The Holy Grail: Prevention of Weight Regain

Losing excess weight is easier than keeping it off.

Neither is exactly a walk in the park.

Prevention of weight regain is the most problematic area in the field of weight management.  You may have heard that “diets don’t work,” but they do.  Many different weight loss programs work short-term, if “work” is defined as loss of five, 10, or more pounds while you adhere to the program for several weeks or months.  The problem is that the lost pounds usually return.

Why?  You get bored with the diet, or your willpower flags, or the diet simply stops working, or the transition from weight loss to maintenance is unclear, or you just feel too bad to go on, or you lose your commitment, or you take a job as a taste tester for Baskin-Robbins Ice Cream, or whatever. 

Most diets ultimately fail in the long run because people go back to their old habits. 

Read on for the secret to prevention of weight regain.  They apply to a majority of weight-loss methods, although many programs ignore this problem because the cure is a hard pill to swallow. 

Moving Ahead

For purposes of further discussion, I will assume that you have already lost excess weight down to your goal and now we must focus on staying thereabouts from here on out.  Finally down to your goal!  A grand accomplishment!  You’ve got a new wardrobe, or the old clothes fit again.  You have more energy and feel younger.  Maybe you cured or improved some health problems.  Perhaps you’re getting more attention from the opposite sex (ooh la la!). 

Our species’ scientific name is Homo sapiens.  It is from the Latin sapere, which means “to be wise.”  Wisdom is the ability to make correct judgments and decisions.  Undoubtedly, your success at weight loss required correct judgments and decisions.  You are not done yet.  You will need sustained wisdom to avoid weight regain.

Be wise about this especially: you can never again eat all you want, whenever you want, over sustained periods of time.  

Now that you have reached your goal weight, you must restrain yourself on a daily basis.  Think about it.  You became overweight because you didn’t watch what you ate and didn’t exercise enough.  You can’t go back to your old ways.  Reject this advice, and you have a 100 percent chance of regaining your lost weight. 

Have you heard of the Energy Balance Equation?

Calorie Intake minus Calories Burned

         =  Change in Body Fat

You have been able to lose fat weight because you ate less energy (calories) than your body required for metabolism and physical activity.  Your body remedied the energy deficit by converting fat into energy.  A pound of fat contains 3,500 calories of energy.  If you lost a pound per week, your body on average converted 500 calories of fat daily into energy (7 days x 500 calories = 3,500 calories = 1 pound of fat). 

Now that you are at your goal weight and want to stay there, you need to add 500 calories per day back into the equation.  Add the calories by eating more food, exercising less, or a combination of the two. But if you add back more than 500, you will regain weight.

The true measure of a successful weight management program is not simply how much weight is lost, but whether the lost weight stays lost over the long run.  What distinguishes weight losers who keep the weight off from those who gain it back?  Two factors, mostly:

          1.  Restrained eating
          2.  Regular physical activity
.

“Successful losers” apply self-restraint on an almost daily basis, avoiding food that they know will lead to weight regain.  They limit how much they eat.  They consciously choose not to return to their old eating habits, despite urges to the contrary.  The other glaring difference is that, compared to regainers, the successful losers remain physically active.  They exercised while losing weight, and continue to exercise in the maintenance phase of their program.  This is true in at least eight out of 10 cases.  It’s clear that regular exercise is not always needed, but it dramatically increases your chances of long-term success. 

In a nutshell, my maintenance phase prescription for you is: Keep exercising, and eat a little more.  Keep exercising, and eat a little more.

Go out of your way to be physically active for 30 to 45 minutes on at least four days per week, if not all days.  Walking is fine.  The more you exercise, the more you can eat without getting fat again. 

At the end of your weight-loss phase and the beginning of the maintenance phase, it is surprisingly easy to start overeating.  Forewarned is forearmed.  Avoid this landmine any way you can.  It helps to continue monitoring food consumption and exercise on your food diary while eating an additional 200–500 calories per day.  Continue weighing daily.  Keep exercising.  After a month or two of this regimen, you’ll have an intuitive sense of what and how much you should be eating without regaining weight.  Then stop the daily log routine. 

Another option for transition to the maintenance phase: if you have been exercising regularly but loathe it, you could stop exercising and stay on your current calorie level diet.  In other words, don’t start eating more.  See what happens with your weight.  Perhaps you could later eat an extra 100 to 200 daily calories without gaining weight.  Continue recording your daily intake and weight for a couple months.  

