Archive for November, 2010

Weight Loss Maintenance

Tuesday, November 30, 2010 // Uncategorized

Some people lose weight easily, but have a difficult time keeping it off.  Once weight loss has been achieved, what is the optimal diet to keep it off? The following study assesses the comination of low or high protein along with low or high glycemic versus placebo. The term glycemic has to do with how quickly foods are converted to sugar. Low glycemic foods are slowly converted and high glycemic are quickly converted.
Diet High in Protein, Low on Glycemic Index Helps Prevent Weight Regain
A diet high in protein and low on the glycemic index appears to be optimal for weight control following significant weight loss, according to an international study in the New England Journal of Medicine.
Researchers randomized some 770 overweight or obese adults — who had recently lost at least 8% of their body mass — to one of five maintenance diets: high-protein/low-glycemic-index, high-protein/high-glycemic-index, low-protein/low-glycemic-index, low-protein/high-glycemic-index, or following their country’s dietary guidelines.
At 6 months, the high-protein/low-glycemic-index diet group had lost additional weight (-0.38 kg), while the low-protein/high-glycemic-index diet regained the most weight (1.67 kg). Diets that were high in protein and low on the glycemic index had higher rates of study completion.
The authors conclude that a high-protein/low-glycemic-index diet “appears to be ideal for the prevention of weight regain.”

For those who want more detail, the following is the editorial from that issue of the NEJM which goes into the mechanism by which the diet might work.  “Diet” is a four letter word.  The problem with it is that it implies that there is a beginning and an end.  “Life style modification” is a better term.  The dietary modifications described in this study are easier to adapt for long term use.

Editorial

Weight-Loss Maintenance — Mind over Matter?

David S. Ludwig, M.D., Ph.D., and Cara B. Ebbeling, Ph.D.

N Engl J Med 2010; 363:2159-2161November 25, 2010

Article

Many people can lose weight in the short term by reducing their intake of calories with the use of a variety of diets, ranging from low-fat to very-low-carbohydrate. However, few people successfully maintain their weight loss.1 One explanation for the poor efficacy of conventional diets relates to psychological factors, since the motivation to adhere to restrictive regimens diminishes with time, especially in an environment with virtually instantaneous availability of food. A second, perhaps more fundamental, explanation is that weight loss elicits physiological adaptations — principally an increase in hunger and a decrease in resting energy expenditure2 — that oppose ongoing weight loss.

In the search for more effective strategies, diets that are low in glycemic index and moderately high in protein merit special consideration. The glycemic index describes the way in which foods affect blood glucose levels in the postprandial period, controlled for the amount of carbohydrate.3The glycemic load, the arithmetic product of the glycemic index and the amount of carbohydrate, predicts postprandial glycemic response among foods with widely varying carbohydrate contents.4Most highly processed grain products have a high glycemic index, whereas minimally processed grains, whole fruits, legumes, and nonstarchy vegetables tend to have a moderate or low glycemic index.

The mechanisms relating glycemic response to the regulation of body weight have been examined in controlled feeding studies.5Meals with a low glycemic index or glycemic load elicit acute hormonal and metabolic changes that may decrease hunger and energy intake. During weight loss, a reduction in glycemic load may attenuate the decline in resting energy expenditure that is thought to promote weight regain.6Recently, a meta-analysis indicated that diets in which there was a reduction in the glycemic index produced moderately more weight loss than control diets,7 although the quality of the clinical trials has been limited by their small size, a failure to show adherence to treatment, and confounding.

The glycemic response to carbohydrates is lowered when protein is ingested simultaneously, since protein delays gastric emptying and stimulates insulin secretion. Protein also displaces carbohydrates, as opposed to fat, from the diet because foods high in protein are also typically high in fat. Therefore, higher-protein diets tend to have a reduced glycemic load and might promote weight loss, at least in part, through the mechanisms discussed above.

