Tag Archives: diabetes

Can Diabetes Be Prevented?

Not Paula Deen

Paula Deen’s recent announcement of her type 2 diabetes got me to thinking about diabetes prevention again.  If you’re at high risk of developing diabetes you can reduce your risk of full-blown type 2 diabetes by 58% with intensive lifestyle modification.  Here’s how it was done in a 2002 study:

The goals for the participants assigned to the intensive lifestyle intervention were to achieve and maintain a weight reduction of at least 7 percent of initial body weight through a healthy low-calorie, low-fat diet and to engage in physical activity of moderate intensity, such as brisk walking, for at least 150 minutes per week. A 16-lesson curriculum covering diet, exercise, and behavior modification was designed to help the participants achieve these goals. The curriculum, taught by case managers on a one-to-one basis during the first 24 weeks after enrollment, was flexible, culturally sensitive, and individualized. Subsequent individual sessions (usually monthly) and group sessions with the case managers were designed to reinforce the behavioral changes.

Although the Diabetes Prevention Program encouraged a low-fat diet, another study from 2008 showed that a low-fat diet did nothing to prevent diabetes in postmenopausal women

I don’t know Paula Deen.  I’ve never watched one of her cooking shows.  She looks overweight and I’d be surprised if she’s had a good exercise routine over the last decade.  I’m sorry she’s part of the diabetes epidemic we have in the U.S.  I wish her well.  Amy Tenderich posted the transcript of her brief interview with Paula, who calculates her sweet tea habit gave her one-and-a-half cups of sugar daily).

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

I think excessive consumption of concentrated sugars and refined carbohydrates contribute to the diabetes epidemic.  Probably more important are overweight, obesity, and physical inactivity.

The Mediterranean diet has also been linked to lower rates of diabetes (and here).  Preliminary studies suggest the Paleo diet may also be preventative (and here).

Greatly reduce your risk of type 2 diabetes by eating right, keeping your weight reasonable, and exercising.

Steve Parker, M.D.

PS: Paula, if you’d like a copy of Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet, have your people contact my people.

Reference:  Diabetes Prevention Program Research Group.  Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or MetforminNew England Journal of Medicine, 346 (2002): 393-403.

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LADA Awareness Week

"Who can tell us about LADA?"

This is the first ever LADA Awareness Week, organized by Diabetes Hands Foundation and dLife.  LADA stands for Latent Autoimmune Diabetes in Adults.  I think of it as type 1 diabetes that starts in adulthood, although there are some differences from typical juvenile-onset type 1 diabetes.

Seven-and-a-half to 10% of apparent type 2 adult diabetics have LADA.  It’s caused by the body attacking its own pancreas beta cells and thereby impairing insulin production; in other words, it’s an autoimmune thing.

Here are some generalities (with exceptions, of course) about LADA, compared to typical type 2 diabetes:

  • lower body mass index, often under 25
  • age at onset under 50
  • poorer response to dietary management
  • poorer response to oral diabetic medications
  • acute symptoms at time of diagnosis (e.g., weight loss, thirst, frequent urination, ketoacidosis, malaise, etc.)
  • higher risk of developing diabetic ketoacidosis
  • much more likely to need insulin

How Is LADA Diagnosed?

First of all, the doctor has to consider the possibility, based on the clinical factors above.  The autoimmune nature of the disease is reflected in islet-cell antiobodies (ICA) and antibodies to glutamic acid decarboxylase (anti-GAD).  These are testable in the blood.  One of the two may be enough.  If the disease is far enough along, blood levels of C-peptide will be low.  C-peptide reflects the body’s production of insulin.

For more information on LADA, talk to your doctor or visit this page at dLife.

Steve Parker, M.D.

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Dr. Andreas Eenfeldt Explains LCHF Diet

LCHF Cheese

Dr. Eenfeldt of DietDoctor.com gave a talk at the recent Ancestral Health Symposium in California, on the rationale of the current low-carb, high-fat diet (LCHF) so popular in his home country of Sweden.  It’s very understandable to the general public and is a good introduction to low-carb eating.  The entire YouTube video is 55 minutes; if you’re pressed for time, skip the 10-minute Q&A at the end.

He also discusses the benefits of LCHF eating for his patients with diabetes.

If you reduce carbohydrate, you’re going to replace it with either protein, fat, or both.  As Dr. Eenfeldt recommends, the Ketogenic Mediterranean and Low-Carb Mediterranean Diets replace carbs more with fats than protein.

