, M.D.

Reference: De Konig, Lawrence, et al.  Low-carbohydrate diet scores and risk of type 2 diabetes in menAmercan Journal of Clinical Nutrition, 2011. doi: 10.3945/ajcn.110.004333

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History of Diabetes: Elizabeth Hughes, Insulin Pioneer

One of the very first users of insulin injections lived to be 73.  That amazes me since most of her life was lived before we could keep close track of blood sugar levels with home glucose monitoring.  She died of pneumonia in 1981.  She was a type 1 diabetic since age 11.

Insulin was discovered in Canada

Her name was Elizabeth Hughes, daughter of a New York governor.  She was started in insulin around 1922. 

I read about her in Nutrition Journal earlier this year.  Most of the article was about the use of starvation diets for diabetics in the pre-insulin era .  Ever heard of the Joslin Clinic, a preeminent U.S. diabetes center?  Elliott Joslin was once an advocate of these starvation diets.  Insulin changed that.

The article notes that before insulin therapy was available, the standard diabetic diet was low-carbohydrate, avoiding sugars and starches, sometimes called the “animal diet.”

I also learned that urine became easily testable for sugar in the early part of the 20th century, if not earlier.  Before this, many cases of diabetes (mostly type 2) were undetectable or misdiagnosed.

Even today, type 1 diabetes is a hard row to hoe.  Before 1922, it was even worse.  As bad as it can get.

Steve Parker, M.D.

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