In addition, diets that are based on these principles may be less psychologically burdensome, because they do not severely restrict any macronutrient or major food group. However, the 2010 U.S. Department of Agriculture Dietary Guidelines Advisory Committee considers the effectiveness of reducing the glycemic index to be unproven. Similarly, there is a lack of consensus regarding the optimal protein level for achieving and maintaining weight loss. A study in this issue of the Journal from the Diet, Obesity, and Genes (Diogenes) project8 addresses these knowledge gaps.

Investigators from eight European countries randomly assigned 773 participants who had lost at least 8% of their initial body weight to one of four test diets, using a two-by-two factorial design (low-glycemic-index vs. high-glycemic-index diets and low-protein vs. high-protein diets), or to a fifth, control, diet. Assessment of dietary intake showed that there was a modest difference of about 5 glycemic-index units between the low-glycemic-index and high-glycemic-index groups and a difference of about 5 percentage points in protein content between the high-protein and low-protein groups. After 6 months, body weight differed by about 2 kg among the groups, with a direct relationship to glycemic load — lowest in the group assigned to the low-glycemic-index–high-protein diet, intermediate in the groups assigned to the low-glycemic-index–low-protein and the high-glycemic-index–high-protein diets, and highest in the group assigned to the high-glycemic-index–low-protein diet. Of note, study completion rates were significantly better among participants in the low-glycemic-index and high-protein diet groups.

The study has several notable strengths, including the large number of participants and a multicenter, multinational design, providing evidence of effectiveness and generalizability. The apparent control for treatment intensity and behavioral methods across groups (although not across countries) allows for a fair testing of dietary hypotheses. Furthermore, the investigative team appears to have had scientific balance; one senior member had espoused a skeptical view of the glycemic index,9 providing confidence that the study was conducted and interpreted without unconscious bias. The primary limitation of the study is the short duration of follow-up. A 2-kg difference in body weight, by itself, has limited practical implications. But a diet that could effectively prevent weight regain over the long term would have major public health significance. In this regard, the 12-month and longer follow-up data will be informative.

The observed effects on body weight were obtained from small mean differences in glycemic index and protein among the groups. In principle, more powerful methods for effecting behavioral change and improved availability of low-glycemic-index foods may facilitate the long-term adoption of diets with a substantially lower glycemic load and result in larger effects on body weight. Moreover, a low-glycemic-index diet may reduce the risk of diabetes and heart disease independently of body weight,5and data addressing this possibility will be forthcoming from the Diogenes trial.

The present study contrasts, but does not necessarily conflict, with data reported by Sacks et al.,10who assigned 811 people to one of four diets that differed in the percentage of total energy derived from carbohydrate, protein, and fat. In contrast to the protocol in the Diogenes trial, participants in all four groups were counseled to consume carbohydrates with a low glycemic index. Similar to the results in the Diogenes trial, the protein content of the diets at 6 months differed by only about 5 percentage points. After 2 years, no significant difference in body weight was found among the groups, although among subjects who completed the study, those who consumed higher-protein diets weighed about 1 kg less than those who consumed lower-protein diets (P=0.11).10Together, these two studies suggest that the ratio of carbohydrate to fat has relatively little importance for weight control among persons consuming a low-glycemic-index diet, and higher protein intake may have additional benefits.

The Diogenes study provides reassurance regarding three long-standing concerns about glycemic index: that measured values apply to individual foods only and have no relevance to mixed meals, that effects observed in clinical trials arise from confounding by macronutrients or fiber, and that the concepts are confusing and impractical for the general public. Indeed, the higher study-completion rate in the low-glycemic-index groups provides compelling evidence of the practicality of low-glycemic-index diets.

