Tag Archives: obesity

October 28, 2011 · 6:21 AM

Does Loss of Excess Weight Improve Longevity?

High WHR

Intentional weight loss didn’t have any effect either way on risk of death, according to recent research out of Baltimore.  Surprising, huh?

Obesity tends to shorten lifespan, mostly due to higher rates of cancer and cardiovascular disease like heart attacks and strokes.  Doctors and dietitians all day long recommend loss of excess weight, figuring it will reduce the risk of obesity-related death and disease.  Many of them are unaware that’s not necessarily the case.  It’s called the “obesity paradox“: some types of overweight and obese patients actually seem to do better (e.g., live longer) if they’re above the so-called healthy body mass index of 18.5 to 24.9.  For instance: those with heart failure, coronary artery disease, and advanced kidney disease.

It’s never really been clear whether the average obese person (body mass index over 30) improves his longevity by losing some excess weight.  That’s what the study at hand is about.

Methodology

Baltimore-based investigators followed the health status of 585 overweight or obese older adults over the course of 12 years.  Half of them were randomized to an intentional weight loss intervention.  All of them had a high blood pressure diagnosis.  Average age was 66.  Average body mass index was 31.  Details of the weight-loss intervention are unclear, but it was probably along the lines of “eat less, exercise more.”

What Did They Find?

The weight-loss group lost and maintained an average of 4.4 kg (9.7 lb) over the 12 years of the study.  This is about 5% of initial body weight, the minimal amount thought to be helpful for improvement in weight-related medical and metabolic problems.  Most of the weight loss was over the first three years.

The men assigned to the weight-loss program had about half the risk of dying over the course of the study, compared to the men not assigned to weight loss.  The authors don’t seem to put much stock in it, however, stating that “…no significant difference overall was found in all-cause mortality between older overweight and obese adults who were randomly assigned to an intentional weight-loss intervention and those who were not.” 

Comments

With regards to the men losing weight, we’re only talking about 100-150 test subjects, a relatively small number.  So I understand why the researchers didn’t make a big deal of the lower mortality: it may not be reproducible.

This same research group did a similar study of 318 arthritis patients and intentional weight loss, finding a 50% lower death rate over eight years.

The authors reviewed many similar studies done by other teams, noting increased death rates from weight loss in some studies, and lesser death rates in others. 

When the studies are all over the place like this, it usually means there’s no strong association either way.  Nearly all the pertinent studies were done on relatively healthy, middle-aged and older folks.  The most reliable thing you can say about the issue is that loss of excess fat weight doesn’t increase your odds of premature death. 

 Remember that patients with coronary heart disease, congestive heart failure, or advanced kidney disease tend to live longer if they’re overweight or at least mildly obese.  It’s the obesity paradox.  Will they live longer or die earlier if they go on a weight-loss program?  We don’t know.

We do know that intentional weight loss helps:

  • prevent type 2 diabetes
  • maintain reasonable blood pressures (avoiding high blood pressure)
  • improves lower limb functional ability

Maybe that’s enough.

Steve Parker, M.D.

Reference: Shea, M.K., et al.  The effect of intentional weight loss on all-cause mortality in older adults: results of a randomized controlled weight-loss trial.  American Journal of Clinical Nutrition, 94 (2011): 839-846.

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October 9, 2011 · 2:18 AM

Does Diminished Work Activity Explain Our 50-Year Overweight Trend?

Daily work-related energy expenditure over the last half-century in the U.S. has decreased by over 100 calories.  This may well explain the increase in body weights we’ve seen, according to a 2011 article in PLoS ONE.

I sorta hate to open this can o’ worms, but it’s important.  As a population, are we fat because we eat too much or because we burn too few calories in physical activity?  Or is it a combination?  The correct answer may help us learn how to reverse the trend.

Methodology

Authors of the study at hand estimated the amount of energy (calories) necessary to perform various jobs, then noted changes in numbers of people employed in those jobs over time.  In the early 196os, for example, nearly half of U.S. jobs required at least moderate intensity physical activity, compared to less than 20% demanding that degree of energy now.  The authors note the dramatic shift from manufacturing to service-type jobs over the last 50 years.  Service jobs, like mine, often entail a lot of sitting and standing around. 