Weigh yourself daily during the first two months of your maintenance-of-weight-loss phase. After that, weigh weekly.  Daily weights will remind you how hard you worked to achieve your goal.  When you look now at a brownie, candy bar, or piece of pie, you ask yourself, “Do I really want to walk an extra hour or jog an extra three miles today to burn off those calories?” If so, enjoy. Otherwise, forego the unneeded calories. 

Be aware that you might regain five or 10 pounds of fat now and then.  You probably will.  It’s not the end of the world.  It’s human nature.  You’re not a failure; you’re human.  

But draw the line and get back on your old weight-loss program for one or two months.  Analyze and learn from the episode.  Why did it happen?  Slipping back into your old ways? Slacking off on exercise?  Too many special occasion feasts?  Allowing junk food back into the house?  Learn which food item is your nemesis—the food that consistently torpedoes your resolve to eat right.  For example, I have two—candy, and sweet baked goods such as cookies and muffins.  If I just look at them I add a pound.  Remember an old ad campaign for a potato chip: “Betcha can’t eat just one!”?  Well, I can’t eat just one cookie.  So I don’t get started.  I might eat one if it’s the last one available.  Or I satisfy my sweet craving with fresh fruit or a diet soda.  Just as a recovering alcoholic can’t drink any alcohol, perhaps you should totally abstain from…?  You know your own personal gastronomic Achilles heel.  Or heels.  Experiment with various strategies for vanquishing your nemesis. 

It’s OK to overindulge in food infrequently (10–12 times per year), on special occasions such as birthdays, wedding anniversaries, holidays.  But you must counteract the extra calories by cutting down intake or by exercising more, either before or after the feast.  No big deal.

Click to read additional ideas on prevention of weight regain.

Steve Parker, M.D.

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Does Lipid Overload Cause Diabetes?

An up-and-coming theory to explain type 2 diabetes suggests that abnormal lipid metabolism, not glucose/sugar metabolism, is the primary metabolic defect.  Roger H. Unger, M.D., wrote about this in the March 12, 2008, issue of the Journal of the American Medical Association.

Early in the writing of this blog entry, I realized it is much too technical for most of my readers.  If you are not interested in physiology, you can quit reading now.  It’s OK  . . . really.  This may be the most boring blog post of mine you have ever read.  I’m writing this to solidify my own understanding of a new theory.

I assure you my prose in The Advanced Mediterranean Diet weight-loss book is not nearly this technical.

Still with me?  [Get out now while you’re still awake!] 

Definitions and Physiology

Diabetes is defined by high blood glucose (sugar) levels. 

ResearchBlogging.orgThe lipid family includes triglycerides (fats and oils), sterols (e.g., cholesterol), and phospholipids (e.g., lecithin, a major cell membrane component).  Fats are almost entirely composed of trigylcerides.  When fats are broken down, fatty acids are produced.  On the other hand, fatty acids can be joined together, along with glycerol, to form triglycerides. 

Glycogen is a storage form of glucose in liver and muscle tissue.  In olden days, some called it “animal starch.” 

Insulin is a protein hormone produced by pancreatic beta cellsInsulin has multiple actions, not just blood sugar lowering:  

  1. lowers blood glucose levels by driving glucose into cells
  2. inhibits breakdown of glycogen into glucose
  3. inhibits formation of new glucose molecules by the body
  4. stimulates glycogen formation
  5. promotes storage of triglycerides in fat cells (i.e., lipogenesis, fat accumulation)
  6. promotes formation of fatty acids (triglyceride building blocks) by the liver
  7. inhibits breakdown of stored triglycerides
  8. supports protein synthesis 

Fatty acids in muscle tissue block the uptake of glucose from the bloodstream by muscle cells.  Fatty acids in liver tissue impair the ability of insulin to suppress breakdown of glycogen into glucose, and impairs the ability of insulin to suppress production of new glucose molecules.  In other words, an “excessive fatty acid” environment in liver and muscle tissue promotes elevated glucose levels.

Got that?  [This is very difficult material.]  Now on to . . . 