Several recent clinical trials have shown no significant difference in weight loss among various popular diets, leading to the notion that dietary composition is less important than adherence to a diet, whatever it might be. However, this conclusion does not consider the fundamental relationship between psychology and physiology. A person’s ability to maintain adherence over time may be influenced by the way in which a diet affects hunger and metabolism. Additional research is needed to clarify the mechanisms by which dietary composition regulates body weight and to devise novel strategies to effect behavioral changes.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

Source Information

From the Optimal Weight for Life Program, Department of Medicine, Children’s Hospital; and the Department of Pediatrics, Harvard Medical School — both in Boston.

References

References

  1. 1

    Dansinger ML, Tatsioni A, Wong JB, Chung M, Balk EM. Meta-analysis: the effect of dietary counseling for weight loss. Ann Intern Med 2007;147:41-50
    Web of Science | Medline

  2. 2

    Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995;332:621-628[Erratum, N Engl J Med 1995;333:399.]
    Full Text | Web of Science | Medline

  3. 3

    Jenkins DJ, Wolever TM, Taylor RH, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362-366
    Web of Science | Medline

  4. 4

    Brand-Miller JC, Thomas M, Swan V, Ahmed Z, Petocz P, Colagiuri S. Physiological validation of the concept of glycemic load in lean young adults. J Nutr 2003;133:2728-2732
    Web of Science | Medline

  5. 5

    Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA 2002;287:2414-2423
    CrossRef | Web of Science | Medline

  6. 6

    Pereira MA, Swain J, Goldfine AB, Rifai N, Ludwig DS. Effects of a low-glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss. JAMA 2004;292:2482-2490
    CrossRef | Web of Science | Medline

  7. 7

    Thomas DE, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load diets for overweight and obesity. Cochrane Database Syst Rev 2007;3:CD005105-CD005105
    Medline

  8. 8

    Larsen TM, Dalskov S-M, van Baak M, et al. Diets with high or low protein content and glycemic index for weight-loss maintenance. N Engl J Med 2010;363:2102-2113
    Full Text

  9. 9

    Astrup A. Dietary management of obesity. JPEN J Parenter Enteral Nutr 2008;32:575-577
    CrossRef | Web of Science | Medline

  10. 10

    Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 2009;360:859-873
    Full Text | Web of Science | Medline

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Memoirs of an Obese Physician

Tuesday, November 16, 2010 // Uncategorized

I’m not obese.  This isn’t about my essay.

 Since I exercise daily and watch my daughter at sporting events, I get sun exposure, more than I want.  Even with sunscreen, I get tanned.  Someone told me once that you should never trust a tan physician.    I countered with,”No, you should never trust a tan dermatologist or a fat cardiologist”.  It was a joke.  I came upon this essay in The Annals of Internal Medicine” today.

It will make me think twice before offering the last half of that advice again.

  • On Being a Doctor

Memoirs of an Obese Physician

  • Joseph F. Majdan, MD
  •  


    1. From Jefferson Medical College, Philadelphia, PA 19107.

    Because of society’s negative view of obesity, obese people continue to suffer indignities and prejudices even in this “politically correct” world. Physicians also harbor a similar prejudicial view of obese patients (1). As a medical student and now as an attending physician and as someone who has been obese for much of my life, I have had to face both simmering and overt prejudice from the profession I hold in the highest esteem. 

    I vividly recall that during medical school, a physician approached me as I stood with my tray in the cafeteria line. He said loudly for all to hear, “You know you should watch what you eat. Don’t you see yourself?” At morning report during my third-year medicine clerkship, there was too much light in the room for a slide presentation to be shown. A teaching attending yelled out, “Have Joe stand by the window; he can blot out the light.” At that moment, I wished my beeper would have gone off so I could have escaped from the laughter. During that same clerkship, our teaching attending regularly marched our whole team up 9 flights of steps on a humid summer day in Philadelphia because “one of you has to lose weight,” he said as he smirked at me. While putting on my scrubs during my surgery clerkship, an attending surgeon looked at me with disgust and sarcastically bellowed, “Hey, hey, hey, it’s Fat Albert!” As a result of these comments, I became increasingly self-conscious and with that ensued low self-esteem that persisted for years. I dieted and dieted again, a cycle that would continue to be part of my life in an attempt finally to become “normal” in the eyes of my profession. As a compulsive person, I was successful in losing weight, but as is the unfortunate fate of a large percentage of obese individuals (2), I always slowly regained it. 