They chose to ignore how much energy we expend in exercise, figuring what we do in a 40-hour work week overwhelms the 1-2 hours of  exercise we may do.

Researchers’ Findings and Conclusions

They found that work-related daily energy expenditure has decreased by over 100 calories over the last half-century, which (in the authors’ view) would account for a significant portion of the increased body weight we’ve seen.  Since physically demanding jobs are unlikely to see a resurgence, the authors advocate physically active lifestyles away from workplace. 

Discussion

Surveys indicate that only one in four of us fulfill the federal physical activity guidelines: 150 minutes a week of moderate intensity activity or 75 minutes a week of vigorous intensity activity.  When activity is actually measured with an accelerometer, only one in 20 achieve that lofty goal.  We over-estimate how much we exercise, and under-estimate how much we eat.

(If you want to emulate a Paleolithic lifestyle, you should probably shoot for an hour of exercise daily, not 20 minutes as above.)

The researchers cite studies showing significantly increased average per capita calorie consumption in the U.S. over the last several decades.  Some experts estimate the caloric increase is in the range of 500 a day for adults; the authors here think that’s too high but don’t offer a specific alternative. Looking at one of their references (Hall et al), they must think the increase is closer to 200 calories a day, comparing 2005 to 1975.

Several studies suggest that average daily energy expenditure has not decreased in developed countries, at least from the 1980s to the present.   A strength of the current study at hand is that it spans about 50 years, up to 2008.

My sense is that both calorie consumption (too much) and physical activity (too little) contribute to our overweight problem that started 40 or 50 years ago.  Excessive consumption is the predominant factor.  To “exercise off”  the calories in a Snickers candy bar, you’d have to jog for an hour.  If you’re watching your weight, you’ll have more success if you just skip the Snickers.

In case you couldn’t tell,  I still believe in the “calories in/calories out” model of overweight and obesity, aka “the energy balance equation.”  At the same time, I believe certain foods  are more fattening than others: concentrated sugars and refined starches.

Steve Parker, M.D.

References:

Church, T.S., et al.  Trends over 5 decades in U.S. occupation-related physical activity and their associations with obesity.  PLoS ONE, 2011, 6(5): e19657.  doi: 10.1371/journal.pone.0019657  

Swinburn, B., et al.  Increased food energy supply is more than sufficient to explain the U.S. epidemic of obesity.  American Journal of Clinical Nutrition, 2009 (90): 1,453-1,456.  

Hall, K.D., et al.  The progressive increase of food waste in America and its environmental impact.  PLoS ONE, 2009, 4(11): e7940.  doi: 10.1371/journal.pone.0007940

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September 9, 2011 · 2:00 AM

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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June 2, 2011 · 2:00 AM

Exercise, Part 10: What If I’m Markedly Obese?

The more overweight you are, the harder it will be to exercise.  At some point even light exercise becomes impossible.  Average-height women tipping the scales at about 280 pounds (127 kg) and men at 360 pounds (164 kg) aren’t going to be able to jog around the block, much less run a marathon.  These weights are 100 percent over ideal or healthy levels.  An actual “exercise program” probably won’t be possible until some weight is lost simply through very-low-carb eating, calorie restriction, or bariatric surgery.  The initial exercise goal for you may just be to get moving through activities of daily living and perhaps brief walks and calisthenics while sitting in a chair.

"I'll get started after I finish this cigarette."

Markedly obese people who aren’t up to the aforementioned extreme weights can usually tolerate a low-intensity physical activity program.  At 50 percent over ideal weight, an average-height woman of 210 pounds (95 kg) is carrying 70 excess pounds (32 kg) of fat.  Her male counter-part lugs around 90 pounds (41 kg) of unnecessary fat.  This weight burden causes dramatic breathlessness and fatigue upon exertion, and makes the joints and muscles more susceptible to aching and injury.  If you’re skinny, just imagine trying to walk or run a mile carrying a standard five-gallon (19 liter) water cooler bottle, which weighs only 43 pounds (19.5 kg) when full.  The burden of excess fat makes it quite difficult to exercise.    