The Lipocentric Theory of Type 2 Diabetes

Type 2 diabetes may be caused by:

  1. Eating too many calories [especially carbohydrates?], leading to…
  2. High insulin levels, leading to…
  3. Stimulation of fat production, leading to…
  4. Increased body fat, leading to…
  5. Deposition of lipids in cells where they don’t belong (that is, not in fat cells), leading to…
  6. Resistance to insulin’s effects on glucose metabolism, leading to…
  7. Lipid accumulation in pancreatic beta cells, damaging them, leading to…
  8. Elevated blood glucose levels, i.e., diabetes.

Perhaps the key to understanding this is to know that “insulin resistance” refers to insulin having less ability to suppress glucose production by the liver, or less ability of various tissues to soak up circulating glucose.  Insulin resistance thereby leads to elevated glucose levels.  But insulin’s effect of “producing fats” (lipogenesis) continues unabated.  Excessive fats, actually fatty acids, accumulate not only in fat cells, but also in liver cells, muscle cells, pancreatic beta cells, and others.  This lipid overload can damage those cells.

If This Theory Is Correct, So What?

Steps #1 and 2 of the lipocentric theory involve excessive caloric intake and high circulating insulin levels, leading to problems down the road.  So overweight people should restrict calories and try to lose at least a modest amount of weight.  Particularly if already having type 2 diabetes or prone to it.   

And what about people with type 2 diabetes who have insulin resistance and have poorly controlled glucose levels?  Most of these have high insulin levels already, contributing to a fat-producing state.  Adding more insulin, by injection, wouldn’t seem to make much sense if there are other alternatives.  The extra insulin would bring glucose levels down, but might also cause lipid overload with associated cellular damage. 

Effective clinical strategies according to Dr. Unger would include 1) caloric restriction, which helps reduce weight, high insulin levels, and fat production, and 2) if #1 fails, add anti-diabetic drugs that reduce caloric intake [exenatide?], that reduce lipid overload [which drug?], or that do both.  

Dr. Unger suggests consideration of bariatric surgery, for caloric restriction and cure of diabetes.

Compared with dietary fats and proteins, carbohydrates generally cause higher circulating insulin levels.  And type 2 diabetics taking insulin shots need higher doses for higher intakes of carbohydrate.  So it makes sense to me to consider preferential reduction of carbohydrate consumption if someone’s going to reduce caloric intake.

Dr. Unger and I agree that reduction of excessive food intake and excess body fat is critically important for overweight people with type 2 diabetes.

Steve Parker, M.D.

References: Unger, R. (2008). Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention JAMA: The Journal of the American Medical Association, 299 (10), 1185-1187 DOI: 10.1001/jama.299.10.1185

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Let Freedom Ring!

Arizona’s Constitution of 1912 has always held that “the right of the individual citizen to bear arms in defense of himself or the state shall not be impaired.”

Arizona’s governor a few months ago signed into law a bill restoring Arizonans’ freedom to carry firearms discreetly without a permit.  Previously, we had to ask the state for written permission, but could carry a handgun openly.  The “open carry” option sometimes scared hoplophobes.  And some of us didn’t want the bad guys to know we were armed.

Remember: When seconds count, the police are only minutes away.

Steve Parker, M.D.

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Quote of the Day

Being fat is hard…

Losing weight is hard…

Maintaining weight loss is hard…

 

Choose your hard.

 

I got this from Magicsmom at the Low Carb Friends message board, but she didn’t know the source.  Do you?

Steve Parker, M.D.

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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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Filed under Carbohydrate, Causes of Diabetes, coronary heart disease, Glycemic Index and Load, Overweight and Obesity

FDA Warns About Lipodissolve

I wrote elsewhere about mesotherapy (also known as lipodissolve) in April, 2008.  It’s a technique designed to “dissolve” localized fat deposits under the skin.

The U.S. Food and Drug Administration this month is alerting consumers that

  • it has not evaluated or approved products for use in lipodissolve
  • it is not aware of evidence supporting the effectiveness of the substances used in lipodissolve for fat elimination
  • the safety of these substances, when used alone or in combination, is unknown
  • it is not aware of clinical studies to support medical uses of lipodissolve

In addition, FDA has reports of unexpected side effects in people who’ve undergone the lipodissolve procedure. These side effects include

  • permanent scarring
  • skin deformation
  • deep, painful knots under the skin in areas where the lipodissolve treatments were injected

This is good to know before you invest time and money in the procedure.   

Steve Parker, M.D.

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Whole Grains in Diabetics: A Double-Edged Sword

 Whole grain and bran consumption are linked to reduced overall death rates and cardiovascular disease deaths in white women with type 2 diabetes, according to recent research from Boston-based investigators.