    During my internal medicine residency, staff physicians would often—unilaterally and in the presence of colleagues and nurses—offer me their unsolicited opinions on how and why I should lose weight. I wondered why physicians would be so insensitive and callous. Some fellow residents asked me whether my lab coats were made by Omar the Tentmaker. I remember one call from a fellow classmate who was chief medical resident at another institution in Philadelphia; she asked to borrow my white intern trousers so that she could project slides onto them for a housestaff skit that she was organizing. She thought it “would be hilarious.” Instead of getting angry, I gave the excuse that I had thrown them away. To this day, I regret not telling her how unprofessional she was. My lack of self-esteem and feeling “second class” continued to haunt and to anger me. 

    I decided to pursue cardiology and started interviewing for a fellowship. At one interview at a university hospital in Philadelphia, the fellowship director eyed me up and down and curtly asked, “Do you have the stamina and health to survive a cardiac fellowship?” At another interview, a cardiologist told me to sit in another chair since “I don’t want to have to buy a new chair.” I learned quickly that the thinner the attending, the more disdain for my size. Yet, I sat there and accepted their behavior; I felt unworthy of respect. 

    I completed my cardiology fellowship and came on staff at the same university hospital. I quickly established myself as both a clinician and a teacher. I received 11 teaching awards from both students and residents, including the class portrait from the graduating class of 1986, the highest honor a faculty member can achieve at our institution. Even at this moment of achievement, however, a fellow attending took it upon himself to admonish me in the physician’s lounge by saying, “You look too fat in the portrait. You know, they should only paint portraits of those who have done something worthwhile for the university. How could you with your size?” As the portrait was unveiled, I wished I had been portrayed as thinner. 

    I continued my cycle of losing large amounts of weight by religiously following various diet programs: OPTIFAST, Medifast, Weight Watchers, Jenny Craig—you name the diet, I tried it. I was successful in shedding large amounts of weight, but each time it lasted only for a while. During these thinning cycles, fellow physicians and nurses would come up to me while I was getting my lunch and scan my tray, saying, “You don’t want to get as fat as you were, so I just wanted to make sure you were watching what you were eating.” Once I was even asked whether I had cancer. One patient told me of her request to her physician to be referred to me. The physician responded, “Why do you want to go to him? He’s fat.” She came to me nonetheless. Other physicians openly told my friends that they would never refer anyone to me because of my obesity. I felt I had to prove myself more than the “normal” physician. A surgeon stopped me on the floors and told me I needed gastric bypass surgery; another internist sat down next to me at a nurses’ station and openly guessed my weight, then pontificated on what my approach to weight loss should be. A fellow cardiologist stopped me on the street to tell me I looked “disgusting” and asked whether I “had no shame.” 

    This constant insensitive, unprofessional attitude of fellow colleagues who preached empathy to their students and residents and evaluated them for it caused me to see them as hypocritical. My low self-esteem rendered me silent to the comments, but it also made me angrier with myself for not defending myself. 

    Sometimes we have to teach others how to treat us. Physician attitudes toward obese patients have been shown to be negative, and they tend to stereotype their obese patients as being lazy (3). Another study found that physicians view obese patients as ugly, weak-willed, sloppy, and lazy (1). One editorial stated that attending physicians develop growing cynicism toward obese patients about convincing them to lose weight, because the physicians feel that their preaching goes unheeded (4). It is interesting, though, that physicians do not hold the same cynicism and negative views toward patients with diseases that are similarly resistant to therapy. When has a physician blamed the patient when cancer recurs? 

