Book Review: Why We Get Fat

Gary Taubes’s new book, Why We Get Fat: And What To Do About It, comes on the market later this month.  I give it five stars per Amazon.com’s ranking system (I love it).

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

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

Paradigm Shift

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

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

So, Why DO We Get Fat?

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

What To Do About It

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

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

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

This’N’That

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

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

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

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

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

Minor Bone of Contention RE: Coronary Heart Disease

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

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

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

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

Going Forward

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

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

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

Steve Parker, M.D.

Update December 18, 2010: I found Mr. Taubes’s reference for stating that Paleolithic diets provide about a third of calories from carbohydrate (22-40%), based on modern hunter-gatherer societies).  See References below.   

References:
Coronary heart disease autopsy data:  American Journal of Medicine, 110 (2001): 267-273.
Reduced heart attacks:  Circulation, 12 (2010): 1,322-1,328.
Reduced incidence of coronary heart disease:  www.UpToDate.com, topic: “Epidemiology of Coronary Heart Disease,” accessed December 11, 2010.
Death rates for coronary heart disease:  Journal of the American Medical Association, 294 (2005): 1,255-1,259.

Cordain, L., et al.  Plant-animal subsistance ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.  American Journal of Clinical Nutrition, 71 (2000): 682-692.

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

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

Update April 22, 2013: 

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

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Filed under Book Reviews, coronary heart disease, Fat in Diet, Mediterranean Diet

Ketogenic Diet for Alzheimer’s Disease?

Alzhiemer's is "the long goodbye..."

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

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

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

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

What is this “ketogenic diet” for epilepsy?

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

So what?

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

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

Steve Parker, M.D.

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

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Filed under Fat in Diet, ketogenic diet

Heart Patients, Listen Up: Mediterranean Diet to the Rescue

The Mediterranean diet preserves heart muscle performance and reduces future heart disease events, according to Greek researchers reporting in the American Journal of Clinical Nutrition, May 19, 2010. 

Reuters and other news services have covered the story.

The Mediterranean diet is well-established as an eating pattern that reduces the risk of death or illness related to cardiovascular disease—mostly heart attacks and strokes.  Most of the studies in support of the heart-healthy diet looked at development of disease in general populations.  The study at hand examined whether the diet had any effect on patients with known heart disease, which has not been studied much.

How Was the Study Done? 

 The study population was 1,000 consecutive patients admitted with heart disease to a Greek hospital between 2006 and 2009.  In this context, heart disease refers to a first or recurrent heart attack (70-80% of participants) or unstable angina pectoris.  Acute heart attacks and unstable angina are “acute coronary syndromes.”  Average age was 64.  Sixty percent had a prior diagnosis of cardiovascular disease (coronary heart disease or stroke).  Thirty percent had diabetes.  At the time of hospitalization, half had diminished function of the main heart pumping chamber (the left ventricle), half had normal pump function.  Men totalled 788; women 212.

On the third hospital day, participants were given a 75-item food frequency questionnaire asking about consumption over the prior year.  If a potential enrollee died in the first two hospital days, he was not included in the study.  A Mediterranean diet score was calculated to determine adherence to the Mediterranean diet.  Mediterranean diet items were nonrefined cereals and products, fruits, nuts, vegetables, potatoes, dairy products, fish and seafood, poultry, red meats and meat products, olive oil, and alcohol. 

Left ventricle function was determined by echocardiogram (ultrasound) at the time of study entry, at the time of hospital discharge, and three months after discharge.  Systolic dysfunction was defined as an ejection fraction of under 40%.  [Normal is 65%: when the left ventricle is full of blood, and then squeezes on that blood to pump it into the aorta, 65% of the blood squirts out.]

Participants were then divided into two groups: preserved (normal) systolic left ventricular function, or diminished left ventricular function. 

They were followed over the next two years, with attention to cardiovascular disease events (not clearly defined in the article, but I assume including heart attacks, strokes, unstable angina, coronary revascularization, heart failure, arrhythmia, and death from heart disease or stroke.

Results

  • Four percent of participants died during the initial hospitalization.
  • At the three month follow-up visit, those with greater adherence to the Mediterranean diet (a high Mediterranean diet score) had higher left ventricular performance (P=0.02).
  • At the time of hospital admission, higher ejection fractions were associated with greater adherence to the Mediterranean diet (P<0.001).
  • Those who developed diminished left ventricular dysfunction had a lower Mediterranean diet score (P<0.001)
  • During the hospital stay, those in the highest third of Mediterranean diet score had lower in-hospital deaths (compared with the lower third scores) (P=0.009).
  • Among those who survived the initial hospitalization, there was no differences in fatal cardiovascular outcomes based on Mediterranean diet score.
  • Food-specific analysis tended to favor better cardiovascular health (at two-year follow-up) for those with higher “vegetable and salad”  and nut consumption.  No significant effect was found for other components of the Mediterranean diet score.
  • Of those in the highest third of Mediterranean adherence, 75% had avoided additional fatal and nonfatal cardiovasclar disease events as measured at two years.  Of those in the lowest third of Mediterranean diet score, only 53% avoided additional cardiovascular disease events.   

The Authors’ Conclusion

Greater adherence to the Mediterranean diet seems to preserve left ventricular systolic function and is associated with better long-term prognosis of patients who have had an acute coronary syndrome.

My Comments

I agree with the authors’ conclusion.

We’re assuming these patients didn’t change their way of eating after the initial hospitalization.  We don’t know that.  No information is given regarding dietary instruction of these patients while they were hospitalized.  In the U.S., such instruction is usually given, and it varies quite a bit.