This is an important association since diabetics are prone to develop cardiovascular disease and suffer premature death.  Anything that can easily counteract those trends is welcome.

Several prior studies have found lower rates of cardiovascular disease in the general public eating whole grains.  I’m referring to fewer heart attacks and strokes, and fewer deaths from cardiovascular disease.

On the other hand, the carbohydrate content of whole grain products has the potential to complicate day-to-day management of diabetes by spiking blood sugars too high.  Too-high blood sugars aren’t healthy.  So, there’s the double edge.

What’s the Evidence That Whole Grains and Bran Prevent Death in Diabetics ?

ResearchBlogging.orgThe Harvard researchers followed 7,822 type 2 diabetic women in the massive Nurses’ Health Study over 26 years, during which 852 women died from any cause, including 295 from cardiovascular disease (195 from coronary heart disease, 100 from stroke).  Food-frequency questionnaires were administered periodically to the participants, with attention to whole grain and its components: cereal fiber, bran, and germ.  The hard clinical end-point in this study was death—from any and all causes, and from cardiovascular disease.   

Results

  • After adjustment for age and lifestyle and other dietary factors, only bran consumption was inversely associated with all-cause mortality: 25% lower risk of death for those eating an average of 10 g per day compared to 1 g per day.  In other words,the women who ate the most bran had the lowest risk of dying from any cause.
  • After adjustment for age and lifestyle and other dietary factors, whole grain intake trended towards protection against all-cause death, but not quite to the point of statistical significance.  Average highest consumption was 33 g per day, compared to lowest intake at 5 g per day. 
  • Bran consumption was consistently associated with lower risk of cardiovascular death: 35% lower risk comparing highest (10 g/day) with lowest consumption (1 g/day). 
  • “Added bran” was as protective against cardiovascular death as naturally occuring bran. 
  • Whole grain tended to protect against cardiovascular death, but did not reach statistical significance in the model adusting for lifestyle and other dietary variables (even when comparing 33 g/day to 5 g/day)
  • Whole grain and cereal fiber were inversely associated with all-cause and cardiovascular mortality when the investigators adjusted only for age, disregarding the possible effects of smoking, alcohol, overweight, physical activity, family history of heart disease, hormone therapy, duration of diabetes, total energy intake, fat intake (polyunsatrurated, trans-, saturated), magnesium, and folate.

The Researchers’ Conclusions

Whole-grain and bran intakes were associated with reduced all-cause and cardiovascular disease-specific mortality in women with diabetes mellitus. These findings suggest a potential benefit of whole-grain intake in reducing mortality and cardiovascular risk in diabetic patients.

The authors point out that whole grain and its components may be protective since they:

  • reduce blood lipids
  • lower blood pressure
  • reduce hyperinsulinemia and improve glucose control
  • improve performance of the arterial wall lining (endothelium)
  • reduce oxidative stress and iflammation

My Comments

Whole grain and bran consumption may indeed protect against death and cardiovascular disease in diabetic white women, but the effect is by no means dramatic.  I had speculated earlier whether whole grain intake might be particularly protective in diabetics, but this study suggests not.  Clearly, whole grains are no panacea. 

Diabetics hoping to avoid cardiovascular disease are well-advised to pay attention to—and modify—non-dietary risk factors for heart disease, such as obesity, smoking, and sedentary lifestyle.  Non-dietary issues probably outweigh the effects of diet, assuming blood sugars are reasonably controlled.

The traditional Mediterranean diet—prominently featuring whole grains—is associated with longer lifespan and less cardiovascular disease.   Canadian researchers in 2009 found moderately strong evidence that whole grains protect against coronary heart disease in the general population.  Yet a 2009 study did not find cereals contributing to the longer lifespan. 

I’m starting to think that the effect of diet on chronic disease is not as powerful as we have hoped.  

Steve Parker, M.D.

Reference: 
He, M., van Dam, R., Rimm, E., Hu, F., & Qi, L. (2010). Whole-Grain, Cereal Fiber, Bran, and Germ Intake and the Risks of All-Cause and Cardiovascular Disease-Specific Mortality Among Women With Type 2 Diabetes Mellitus Circulation, 121 (20), 2162-2168 DOI: 10.1161/CIRCULATIONAHA.109.907360

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Metformin Raises Risk of Vitamin B-12 Deficiency

ResearchBlogging.orgA recent study out of the Netherlands shows that type 2 diabetics taking insulin and metformin are at risk of clinically significant vitamin B12 deficiency.