Steve Parker, M.D.

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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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Nutty Treatment for Diabetes

Mixed Nuts Improve Diabetes

Eating nuts improves blood sugar control and cholesterol levels in type 2 diabetics, according to a recent research report in Diabetes Care.

Canadian researchers randomized 117 type 2 diabetics to eat their usual types of food, but also to be sure to eat either

  •  mixed nuts (about 2 ounces a day)
  •  muffins (I figure one a day)
  • or  half portions of each. 

They did this daily for three months.  Compared to the muffin group, the full nut group ate quite a bit more monounsaturated fatty acids.  (I don’t have full study details because I have access only to the article abstract.)

Results

Hemoglobin A1c, a reliable measure of blood sugar control, fell by 0.21% in the mixed nut group.  That’s a move in the right direction.  LDL cholesterol, the “bad cholesterol” linked to heart and vascular disease, also dropped significantly. 

So What?

The investigators suggest that replacement of certain carbohydrates with 2 ounces of daily mixed nuts is good for people with type 2 diabetes.

I must mention that nuts are  a mandatory component of the Ketogenic Mediterranean Diet  and the Low-Carb Mediterranean Diet, and a recommended option on the Advanced Mediterranean Diet

Steve Parker, M.D.

References:  Jenkins, David J.A., et al.  Nuts as a replacement for carbohydrates in the diabetic dietDiabetes Care, June 29, 2011.  doi: 10.2337/dc11-0338

PS: The lead author of this study is the same David Jenkins of glycemic index fame.

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Mediterranean Diet for Diabetes

In 2009, Current Diabetes Reports published “The usefulness of a Mediterranean-based diet in individuals with type 2 diabetes,” by Catherine M. Champagne, Ph.D., R.D., L.D.N.  Unfortunately, the full article isn’t available to you at no cost.  But I read it.  Her article is a review of available scientific evidence related to the Mediterranean diet as applied to a diabetic population.  Here’s a quote:

This diet is a viable treatment option; advisors should stress not only adherence to a fairly traditional Mediterranean eating plan but also a lifestyle that includes sufficient physical activity.

I’ve been publishing my series on exercise here in dribs and drabs for the last several months.

Dr. Champagne was very favorably impressed with the DIRECT trial of Shai et al, which I covered extensively elsewhere.  DIRECT compared three diets over 24 months: Atkins, Mediterranean/calorie-restricted, and low-fat/calorie-restricted.  Mind you, it was a weight loss study, but a fair number of diabetics participated.  Mediterranean-style eating showed the most beneficial effects for diabetics. 

The author also mentions evidence that a modified Mediterranean diet may help counteract the build-up of fat in the liver, seen in up to 70% of type 2 diabetics.  I wrote recently about how a very-low-carb diet beat the low-fat diet so often recommended for this condition (hepatic steatosis or non-alcoholic fatty liver disease).

ResearchBlogging.orgIf you want full online access to Champagne’s 6-page article, you can purchase it for $34 (USD) at SpringerLink.  I cite many of the same scientific sources and provide a whole lot more in my 216-page Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet, at Amazon.com for $16.95 or $9.99 (the Kindle edition) or in multiple ebook formats from Smashwords.

Steve Parker, M.D.

Reference: Champagne, Catherine (2009). The usefulness of a Mediterranean-based diet in individuals with type 2 diabetes. Current Diabetes Reports DOI: 10.1007/s11892-009-0060-3

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Book Review: Carbohydrates Can Kill

I recently read Carbohydrates Can Kill, by Robert K. Su, M.D., written in 2009.  Per Amazon.com’s rating system, I give it four stars ( I like it).

♦   ♦   ♦

Many developed Western societies have a love affair with carbohydrates, particularly concentrated sugars and highly processed grains and starches.  The U.S. is a good example.  Our skyrocketing rates of overweight and obesity (68% of adults) are testament to that.  Obesity is strongly linked to cancer, high blood pressure, heart attacks, diabetes, strokes, and premature death.  It’s not too much of a stretch to blame carbohydrates for at least a portion of these diseases and others.  Dr. Robert Su thoroughly reviews these connections in Carbohydrates Can Kill.

Blissfully unaware of his prediabetes

Blocked heart arteries are the No.1 cause of death in developed countries.  A growing trend among the experts is to abandon the theory that total and saturated fats cause heart disease, pointing instead to excessive consumption of sugars and processed grains and other starches.  Dr. Su makes a fairly convincing case for the carbohydrate theory of heart disease.  He’s also convinced that carbs cause high blood pressure, dementia, many cancers, diabetes, overweight, perhaps even most diseases. 

