Back in 2005, Jeff Friedman, who discovered the hormone leptin, appeared in conversation with NPR's Ira Flatow as part of a lecture series presented by Rockefeller University, where he heads their Laboratory of Molecular Genetics. The presentation was entitled "A War on Obesity, Not the Obese." A .pdf file of the transcript can be downloaded here. It's pretty long (26 pages), but I think Friedman does an excellent job explaining what we know about the science of obesity and the ethical implications of the "war on obesity."
"I think that to the extent that increased weight has health
consequences, people should do their best. It certainly is a good thing
to be fit. And it is a good thing to eat a heart healthy diet. And it’s
probably a good thing to make one’s best efforts to keep one’s weight
under control. So that means not doing much different than what
Hippocrates would have recommended. But I think at the same time we
have to recognize that those measures are rather limited in their
efficacy and that to make the leap therefore that people who are not
successful at keeping their weight off are at fault is just wrong
headed."
I don't agree with absolutely everything Friedman says in the interview, but we're definitely on the same page with the quote above.
Friday, February 22, 2008
Thursday, February 21, 2008
How bad are artificial sweeteners?
The Calorie Control Council is having a bad month. The group, which represents "the low-calorie and reduced-fat food and beverage industry" has got to be hurting after a couple of high-profile studies getting media coverage in the last month cast doubt on the healthfulness of some of these products.
The first of these studies, by Lutsey et al. (1) showed that higher consumption of diet soda was associated with an increased risk of metabolic syndrome. What is metabolic syndrome? It's when you have three or more of the following: waist circumference >102 cm in men or >88 cm for women; triglycerides >150 mg/dl, HDL cholesterol <>130 mm Hg, diastolic blood pressure >85 mm Hg or use of antihypertensive medication; and fasting glucose > 100 mg/dl or treatment for elevated glucose. These things are of concern because they confer a heightened risk for heart disease and type II diabetes.
What these authors did was looked at a group of people who didn't have Metabolic Syndrome and gave them a long quiz about how much they consumed of 66 different foods and beverages. Then they looked for associations between people eating more or less of certain foods and whether they had developed Metabolic Syndrome after 9 years of followup. I will refer to Metabolic Syndrome as "MetSyn" for the rest of this blog post because I am a bit of a lazy typist.
The authors found that a "Western dietary pattern" and high consumption of meat (especially hamburgers and hot dogs), fried foods, and, surprisingly diet soda were associated with increased rates of MetSyn, and high consumption of dairy was associated with a lower risk. The authors were also surprised that they didn't see any association of MetSyn risk with whole grain or fruit and vegetable intake. They say the dairy (2-4) and diet soda (5) findings were also found in previously published studies by other groups. They controlled for age, race, sex, education, total caloric intake, baseline overweight, smoking, exercise, and what seem to me to be all the other obvious possible cofactors.
So what can we say about the health risks of diet soda? This is an epidemiologic study, so it just establishes an association, not a causal relationship or a mechanism. It may be that some component of diet soda has a biological effect on people who drink it that makes them more prone to MetSyn. Or it could be that some other behavior or genetic variant that predisposes people to drink more diet soda also predisposes them towards MetSyn. At any rate, it's quite a strong association. The authors of this study found that people who drank the most diet soda had a 34% higher risk of developing metabolic syndrome than people who drank the least. They say that data from the Framingham Heart study showed that drinking 1 or more diet sodas a day increases your risk of metabolic syndrome by 56% (5). They didn't see any association with sweetened beverages.
These data seem pretty striking, although it is notable that a lot of things you might expect to be associated with Metabolic Syndrome risk weren't, according to their study (like fruits and vegetables and whole grains, which are supposed to be protective against obesity). As the authors say, "[a]dditional research on the relation between diet soda and incident MetSyn is clearly warranted."
The second study is not yet published but is slated to appear in next month's issue of Behavioral Neuroscience. In this study, they divided male rats into two groups: one group was fed yogurt sweetened with glucose (sugar) in addition to their normal chow, and the other was fed yogurt sweetened with saccharin along with chow. They apparently found that the rats in the saccharin group ate more calories, gained more weight and body fat, and had a decreased metabolic response to food, indicating that saccharin somehow predisposes rats (and possibly their human cousins) to weight gain.