B12 deficiency may cause anemia, nerve damage (neuropathy), and dementia, among other problems.

Metformin is the cornerstone of drug therapy for type 2 diabetes.  One reason is that it’s associated with improved cardiovascular disease outcomes—a claim few diabetic drugs can make.  Prior studies established that metformin interferes with B12 absorption.  The study at hand indicates that such malabsorption can reach a clinically significant degree, and that the falling blood levels are progressive over time.

No B12 here

How Was the Study Done?

Three diabetes clinic in the Netherlands provided 390 patients with type 2 diabetes between the ages of 30 and 80.  They were all treated with 1) insulin and metformin 850 mg three times daily, or 2) insulin and placebo three times daily.  B12 levels were drawn periodically over the course of the 4-year study.  Seventy-two percent of participants completed the study (the drop-outs included 30 on metformin and 16 on placebo).

What Did the Investigators Find After Four Years?

  • Compared with the placebo group, B12 levels in the metformin group dropped an average of 19%.
  • Compared to the placebo group, the metformin cohort had a 7% risk of developing B12 deficiency (blood level under 150 pmol/l) and 11% risk of dropping into the “low B12” category (level 150-220 pmol/l).

Clinical Implications

It’s unclear whether these findings apply to diabetics not taking insulin or to other ethnicities and nationalities.  I suspect they do.

The risk of developing B12 deficiency with metformin is not huge, but it seems to be real.  Once B12 deficiency does it’s damage, it may not be totally reversible.  So it’s important to know about this issue if you take or prescribe metformin.  At this point I wouldn’t depend on my doctor to be aware of this adverse drug effect, nor to remember to check B12 levels periodically.

The researchers recommend that B12 levels be checked “regularly” in patients taking metformin, without defining a time frame.  I suggest every year or two—closer to yearly if the patient has other risk factors for B12 deficiency, such as malnutrition, advanced age, removal of part of the stomach, some weight-loss surgeries, vegan diet, celiac disease, and Crohn’s disease.

Steve Parker, M.D.

de Jager, J., Kooy, A., Lehert, P., Wulffele, M., van der Kolk, J., Bets, D., Verburg, J., Donker, A., & Stehouwer, C. (2010). Long term treatment with metformin in patients with type 2 diabetes and risk of vitamin B-12 deficiency: randomised placebo controlled trial BMJ, 340 (may19 4) DOI: 10.1136/bmj.c2181

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Cinnabon Schninnamon

I woke up today and found my wife had brought home six Cinnabon cinnamon rolls.  I had mentioned off-hand a few days ago how much I missed them.  She interpreted that as a request [it wasn’t].

I couldn’t say “no” now, could I?

No, I couldn’t.

According to Calorie Count, the classic Cinnabon roll provides:

  • 730 calories
  • 216 calories from fat (24 g)
  • 114 g of carbohydrate
  • 1.5 g fiber

Looking at the carb count, you can understand how the typical American gets 250-300 g of carb daily.  For the last nine months, I’ve been eating 50 g or less, and about 2000 calories/day.

I ate the Cinnabon as a meal, rather than as dessert after—and in addition to—a meal.  If you’re gonna cheat during a weight-control program—and who doesn’t?—that may be a good way to do it.

Compare the Cinnabon with a 700-cal large green salad with tomato, onion, olive oil vinaigrette, topped with tuna or chicken.  Which has “more nutrition”? 

Did I enjoy the Cinnabon?  You bet!  Will I be able to resist the temptation of the ones remaining?  I hope so.

Steve Parker, M.D.

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London’s Low-Carb Diet Fad of 1865

Dr. Robert Atkins didn’t invent low-carb dieting.  William Banting (1797-1878) sparked a low-carb diet craze in London with his low-carb weight-loss diet, first published in 1863.  Even that probaby wasn’t the first low-carb diet.

According to Wikipedia, Banting was a distant relative of Frederick Banting, the co-discoverer of insulin in 1921.

Mr. Banting attributes his successful program design to a “medical gentleman,” Mr. Harvey, of Soho Square, London. 

Click to read Mr. Banting’s 1865 “Letter on Corpulence” at Internet Archive.

Steve Parker, M.D.

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