This book addresses overweight, adverse health effects of obesity, nutrition and digestion in detail, and numerous scientific studies supporting his ideas.

One of the most interesting things to me was Dr. Su’s personal medical story.  At age 62, he found himself 40 pounds (18 kg) overweight, blood pressure 205/63, and having apparent reversible heart pains (angina) when stressed or exercising.  The combination of salt restriction and exercise didn’t help.  Reducing carbs to 60-70 g/day and continued exercise (walking and stair-climbing) did the trick, helping him lose 30 pounds and controlling angina and high blood pressure.  I expected him at any time to reveal he had a heart attack, stroke, or heart bypass surgery, but he dodged those bullets.  His problems at 62 were a wake-up call.  He didn’t want to end up prematurely dead or disabled, a burden to his family and unable to spend quality time with them.  So he undertook major lifestyle changes.  Very inspirational. 

In addition to a medical degree, Dr. Su has a degree in pharmacy.  He knew he’d be put on multiple drugs if he went to a doctor for treatment of his symptoms.  Like me, he’s wary of drug side effects and wanted to avoid them, opting for diet and exercise instead.  He gambled and won.  I’m sure at least a few others would not be so lucky.

Dr. Su cites evidence that high blood sugars cause inflammation, which can predispose to cancer.  Diabetics do indeed have a higher risk of certain cancers, yet he didn’t mention that diabetics have a lower risk of prostate cancer. 

Dr. Su is anti-alcohol.  The studies are mixed on the overall health effects of alcohol, but the bulk of the studies link low-to-moderate consumption of alcohol with less cardiovascular disease and longer lifespan.  Clearly, heavy drinking can be lethal.

Like all books, CCK isn’t perfect.  First, it could have used better editing to eliminate grammatical errors and wordiness.  Next, I suspect Dr. Su is getting a little ahead of the science when he states that “….most diseases, if not all, are directly or indirectly caused by too much blood sugar.”  If carbohydrates are so deadly (mediated via high blood sugar), why do the Kitavan’s of Melanesia have such low rates of heart attack, stroke, overweight, and diabetes, despite a diet deriving 69% of total calories from carbohydrates?  (Calories from carbohydrates in the U.S. are about 50% of the total.)  Granted, Kitavan’s carbs are mostly unrefined.  Could the Kitavans be genetically protected from carb toxicity? 

So, what do we do if carboydrates are so dangerous?  Dr. Su recommends limiting carb consumption to a maximum of 100 grams a day.  (By way of reference, average U.S. carb consumption is 250 grams a day.)  Simple sugars and highly processed grains and starches should be avoided.  Additionally, he recommends a yearly glucose tolerance test to determine fasting blood sugar, then blood sugar readings every 15-20 minutes after an unspecified meal for two or three hours.  I wonder if a single hemoglobin A1c blood test would suffice.  I agree with Dr. Su that fasting blood sugars should be under 110 mg/dl (6.1 mmol/l)—if not lower—and all blood sugars after meals under 150 mg/dl (8.3 mmol/l).

Dr. Su is a tireless advocate for carbohydrate-restricted eating.  Visit his website: carbohydratescankill.com.  If his diet and exercise ideas were widely adopted in the U.S., we’d be a healthier country.  This book is a worthy read for anyone with overweight, obesity, diabetes, prediabetes, or otherwise enamored of concentrated sugars and highly processed grains and other starches.  Note that one of every three U.S. adults has prediabetes, including half of all those over 65, and most of them are unaware.

Steve Parker, M.D.

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Vitamins Slow Rate of Brain Shrinkage in Elderly

A cocktail of three common vitamins slowed the rate of brain shrinkage over two years  in elderly patients with mild cognitive impairment, according to researchers at the University of Oxford.  Less brain shrinkage should translate to better brain functioning.  People with diabetes need to know about this since diabetes is associated  with age-related cognitive impairment and dementia.  The dementia connection is debatable.

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

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

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

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

That’s why I was excited to see a research report in which brain atrophy was slowed with three simple daily vitamins: folic acid 800 mcg, B12 500 mcg, and B6 20 mg.  (One Centrum vitamin, by comparison, provides folic acid 400 mcg, B12 6 mcg, and B6 2 mg).  The investigators will report later on whether the vitamins helped prevent mental decline.