While there are still a lot of unanswered questions resulting from these studies (particularly from the latter one, which has still not even been published, meaning that what we know about it comes from a press release), I know that this news made me think twice about my own Diet Coke habit. But are artificial sweeteners to blame for the increased risk of MS with diet soda consumption? Are all artificial sweeteners alike? Do humans and rats respond the same way to artificial sweeteners, particularly given that humans have access to a much more varied diet than lab rats?
For now, I've cut way back on the Diet Coke...it's more expensive than water or tea anyway and there's no reason why I need to drink it.
1. Lutsey PL, Steffen LM, Stevens J. Dietary Intake and the Development of the Metabolic Syndrome. The Atherosclerosis Risk in Communities Study. Circulation e-pub ahead of print, January 22, 2008.
2. Azadbakht L, Mirmiran P, Esmillzadeh A, Azizi F. Dairy consumption is inversely associated with the prevalence of the metabolic syndrome in Tehranian adults. American Journal of Clinical Nutrition 82:523-530, 2005.
3. Mennen LI, Lafay L, Feskens EJM, Novak M, Lepinay P, Balkau B. Possible protective effect of bread and dairy products on the risk of metabolic syndrome. Nutrition Research 20: 335-347, 2000.
4. Pereira MA, Jacobs DR Jr., Van Horn L, Slattery ML, Kartashov AI, Ludwig DS. Dairy consumption, obesity, and the insulin resistance syndrom in young adults: the CARDIA Study. Journal of the American Medical Association 287: 2081-2089, 2002.
5. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, D'Agostino RB, Gaziano JM, Vasan RS. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation 116: 480-488, 2007.
The first of these studies, by Lutsey et al. (1) showed that higher consumption of diet soda was associated with an increased risk of metabolic syndrome. What is metabolic syndrome? It's when you have three or more of the following: waist circumference >102 cm in men or >88 cm for women; triglycerides >150 mg/dl, HDL cholesterol <>130 mm Hg, diastolic blood pressure >85 mm Hg or use of antihypertensive medication; and fasting glucose > 100 mg/dl or treatment for elevated glucose. These things are of concern because they confer a heightened risk for heart disease and type II diabetes.
What these authors did was looked at a group of people who didn't have Metabolic Syndrome and gave them a long quiz about how much they consumed of 66 different foods and beverages. Then they looked for associations between people eating more or less of certain foods and whether they had developed Metabolic Syndrome after 9 years of followup. I will refer to Metabolic Syndrome as "MetSyn" for the rest of this blog post because I am a bit of a lazy typist.
The authors found that a "Western dietary pattern" and high consumption of meat (especially hamburgers and hot dogs), fried foods, and, surprisingly diet soda were associated with increased rates of MetSyn, and high consumption of dairy was associated with a lower risk. The authors were also surprised that they didn't see any association of MetSyn risk with whole grain or fruit and vegetable intake. They say the dairy (2-4) and diet soda (5) findings were also found in previously published studies by other groups. They controlled for age, race, sex, education, total caloric intake, baseline overweight, smoking, exercise, and what seem to me to be all the other obvious possible cofactors.
So what can we say about the health risks of diet soda? This is an epidemiologic study, so it just establishes an association, not a causal relationship or a mechanism. It may be that some component of diet soda has a biological effect on people who drink it that makes them more prone to MetSyn. Or it could be that some other behavior or genetic variant that predisposes people to drink more diet soda also predisposes them towards MetSyn. At any rate, it's quite a strong association. The authors of this study found that people who drank the most diet soda had a 34% higher risk of developing metabolic syndrome than people who drank the least. They say that data from the Framingham Heart study showed that drinking 1 or more diet sodas a day increases your risk of metabolic syndrome by 56% (5). They didn't see any association with sweetened beverages.
These data seem pretty striking, although it is notable that a lot of things you might expect to be associated with Metabolic Syndrome risk weren't, according to their study (like fruits and vegetables and whole grains, which are supposed to be protective against obesity). As the authors say, "[a]dditional research on the relation between diet soda and incident MetSyn is clearly warranted."