    An understanding of the causes of obesity, as well as effective treatment, remains to be discovered (5); more research is urgently needed in this area. Starting in medical school, obesity should be addressed and approached with a true understanding of the difficulties the condition presents, as well as treatment options. Professionalism and sensitivity toward obese patients must start with physicians. Equally important, attending physicians should be brought before professionalism committees for callous treatment of both their obese colleagues and patients. The obese patient demands the respect and understanding that all of us deserve. 

     

    Joseph F. Majdan, MD 

    Jefferson Medical College 

    Philadelphia, PA 19107 

    Article and Author Information

    • Requests for Single Reprints: Joseph F. Majdan, MD, Jefferson Medical College, 1001 Locust Street, Suite 409B, Philadelphia, PA 19107. 

    Previous Section  

    References

    1. 1.↵
    2. Foster GD,
    3. Wadden TA,
    4. Makris AP,
    5. Davidson D,
    6. Sanderson RS,
    7. Allison DB

    et al.Primary care physicians’ attitudes about obesity and its treatment.Obes Res200311116877pmid:14569041

    Foster GD, Wadden TA, Makris AP, Davidson D, Sanderson RS, Allison DB, et al. Primary care physicians’ attitudes about obesity and its treatment. Obes Res. 2003;11:1168-77. [PMID: 14569041]

    MedlineWeb of Science

  • 2.↵
    The management of obesityN Y State J Med1958587987pmid:13493797

    The management of obesity. N Y State J Med. 1958:58:79-87. [PMID: 13493797]

    Medline

  • 3.↵
  • Warner CH,
  • Warner CM,
  • Morganstein J,
  • Appenzeller GN,
  • Rachal J,
  • Grieger T
  • Military family physician attitudes toward treating obesity.Mil Med200817397884pmid:19160616

    Warner CH, Warner CM, Morganstein J, Appenzeller GN, Rachal J, Grieger T. Military family physician attitudes toward treating obesity. Mil Med. 2008;173:978-84. [PMID: 19160616]

    Medline

  • 4.↵
  • Alpert JS
  • “So, doctor, what’s so bad about being fat?” Combating the obesity epidemic in the United States [Editorial].Am J Med201012312pmid:20102980Alpert JS. “So, doctor, what’s so bad about being fat?” Combating the obesity epidemic in the United States [Editorial]. Am J Med. 2010;123:1-2. [PMID: 20102980]Medline

  • 5.↵
  • Yanovski SZ
  • Are anorectic agents the ‘magic bullet’ for obesity? [Editorial].Arch Fam Med1993210257pmid:8111481Yanovski SZ. Are anorectic agents the ‘magic bullet’ for obesity? [Editorial]. Arch Fam Med. 1993;2:1025-7. [PMID: 8111481]Abstract/FREE Full Text

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    Supplements Take More Hits

    Wednesday, November 10, 2010 // Uncategorized

    Health does not come in a pill.

    There is no evidence that taking dietary supplements is of benefit.  Some people think that it can’t hurt, but maybe it can.  Here  are some new alerts from Journal Watch.  

    FYI:  There are different types of stroke.  The embolic type usually are blood clots which originate in the heart.  Thrombotic strokes are the most common type.  This is where a blood clot forms in an artery.  Hemorrhagic strokes are when a blood vessel ruptures and bleeds.

    Association Found Between Vitamin E Supplements and Hemorrhagic Stroke
    Vitamin E supplements have no effect on overall stroke incidence, but when stroke type is examined, the supplements significantly increase risk for hemorrhagic stroke, according to a BMJ meta-analysis.
    Researchers examined data from nine trials encompassing some 120,000 subjects who’d been randomized to receive vitamin E or placebo and were followed for more than 1 year. Rates of stroke overall did not differ between groups. However, when the type of stroke was examined, ischemic strokes were significantly fewer among the vitamin recipients, while hemorrhagic strokes were significantly increased — by some 20%.
    The authors say that the contrasting effects have tended to obscure vitamin E’s hemorrhagic risks. They write that the mechanism behind the effect is unknown and that it may stem from vitamin E’s interference with a vitamin-K-dependent clotting factor. They conclude that “indiscriminate widespread use of vitamin E should be cautioned against.”