If you’re markedly obese, several tricks will enhance your exercise success.  I want you to avoid injury, frustration, and burn out.  Start with light activity for only 10 or 15 minutes, gradually increase session length (e.g., by two to four minutes every two to four weeks) and increase exercise intensity only after several months.  Your joints and muscles may appreciate easy, low-impact exercises such as stationary cycling, walking, swimming, and pool calisthenics/water aerobics.  You may also benefit from the advice of a personal fitness trainer arranged through a health club, gym, or YMCA/YWCA.  Check out several health clubs before you join.  Some of them are primarily meat markets for beautiful slender yuppies.  You may feel more comfortable in a gym that welcomes and caters to overweight people. Hospitals are increasingly developing fitness centers with obese orthopedic, heart, and diabetic patients in mind.

Steve Parker, M.D.

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May 9, 2011 · 2:00 AM

Book Review: The Dukan Diet

With a suspicion that the Dukan Diet may be the next diet fad in the U.S., I read The Dukan Diet: 2 Steps to Lose the Weight, 2 Steps to Keep It Off Forever by Pierre Dukan (2011, first American edition).  On Amazon.com’s rating system, I give it two stars.

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Think of Dukan as a Low-Fat Atkins Diet.

The Dukan Diet is apparently very popular in Europe.  It’s comprised of four phases. The Attack Phase, also called “Pure Protein,” lasts usually two to seven days.  Eat all you want from the protein-rich food list, mostly skinless chicken, low-fat meat, fish, and nonfat dairy.  No carbs at all except for the dairy.  The Cruise Phase is next: Alternate Pure Protein days with proteins and non-starchy vegetables until you’re at your goal weight.  Eat all you want from the low-carb veggie list.  Consolidation Phase lasts five days for every pound lost.  Eat more variety but limited quantities: two slices of whole grain bread, one portion each of fruit and cheese daily, one or two servings of starchy carbs (e.g., legumes, flour, cereals), plus two “celebration meals” a week, carefully defined.  Proteins and low-carb veggies are still unlimited.  Finally, the Permanent Stabilization Phase is lifelong and similar to Consolidation Phase, but requires one Pure Protein day per week, such as Thursdays.  Also, take no stairs or elevators.  All phases include prescribed servings of oat bran.

During the active weight loss phases, this diet is low-fat, low-carb, and high-protein. You don’t have to count carb grams, fat grams, or calories.  Presumably, Dr. Dukan has done all that for you, although he never shares the average calories consumed nor the macronutrient breakdown (i.e., what percentage of calories are derived from protein, fat, or carbs). The latter two phases are still very low-fat but allow a bit more carbs.

I liked this book more than I expected.  It’s obvious the author has copious experience with dieters, especially women.  The writing is clear.  He’s a serious, earnest man, not a charlatan.  Although some will criticize the book’s repetitiveness, it’s a proven educational technique.  For weight management, Dr. Dukan and I agree that 1) weighing daily is good, 2) abstinence from sugar rarely eliminates the longing for sweets, 3) artificial no-calorie sweeteners are OK, 4) the 4-7 pound weight loss in Attack Phase is mostly water, not fat, 5) discipline and willpower are important, 6) after losing weight, you’ll regain it if you ever return to your old ways, and 7) a realistic weight goal is essential. 

Dr. Dukan recommends at least 20-30 minutes a day of walking.  He provides little information on resistance training, although increasing evidence supports it as a great weight control measure.  I wish he’d mentioned high intensity interval training (HIIT).

The book contains numerous recipes, including a week of menus for the Attack Phase.  Disappointingly, none of the recipes include nutritional analysis.

You’ll find an index.  It doesn’t list glycogen.  Insulin, a primary fat-storage hormone, is mentioned on only one page, one sentence.

This is one fat-phobic diet.  In Dr. Dukan’s view, “fat in food is the overweight person’s most deadly enemy.”  All fat consumption contributes to fatness, and animal fats “pose a potential threat to the heart.”  It seems Dr. Dukan never got the memo that total and saturated fat content of foods have little, if anything, to do with heart or other cardiovascular disease. While criticizing Dr. Atkins’ diet for demonizing carbohydrates, Dr. Dukan demonizes fats.  Yet Dr. Dukan does all he can to banish both carbohydrates and fats from his weight loss phases. 