The second study is not yet published but is slated to appear in next month's issue of Behavioral Neuroscience. In this study, they divided male rats into two groups: one group was fed yogurt sweetened with glucose (sugar) in addition to their normal chow, and the other was fed yogurt sweetened with saccharin along with chow. They apparently found that the rats in the saccharin group ate more calories, gained more weight and body fat, and had a decreased metabolic response to food, indicating that saccharin somehow predisposes rats (and possibly their human cousins) to weight gain.
While there are still a lot of unanswered questions resulting from these studies (particularly from the latter one, which has still not even been published, meaning that what we know about it comes from a press release), I know that this news made me think twice about my own Diet Coke habit. But are artificial sweeteners to blame for the increased risk of MS with diet soda consumption? Are all artificial sweeteners alike? Do humans and rats respond the same way to artificial sweeteners, particularly given that humans have access to a much more varied diet than lab rats?
For now, I've cut way back on the Diet Coke...it's more expensive than water or tea anyway and there's no reason why I need to drink it.
1. Lutsey PL, Steffen LM, Stevens J. Dietary Intake and the Development of the Metabolic Syndrome. The Atherosclerosis Risk in Communities Study. Circulation e-pub ahead of print, January 22, 2008.
2. Azadbakht L, Mirmiran P, Esmillzadeh A, Azizi F. Dairy consumption is inversely associated with the prevalence of the metabolic syndrome in Tehranian adults. American Journal of Clinical Nutrition 82:523-530, 2005.
3. Mennen LI, Lafay L, Feskens EJM, Novak M, Lepinay P, Balkau B. Possible protective effect of bread and dairy products on the risk of metabolic syndrome. Nutrition Research 20: 335-347, 2000.
4. Pereira MA, Jacobs DR Jr., Van Horn L, Slattery ML, Kartashov AI, Ludwig DS. Dairy consumption, obesity, and the insulin resistance syndrom in young adults: the CARDIA Study. Journal of the American Medical Association 287: 2081-2089, 2002.
5. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, D'Agostino RB, Gaziano JM, Vasan RS. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation 116: 480-488, 2007.
Should I believe this study?
This post is largely cannibalized from something I posted on a message board, but I think it fits well here, too.
When you read about scientific studies in the newspaper, it can be hard to assess their merit. Here are a few questions to keep in mind for critical reading of science 101:
1. Where was the study published? Was it in a peer-reviewed journal, or was it just presented at a conference? (Findings presented at conferences are not subjected to peer review). In the biological sciences, journals like Science, Nature, and Cell are considered "top-tier." Medical journals, like JAMA, The Lancet, and The New England Journal of Medicine, are considered slightly more suspect, but still respectable. If you don't know the journals, it can be hard to judge, but if it sounds obscure, it probably is. One caveat to this method is that big-name people can sometimes get shitty papers into good journals on the strength of their reputations.
2. Who sponsored the study? Peer-reviewed journals require authors to disclose who financed the research, so this is easier to find out than a lot of people think. Any time a drug company publishes a study showing that its new drug cures cancer, baldness and ennui, I would reserve judgement until the results are verified by an outside party.
3. Are the results of the paper supported by other work in the field pointing in the same direction? That information is usually found in the Introduction section of the paper, where researchers discuss the foundation for the work to be presented. This is particularly important for anything you read about in the mainstream media, as they tend to have a "sensationalism bias" in what gets reported, i.e. if a study's results are unexpected, it's more likely to make the papers.
4. Did the authors draw the appropriate conclusions from the data presented? Does their explanation make sense? Does it account for all of their findings? Is there an alternative explanation, and if so, do they consider it in the Discussion section of the paper? Interpretation of the findings is the most subjective aspect of a scientific paper, but it's also the thing people are most likely to take away from reading it.
When you read about scientific studies in the newspaper, it can be hard to assess their merit. Here are a few questions to keep in mind for critical reading of science 101:
1. Where was the study published? Was it in a peer-reviewed journal, or was it just presented at a conference? (Findings presented at conferences are not subjected to peer review). In the biological sciences, journals like Science, Nature, and Cell are considered "top-tier." Medical journals, like JAMA, The Lancet, and The New England Journal of Medicine, are considered slightly more suspect, but still respectable. If you don't know the journals, it can be hard to judge, but if it sounds obscure, it probably is. One caveat to this method is that big-name people can sometimes get shitty papers into good journals on the strength of their reputations.