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

Methodology

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

Results

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

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

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

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

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

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

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

Comments

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

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

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

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

Steve Parker, M.D.

References: 

Smith, David, et al.  Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: A randomized controlled trial.  PLoS ONE 5(9): e1244.  doi: 10.1371/journal.pone.0012244  [published September 8, 2010]

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

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Exercise, Part 8: Warnings and Precautions for Diabetics

Exercise clearly has many benefits, as discussed in prior installments of this series.  Yet we shouldn’t overlook the potential risks to diabetics either. 

Diabetic Retinopathy

Diabetics with retinopathy (an eye disease caused by diabetes) have an increased risk of retinal detachment and bleeding into the eyeball called vitreous hemorrhage. These can cause blindness. Vigorous aerobic or resistance training may increase the odds of these serious eye complications. Patients with retinopathy may not be able to safely participate. If you have any degree of retinopathy, avoid the straining and breath-holding that is so often done during weightlifting or other forms of resistance exercise. Vigorous aerobic exercise may also pose a risk. By all means, check with your ophthalmologist first. You don’t want to experiment with your eyes.

Diabetic Feet and Peripheral Neuropathy 

Diabetics are prone to foot ulcers, infections, and ingrown toenails, especially if peripheral neuropathy (numbness or loss of sensation) is present. Proper foot care, including frequent inspection, is more important than usual if a diabetic exercises with her feet. Daily inspection should include the soles and in-between the toes, looking for blisters, redness, calluses, cracks, scrapes, or breaks in the skin. See your physician or podiatrist for any abnormalities. Proper footwear is important (for example, don’t crowd your toes). Dry feet should be treated with a moisturizer regularly. In cases of severe peripheral neuropathy, non-weight-bearing exercise (e.g., swimming or cycling) may be preferable. Discuss with your physician or podiatrist.

Hypoglycemia

Low blood sugars are a risk during exercise if you take diabetic medications in the following classes: insulins, sulfonylureas, meglitinides, and possibly thiazolidinediones and bromocriptine. Hypoglycemia is very uncommon with thiazolidinediones. Bromocriptine is so new (for diabetes) that we have little experience with it; hypoglycemia is probably rare or non-existent. See drug details in chapter four. Diabetics treated with diet alone or other medications rarely have trouble with hypoglycemia during exercise.

Always check your blood sugar before an exercise session if you are at risk for hypoglycemia. Always have glucose tablets, such as Dextrotabs, available if you are at risk for hypoglycemia. Hold off on your exercise if your blood sugar is over 200 mg/dl (11.1 mmol/l) and you don’t feel well, because exercise has the potential to raise blood sugar even further early in the course of an exercise session.

As an exercise session continues, active muscles may soak up bloodstream glucose as an energy source, leaving less circulating glucose available for other tissues such as your brain. Vigorous exercise can reduce blood sugar levels below 60 mg/dl (3.33 mmol/l), although it’s rarely a problem in non-diabetics.

The degree of glucose removal from the bloodstream by exercising muscles depends on how much muscle is working, and how hard. Vigorous exercise by several large muscles will remove more glucose. Compare a long rowing race to a slow stroll around in the neighborhood. The rower is strenuously using large muscles in the legs, arms, and back. The rower will pull much more glucose out of circulation. Of course, other metabolic processes are working to put more glucose into circulation as exercising muscles remove it. Carbohydrate consumption and diabetic medications are going to affect this balance one way or the other.

If you are at risk for hypoglycemia, check your blood sugar before your exercise session. If under 90 mg/dl (5.0 mmol/l), eat a meal or chew some glucose tablets to prevent exercise-induced hypoglycemia. Re-test your blood sugar 30–60 minutes later, before you exercise, to be sure it’s over 90 mg/dl (5.0 mmol/l). The peak effect of the glucose tablets will be 30–60 minutes later. If the exercise session is long or strenuous, you may need to chew glucose tablets every 15–30 minutes. If you don’t have glucose tablets, keep a carbohydrate source with you or nearby in case you develop hypoglycemia during exercise.

Re-check your blood sugar 30–60 minutes after exercise since it may tend to go too low.

If you are at risk of hypoglycemia and performing moderately vigorous or strenuous exercise, you may need to check your blood sugar every 15–30 minutes during exercise sessions until you have established a predictable pattern. Reduce the frequency once you’re convinced that hypoglycemia won’t occur. Return to frequent blood sugar checks when your diet or exercise routine changes.