In this study, lower risk of cardiovascular death was linked to the Mediterranean diet only during the initial hospital stay.  Most experts on the Mediterranean diet would have predicted lower cardiovascular death rates over the subsequent two years.  Mysteriously, the authors don’t bother to discuss this finding.

For those who don’t enjoy red wine or other alcoholic beverages, this study suggests that the Mediterranean diet may be just as heart-healthy without  alcohol.  A 2009 study by Trichopoulou et al suggests otherwise.

Steve Parker, M.D.

Reference: Chrysohoou, C., et al.  The Mediterranean diet contributes to the preservation of left ventricular systolic function and to the long-term favorable prognosis of patients who have had an acute coronary event.  American Journal of Clinical Nutrition, May 10, 2010.  doi:10.3945/ajcn.2009.28982

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Filed under coronary heart disease, Health Benefits, Mediterranean Diet

Daily Log for Ketogenic and Low-Carb Mediterranean Diets

Followers of my Ketogenic Mediterranean Diet or Low-Carb Mediterranean Diet may appreciate a Daily Log I’ve put together and published as a one-page PDF.  You actually track seven days of eating on a standard sheet of printer paper.

No wine for him until he's 21!

Daily logs aren’t essential, but may help dieters keep track of the major components of the programs.  For instance, you simply check off when you’ve had your olive oil, vegetables, nuts, fish, wine (or alternative), and supplements.  It also has slots for blood sugar levels.

As long as you have a printer, ink, paper, and electricity, the Daily Log PDF is free.  

I’m trying to make this as easy as possible.  What else can I do for you?

Steve Parker, M.D.

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Alcohol Long-Term May Impair Vision in Diabetics

MedPage Today yesterday reported that chronic consumption of alcohol may impair vision in diabetics.  Drinkers performed less well on vision chart tests than non-drinkers.  It’s not a diabetic retinopathy issue.  Beer and distilled spirits were riskier than wine. 

Glasses, contacts, or Lasik?

The MedPage Today article didn’t comment on the potential health benefits of alcohol consumption.

You can bet I’ll keep an eye on this.

Steve Parker, M.D.

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Filed under Alcohol, Diabetes Complications

Cycloset (Bromocriptine) Finally on the Shelves at Your Pharmacy

More than a year after the U.S. Food and Drug Administration approved Cycloset (bromocriptine mesylate) for treatment of type 2 diabetes, it’s now available at pharmacies.  I updated my brief  bromocriptine drug review of May 14, 2009.

I assume it’s the same bromocriptine that’s been available for years to treat Parkinson’s disease and acromegaly.  Parlodel for Parkinson’s is sold as 2.5 and 5 mg tablets; Cycloset is 0.8 mg.  [Update December 3, 2010: Cycloset is not the same formulation of bromocriptine used to treat other diseases.  See first comment below.]  

Steve Parker, M.D.

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Aerobic vs Strength Training: Which Improves Diabetes More?

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

One type of resistance training

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

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

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

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

Methodology

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

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

Results

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

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

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

Comments

The authors write:

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

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

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

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

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

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

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

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

Steve Parker, M.D.

Reference: Church, T., Blair, S., Cocreham, S., Johannsen, N., Johnson, W., Kramer, K., Mikus, C., Myers, V., Nauta, M., Rodarte, R., Sparks, L., Thompson, A., & Earnest, C. (2010). Effects of Aerobic and Resistance Training on Hemoglobin A1c Levels in Patients With Type 2 Diabetes: A Randomized Controlled Trial JAMA: The Journal of the American Medical Association, 304 (20), 2253-2262 DOI: 10.1001/jama.2010.1710

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Filed under Exercise

Are Airport Body Scans Safe?

The Happy Hospitalist has a timely post about the safety of the infamous airport x-ray scanners.

Steve Parker, M.D.

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Filed under Uncategorized

Quote of the Day

St. Peter's Square, Vatican City

The outstanding event of modern times was the failure of religious belief to disappear.  For many millions, especially in the advanced nations, religion ceased to play much or any part in their lives, and the ways in which the vacuum thus lost was filled, by fascism, Nazism and Communism, by attempts at humanist utopianism, by eugenics or health politics, by the ideologies of sexual liberation, race politics and environmental politics, form much of the substance of the history of our century.  But for many more millions—for the overwhelmimg majority of the human race, in fact—religion continued to be a huge dimension in their lives.

      —Paul Johnson, in his book Modern Times, about the history of the 20th Century

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High-Carbohydrate Eating Promotes Heart Disease in Women

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

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

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

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

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

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

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

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

Practical Applications

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

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

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

Steve Parker, M.D.

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

References: Sieri, S., Krogh, V., Berrino, F., Evangelista, A., Agnoli, C., Brighenti, F., Pellegrini, N., Palli, D., Masala, G., Sacerdote, C., Veglia, F., Tumino, R., Frasca, G., Grioni, S., Pala, V., Mattiello, A., Chiodini, P., & Panico, S. (2010). Dietary Glycemic Load and Index and Risk of Coronary Heart Disease in a Large Italian Cohort: The EPICOR Study Archives of Internal Medicine, 170 (7), 640-647 DOI: 10.1001/archinternmed.2010.15

Barclay, Alan, et al.  Glycemic index, glycemic load, and chronic disease risk – a meta-analysis of observational studies [of mostly women].  American Journal of Clinical Nutrition, 87 (2008): 627-637.

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Filed under Carbohydrate, coronary heart disease, Glycemic Index and Load