2. Who sponsored the study? Peer-reviewed journals require authors to disclose who financed the research, so this is easier to find out than a lot of people think. Any time a drug company publishes a study showing that its new drug cures cancer, baldness and ennui, I would reserve judgement until the results are verified by an outside party.
3. Are the results of the paper supported by other work in the field pointing in the same direction? That information is usually found in the Introduction section of the paper, where researchers discuss the foundation for the work to be presented. This is particularly important for anything you read about in the mainstream media, as they tend to have a "sensationalism bias" in what gets reported, i.e. if a study's results are unexpected, it's more likely to make the papers.
4. Did the authors draw the appropriate conclusions from the data presented? Does their explanation make sense? Does it account for all of their findings? Is there an alternative explanation, and if so, do they consider it in the Discussion section of the paper? Interpretation of the findings is the most subjective aspect of a scientific paper, but it's also the thing people are most likely to take away from reading it.
Conventional Wisdom: Yo-Yo Dieting Slows Your Metabolism
We've all heard that repeated cycles of dieting and weight regain can result in a permanent lowering of the metabolism and a "rebound effect," where dieters end up weighing more than ever. But is there a scientific basis for this claim?
Most people who try to lose weight encounter plateaus as a result of a metabolic slowdown. This phenomenon has been well characterized in scientific studies (1-4). Leibel et al. (4) conducted a particularly convincing study in which 18 obese and 23 never-obese subjects were admitted to the hospital so their food intake and activity could be strictly controlled. These subjects were then over- or under-fed until they had reached a 10% increase or decrease in their body weight. In both the obese and never-obese groups, a 10% increase in body weight resulted in a 16% increase in energy expenditure. Correspondingly, the 10% weight loss groups decreased their energy expenditure by 15%. The authors' interpretation of this study was that these changes in energy expenditure represent an attempt by the body to return to its "setpoint" weight.
So, changes in body weight do seem to result in changes in energy expenditure. But do repeated changes in body weight permanently affect your metabolism?
A number of researchers set out to answer this question using animal studies in the 1980s and 1990s. Ernsberger et al. (5) looked at rats with a specific genetic mutation making them prone to obesity and mimicked yo-yo dieting by putting half of the rats through a process of "weight cycling." The weight cycled rats were fed ad lib for 4-6 weeks, and then switched to a very low calorie diet (16.7% of baseline calories) for 12 days. This cycling of ad lib and restricted feeding was done three times. The researchers found that the cycled rats had a higher final body weight than controls which were fed ad lib throughout the study. They also found that the cycled rats lost slightly less weight each successive time they were put on the very low calorie diet. Similarly, Lim et al. (6) found that weight cycled rats had a lower resting metabolic rate than rats that were consistently food restricted (both groups were restricted to 70% of the food control rats ate), but that exercise on a treadmill eliminated that difference. These studies seemed to validate the hypothesis that yo-yo dieting had lasting effects on metabolism. However, Lu et al. (7) found that weight cycling of rats facilitated the development of insulin resistance, but didn't have any effect on body weight.
In humans, the story appears to be somewhat more consistent. While one paper (8) found that adolescent male wrestlers who engaged in yo-yo dieting had lower energy expenditure than those that didn't, subsequent studies of humans have repeatedly failed to see any permanent effects of yo-yo dieting on weight or metabolism in either obese or lean individuals (9-16).
So why the differing results in the human and animal studies? I can think of a few possible explanations. One possibility is that humans and rats may simply differ physiologically with respect to the effects of repeated weight cycling. Another possibility is that since the rat studies tended to involve a greater degree of restriction, there may be effects of weight cycling that don't kick in until the person or animal is in a severely hypocaloric state. This might also explain why the one human paper that did show an effect of yo-yo dieting was in adolescent male wrestlers...adolescent males have tremendous caloric needs so severe dieting may have more of an impact on this group. A third possibility is that rats exposed to involuntary food restriction with no knowledge of when their food access will return to normal may differ physiologically from people who voluntarily restrict their food intake, knowing that food is available to them if they need it.