These general guidelines don’t apply across the board to each and every diabetic. Our metabolisms are all different. The best way to see what effect diet and exercise will have on your glucose levels is to monitor them with your home glucose measuring device, especially if you are new to exercise or you work out vigorously. You can pause during your exercise routine and check a glucose level, particularly if you don’t feel well. Carbohydrate or calorie restriction combined with a moderately strenuous or vigorous exercise program may necessitate a 50 percent or more reduction in your insulin, sulfonylurea, or meglitinide. Or the dosage may need to be reduced only on days of heavy workouts. Again, enlist the help of your personal physician, dietitian, diabetes nurse educator, and home glucose monitor.

Finally, insulin users should be aware that insulin injected over muscles that are about to be exercised may get faster absorption into the bloodstream. Blood sugar may then fall rapidly and too low. For example, injecting into the thigh and then going for a run may cause a more pronounced insulin effect compared to injection into the abdomen or arm.

Autonomic Neuropathy

This issue is pretty technical and pertains to function of automatic, unconscious body functions controlled by nerves. These reflexes can be abnormal, particularly in someone who’s had diabetes for many years, and are called autonomic neuropathy. Take your heart rate, for example. It’s there all the time, you don’t have to think about it. If you run to catch a bus or climb two flights of stairs, your heart rate increases automatically to supply more blood to exercising muscles. If that automatic reflex doesn’t work properly, exercise is more dangerous, possibly leading to passing out, dizziness, and poor exercise tolerance. Other automatic nerve systems control our body temperature regulation (exercise may overheat you), stomach emptying (your blood sugar may go too low), and blood pressure (it could drop too low). Only your doctor can tell for sure if you have autonomic neuropathy.

Steve Parker, M.D.

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Pilot Study: Paleo Diet Is More Satiating Than Mediterranean-Style

Swedish researchers reported recently that a Paleolithic diet was more satiating than a Mediterranean-style diet, when compared on a calorie-for-calorie basis in heart patients.  Both groups of study subjects reported equal degrees of satiety, but the paleo dieters ended up eating 24% fewer calories over the 12-week study.

The main differences in the diets were that the paleo dieters had much lower consumption of cereals (grains) and dairy products, and more fruit and nuts.  The paleos derived 40% of total calories from carbohydrate compared to 52% among the Mediterraneans.

Even though it wasn’t a weight-loss study, both groups lost weight.  The paleo dieters lost a bit more than the Mediterraneans: 5 kg vs 3.8 kg (11 lb vs 8.4 lb).  That’s fantastic weight loss for people not even trying.  Average starting weight of these 29 ischemic heart patients was 93 kg (205 lb).  Each intervention group had only 13 or 14 patients (I’ll let you figure out what happened to to the other two patients).

I blogged about this study population before.  Participants supposedly had diabetes or prediabetes, although certainly very mild cases (average hemoglobin A1c of 4.7% and none were taking diabetic drugs)

As I slogged through the research report, I had to keep reminding myself that this is a very small, pilot study.  So I’ll not bore you with all the details.

Bottom Line

This study suggests that the paleo diet may be particularly helpful for weight loss in heart patients.  No one knows how results would compare a year or two after starting the diet.  The typical weight-loss pattern is to start gaining the weight back at six months, with return to baseline at one or two years out.

Greek investigators found a link between the Mediterranean diet and better clinical outcomes in known ischemic heart disease patients.  On the other hand, researchers at the Heart Institute of Spokane found the Mediterranean diet equivalent to a low-fat diet in heart patients, again in terms of clinical outcomes.  U.S. investigators in 2007 found a positive link between the Mediterranean diet and lower rates of death from cardiovascular disease and cancer

We don’t yet have these kinds of studies looking at the potential benefits of the paleo diet.  I’m talking about hard clinical endpoints such as heart attacks, heart failure, cardiac deaths, and overall deaths.  The paleo diet definitely shows some promise.

I also note the Swedish investigators didn’t point out that weight loss in overweight heart patients may be detrimental.  This is the “obesity paradox,” called “reverse epidemiology” at Wikipedia.  That’s a whole ‘nother can o’ worms.

Keep your eye on the paleo diet.

Steve Parker, M.D.

Reference: Jonsson, Tommy, et al.  A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart diseaseNutrition and Metabolism, 2010, 7:85.

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Filed under coronary heart disease, Mediterranean Diet