    If Vitamin E is prescribed by an ophthalmologist for macular degeneration that is a different story from someone who is taking Vitamin E for general health reasons.

    {omega}-3 Fatty Acids and Prevention of Dementia

    No evidence of benefit was noted in a 24-month trial.  

    Among many proposed interventions to lower risk for or severity of dementia is supplementation with {omega}-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are commonly found in oily fish. 

    U.K. investigators enrolled 867 patients (age range, 70–79) from general practices; none had diabetes, and all had normal cognition (Mini-Mental State Examination scores ≥24). Participants were randomized to daily supplementation with EPA (200 mg) plus DHA (500 mg) or to olive oil placebo. The EPA and DHA dosages were based on U.K. dietary recommendations for fish consumption. The withdrawal and death rates were similar in the two groups — roughly 14% total. 

    At 24 months’ follow-up, no differences were found between the two groups in a validated assessment of cognitive function based on verbal memory or in secondary outcomes related to global cognitive function, memory, or executive function. Adverse events were minor and similar in both groups, with a small incremental risk for flatulence, loose stools, and belching in the treated group. 

    Comment: This randomized controlled trial is reportedly the longest and largest to evaluate {omega}-3 fatty acid supplementation for prevention of dementia. The negative results are consistent with the conclusions of a recent Institute of Medicine report that showed no clear support for any interventions that are purported to prevent dementia. 

    Thomas L. Schwenk, MD 

    Published in Journal Watch General Medicine May 11, 2010 

    Citation(s):

    Dangour AD et al. Effect of 2-y n–3 long-chain polyunsaturated fatty acid supplementation on cognitive function in older people: A randomized, double-blind, controlled trial. Am J Clin Nutr 2010 Apr 21; [e-pub ahead of print]. (http://dx.doi.org/10.3945/ajcn.2009.29121) Now this last article doesn’t deal with taking supplements, but with the most trndy of vitamins, Vitamin D.  Is taking Vitamin D good?  Does checking Vitamin D levels influence survival?  Bottom line:  We don’t know.

    Does Vitamin D Status Affect Mortality?

    No association between vitamin D status and mortality at 7 years was found.  

    These days, many clinicians are checking vitamin D levels routinely. Patients with the lowest levels clearly are at risk for metabolic bone disease, which can be prevented with vitamin D supplementation. Another premise is that screening and supplementation will prevent a variety of disorders involving other organ systems. However, randomized trials in which researchers are examining the effect of vitamin D supplementation on mortality have not yet been completed, and not every observational study has demonstrated an association between vitamin D status and mortality. 

    In this U.S. study, 1500 relatively healthy community-dwelling men (age, ≥65) were randomly selected from participants in the prospective Osteoporotic Fractures in Men study (Contemp Clin Trials 2005; 26:569). At baseline, 25-hydroxyvitamin D levels were <20 ng/mL in 25% of men, and between 20 and 30 ng/mL in 50% of men. During an average follow-up of 7 years, 22% of participants died. In both unadjusted analyses and in analyses adjusted for potentially confounding variables, no significant associations were observed between vitamin D levels (across quartiles) and all-cause, cancer-related, or cardiovascular mortality. 

    Comment: This study reminds us that our understanding of the relation between vitamin D status and various sources of morbidity or mortality is far from complete. Whether screening and supplementation will save lives, prevent cancer, or prevent cardiovascular disease is unknown. 

    Allan S. Brett, MD 

    Published in Journal Watch General Medicine October 26, 2010 

    Citation(s):

    Cawthon PM et al. Serum 25-hydroxyvitamin D, parathyroid hormone, and mortality in older men. J Clin Endocrinol Metab 2010 Oct; 95:4625. (http://dx.doi.org/10.1210/jc.2010-0638

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