Dr. Dukan makes several erroneous statements, including 1) all food is made up of only three nutrients, 2) all alcoholic beverages are high in carbohydrates, 3) all shellfish are carbohydrate-free, 4) he implies that when dieting or fasting, we convert much of our fat into glucose, 5) there are no indispensable fats, 6) fat is bad for the cardiovascular system, 7) vinegar is the only food containing sour taste, 8) fruit is the only natural food containing rapid-assimilation sugars, 9) “Anyone who loses and regains weight several times becomes immune to dieting,” 10) weight loss releases into the bloodstream artery-toxic fat and cholesterol, 11) many overweight folks are unusually good at extracting calories from food, 12) some people can gain weight even while they sleep, 13) exercise is vitally important for losing weight, and 14) the Atkins diet raises triglycerides and cholesterol levels dangerously.

Will the diet work?  I’m sure many have lost weight with it and kept it off.  It does, after all, limit two of the major causes of excess weight: sugars and refined starches. 

In considering rating this book two or three stars, I asked myself if I’d recommend it to one of my patients looking to lose weight.  Initially I had concern that the diet may be deficient in essential fatty acids since it’s so fat-phobic.  “Essential” means necessary for life and health.  Then I figured that the body’s own fat stores would provide adequate essential fatty acids, at least in the first two phases.  The later stages, I’m not so sure.  Carefully choosing specific foods would eliminate the risk, but how many people know how to do that?  Separate from that potential drawback, there are other diets that are better for the non-diabetic population, such as The New Atkins Diet for a New You, Protein Power, the Ketogenic Mediterranean Diet (free on the Internet), and The New Sonoma Diet.  You’ll have no risk of fatty acid deficiency with those.

For people with diabetes or prediabetes, I like Atkins Diabetes Revolution, Dr. Bernstein’s Diabetes Solution, and, of course, Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet.

 If you limit carbs, there’s just no need for fat-phobia.

Steve Parker, M.D.

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May 1, 2011 · 5:52 AM

Low-Carb Diet Better Than Low-Cal for Fatty Liver

Loss of excess weight is a mainstay of therapy for nonalcoholic fatty liver disease.  A very-low-carb diet works better than a reduced-calorie diet, according to a recent study in the American Journal of Clinical Nutrition.

Nonalcoholic fatty liver disease (NAFLD) occurs in 20 to 40% of the general population, with most cases occuring between the ages of 40 and 60.  It’s an accumulation of triglycerides in the liver. 

Nonalcoholic steatohepatitis (NASH) is a subset of NAFLD, perhaps 30% of those with NAFLD.  Steatohepatitis involves an inflammatory component, progressing to cirrhosis in 3 to 26% of cases. 

ResearchBlogging.orgResearchers at the University of Texas Southwestern Medical Center assigned 18 obese subjects (average BMI 35) to either a very-low-carb diet (under 20 grams a day) or a low-calorie diet  (1200 to 1500 calories a day) for two weeks.  Liver fat was measured by magnetic resonance technology.  The low-carb groups’ liver fat decreased by 55% compared to 28% in the other group.  Weight loss was about the same for both groups (4.6 vs 4 kg). 

Bottom Line

This small study needs to be replicated, ideally with a larger group of subjects studied over a longer period.  Nevertheless, it appears that a very-low-carb diet may be one of the best dietary approaches to nonalcoholic fatty liver disease.  And I bet it’s more sustainable than severe calorie restriction.  The Ketogenic Mediterranean Diet, by the way, provides 20-30 grams of carb daily.

Steve Parker, M.D. 

 
Refernce:  Browning JD, Baker JA, Rogers T, Davis J, Satapati S, & Burgess SC (2011). Short-term weight loss and hepatic triglyceride reduction: evidence of a metabolic advantage with dietary carbohydrate restriction. The American journal of clinical nutrition, 93 (5), 1048-52 PMID: 21367948

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December 14, 2010 · 11:07 AM

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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August 13, 2010 · 8:16 AM

Is a Low-Carb Diet Safe For Obese Adolescents?

High-protein, low-carbohydrate diets are safe and effective for severely obese adolescent, according to University of Colorado researchers.

Childhood obesity in the U.S. tripled from the early 1980s to 2000, ending with a 17% obesity rate.  Overweight and obesity together describe 32% of U.S. children.  Some experts believe this generation of kids will be the first in U.S. history to suffer a decline in life expectancy, related to obesity.

Colorado researchers wondered if a low-carb, high-protein diet is a reasonable treatment option.  Why high protein?  It’s an effort to preserve lean body mass (e.g., muscle). 

ResearchBlogging.orgThey randomized 46 adoloscents (age 12–18) to either a high-protein, low-carb diet (HPLC diet) or a calorie-restricted low-fat diet to be followed for 13 weeks.  HPLC dieters could eat unlimited calories as long as they attempted to keep carb consumption to 20 g/day or less.  Low-fat dieters were to choose lean protein sources, aiming daily for 2 to 2.5 grams of protein per kilogram of ideal body weight.  Study participants underwent blood analysis and body compositon analysis by dual x-ray absorptiometry.  These kids weighed an average of 108 kg (238 lb) and average body mass index was 39. 

Analysis of food diaries showed the following:

  • Average caloric intake was 1300-1450/day, toward the lower end for the HPLC dieters
  • Energy composition of the HPLC diet: 32% from protien, 11% from carb, 57% from fat
  • Energy compositon of the LF diet: 21% from protein, 51% from carb, 29% from fat
  • Average daily carb consumption for the HPLCers ended up closer to 40 g (still very low) 

Findings

Both groups lost weight, with the HPLC dieters trending to greater weight loss, but not to a statistically significant degree.  They did, however, show a greater drop in body mass index Z-score, however.  Study authors didn’t bother to explain “body mass index Z-scores,” assuming I would know what that meant.  Average weight in the HPLC group dropped 13 kg (29 lb) compared to 7 kg (15 lb) in the low-fat group.

Total and LDL cholesterol fell in both groups, and insulin resistance improved.  Neither diet had much effect on HDL cholesterol.

As usual, triglycerides fell dramatically in the HPLC dieters.

Nearly 40% of the kids—about the same number in both groups—dropped out before finishing the 13 weeks.

The HPLC group did not see any particular preservation of lean body mass, and actually seemed to lose a bit more than the low-fat group.

There were no serious adverse effects in either group. 

Surprisingly, satiety and hunger scores were the same in both groups.  [Low-carb, ketogenic diets have a reputation for satiation and hunger suppression.]

My Comments

This is a small short-term study with a large drop-out rate; we must consider it a pilot study.  That’s why I’m not as enthusiastic about it as the researchers.  Nevertheless, it does indeed suggest that high-protein, low-carb diets are indeed safe and effective in obese adolescents.  It’s a start.   

Steve Parker, M.D.

Reference: Krebs, N., Gao, D., Gralla, J., Collins, J., & Johnson, S. (2010). Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents The Journal of Pediatrics, 157 (2), 252-258 DOI: 10.1016/j.jpeds.2010.02.010

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June 18, 2010 · 2:00 AM

Sugar-Sweetened Beverages: Bane of Mankind?

Over the last 30 years in the U.S., consumption of sugar-sweetened beverages (SSBs) has increased from3.9% of total calories to 9.2% (in 2001).  In that same time span, the percentage of overweight American adults increased from 47% to 66%.  The obesity percentage rose from15 to 33% of adults. 

[Did the beverages cause the weight gain, or are they just associated?] 

Those are just a few of the many facts shared by the authors of “Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk,” published recently in Circulation.  Sugar-sweetened beverages, by the way, include soft drinks, fruit drinks, energy drinks, and vitamin water drinks. 

ResearchBlogging.orgSounds like an interesting article, doesn’t it?  It’s written by some of the brightest lights in nutritional science, including George Bray and Frank Hu.  Unfortunately, the article is a little too boring and technical for most of my readers.  Here are a few tidbits I enjoyed:

  • Fructose (found in similar amounts in sucrose (table sugar) and high fructose corn syrup) may particularly predispose us to deposit fat in and around our internal abdominal organs (“visceral fat,” which some believe to be more unhealthy than fat  in our buttocks or thighs).
  • Fructose may also lead to fat deposits in cells other than fat cells, potentially interfering with cell function.
  • Fructose may adversely affect lipid metabolism (higher triglyceride levels and lower HDL levels, which could promote heart disease).
  • Fructose raises blood pressure and reduces insulin sensitivity.
  • In the liver, fructose is preferentially converted to lipid, causing high triglyceride levels (associated with heart disease and insulin resistance).  [The authors did not mention the common condition of “fatty liver” (aka hepatic steatosis) in this context.]

Some of the authors conclusions:

  • SSBs are the largest contributor to added-sugar intake in the U.S.
  • SSBs contribute to weight gain.
  • SSBs may cause type 2 diabetes and cardiovascular disease—separate from their effect on obesity—via high glycemic load and increased fructose metabolism, in turn leading to insulin resistance, inflammation, pancreas beta cell impairment, high blood pressure, visceral fat build-up, and adverse effects on blood lipids.

I especially like their final sentence:

For these reasons and because they have little nutritional value, intake of SSBs should be limited, and SSBs should be replaced by healthy alternatives such as water.

Steve Parker, M.D.

Reference: Malik, V., Popkin, B., Bray, G., Despres, J., & Hu, F. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk Circulation, 121 (11), 1356-1364 DOI: 10.1161/CIRCULATIONAHA.109.876185

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December 7, 2009 · 2:00 AM

Are Fructose and High Fructose Corn Syrup Bad for Us?

Table sugar (sucrose) is a combination of glucose and fructose

Darya Pino earlier this month posted at her Summer Tomato blog a video regarding high fructose corn syrup.  The speaker in the video is pediatric endocrinologist Robert Lustig, M.D., of the University of California—San Francisco.
In the U.S. between 1970 and 1990, consumption of high fructose corn syrup increased over 1000%.  During those two decades, the incidence of overweight and obesity nearly doubled.  Many wonder if this is more than just coincidental. Most of this fructose is in soft drinks.  Soft drink consumption per person in 1942 was two servings per week.  In 2000, consumption was two servings per day.  Of course, these drinks typically have few nutrients other than sugars.
I wrote about fructose possibly being “the new trans fat” almost two years ago.

Dr. Lustig is convinced that high fructose corn syrup (HFCS) is a chronic toxin, at least in the amounts many of us eat, and the cause of our current epidemic of childhood and adult obesity and overweight.  Even if this idea is not new to you, you may be interested to hear the biochemistry and physiology behind his position.  If you didn’t enjoy college lectures or are not a food science geek, you probably won’t be able to sit through this 1.5-hour video. 

I enjoyed the heck out of it!  Made me feel like I was back in college again.  Few of my professors were as good as Dr. Lustig at lecturing. 

Here are a few of his other major points:

  • HFCS was invented in Japan in the 1960s, then introduced to U.S. markets in 1975
  • sucrose and fructose are both poisons
  • in the U.S. we eat 63 pounds (28.6 kg) of HFCS and 141 pounds (64.1 kg) of sugar per year [he didn’t define “sugar” in this context]
  • he praises Yudkins book, Pure, White, and Deadly [I’ve written about the Cleave-Yudkin carbohydrate theory of chronic disease]
  • the triglyceride/HDL ratio predicts heart disease much better than does LDL cholesterol
  • chronic high fructose intake causes the metabolic syndrome [does he think it’s the only cause?]
  • only the liver can metabolize fructose, in contrast to every other tissue and organ that can use glucose as an energy supply
  • high fructose consumption increases the risk of gout and high blood pressure
  • fructose interferes with production of our body’s production of nitrous oxide—a natural circulatory dilator—leading to higher blood pressures
  • fructose increases de novo lipogenesis—in other words, it creates body fat
  • fructose interferes with natural chemical messengers that tell your brain you’ve had enough food and it’s time to stop eating
  • high fructose intake reduces LDL particle size, potentially increasing the future risk of cardiovascular disease such as heart attacks [small, dense LDL cholesterol is more damaging to your arteries that large, fluffy LDL]

So What? 

You don’t need polititians to reduce your consumption of sugary soft drinks and high fructose corn syrup—do it yourself starting today.  Read food labels—HFCS is everywhere.  I’ve found it in sausage! 

The food industry greatly reduced use of trans fats in response to consumer concerns, before the polititians ever dabbled in it.  HFCS can go the same route.  Consumption of soft drinks, sports drinks, and other sugary beverages—the major sources of HFCS—is up to you.

Steve Parker, M.D.

PS: The Advanced Mediterranean Diet and Ketogenic Mediterranean Diet are naturally low in fructose.

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