The upshot is that while weight loss can decrease your metabolic rate, this change appears to be reversible with a return to "normal" weight.
1. Ravussin E, Burnand B, Schutz Y, Jéquier E. Energy expenditure before and during energy restriction in obese patients. The American Journal of Clinical Nutrition 41(4): 753-759, 1985.
2. Weigle DS, Sande KJ, Iverius PH, Monsen ER, Brunzell, JD. Weight loss leads to a marked decrease in nonresting energy expenditure in ambulatory human subjects. Metabolism 37(10): 930-936, 1988.
3. Keesey RE, Hirvonen MD. Body weight set-points: determination and adjustment. The Journal of Nutrition 127(9): 1875S-1883S, 1997.
4. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. The New England Journal of Medicine 332(10): 621-628, 1995.
5. Ernsberger P, Koletsky RJ, Baskin JS, Collins LA. Consquences of weight cycling in obese spontaneously hyperactive rats. American Journal of Physiology--Regulatory, Integrative and Comparative Physiology 270(4): R864-R872, 1996.
6. Lim K, Murakami E, Lee S, Shimomura Y, Suzuki M. Effects of intermittent food restriction and refeeding on energy efficiency and body fat deposition in sedentary and exercised rats. Journal of Nutritional Science and vitaminology 42(5): 449-468, 1996.
7. Lu H, Buison A, Uhley V, Jen KL. Long-term weight cycling in female Wistar rats: effects on metabolism. Obesity Research 3(6): 521-530, 1995.
8. Steen SN, Oppliger RA, Brownell KD. Metabolic effects of repeated weight loss and regain in adolescent wrestlers. Journal of the American Medical Association 260(1): 47-50, 1988.
9. Jebb SA, Goldberg GR, Coward WA, Murgatroyd PR, Prentice AM. Effects of weight cycling caused by intermittent dieting on metabolic rate and body composition in obese women. International Journal of Obesity 15(5): 367-374, 1991.
10. Nitzke SA, Voichick SJ, Olson D. Weight Cycling Practices and Long-term Health Conditions in a Sample of Former Wrestlers and Other Collegiate Athletes. Journal of Ath
11. Wadden TA, Bartlett S, Letizia KA, Foster GD, Stunkard AJ, Conill A. Relationship of dieting history to resting metabolic rate, behavior, and subsequent weight loss. American Journal of Clinical Nutrition 56: 203S-208S, 1992.
12. McCargar L, Taunton J, Birmingham CL, Paré S, Simmons D. Metabolic and anthropometric changes in female weight cyclers and controls over a 1-year period. Journal of the American Dietetic Association 93(9): 1025-1030, 1993.
13. Brownell KD, Rodin J. Medical, metabolic, and psychological effects of weight cycling. Archives of Internal Medicine 154(12): 1325-1330, 1994.
14. Muls E, Kempen K, Vansant G, Saris W. Is weight cycling detrimental to health? A review of the literature in humans. International Journal of Obesity and Related Metabolic Disorders 19(Suppl ): S46-S50, 1995.
15. Platte P, Wurmser H, Wade SE, Mercheril A, Pirke KM. Resting metabolic rate and diet-induced thermogenesis in restrained and unrestrained eaters. International Journal of Eating Disorders 20(1): 33-41, 1996.
16. Li Z, Wong E, Maxwell M, Heber D. Weight cycling in a very low-calorie diet programme has no effect on weight loss velocity, blood pressure and serum lipid profile. Diabetes, Obesity and Metabolism 9(3): 379-385, 2007.
Most people who try to lose weight encounter plateaus as a result of a metabolic slowdown. This phenomenon has been well characterized in scientific studies (1-4). Leibel et al. (4) conducted a particularly convincing study in which 18 obese and 23 never-obese subjects were admitted to the hospital so their food intake and activity could be strictly controlled. These subjects were then over- or under-fed until they had reached a 10% increase or decrease in their body weight. In both the obese and never-obese groups, a 10% increase in body weight resulted in a 16% increase in energy expenditure. Correspondingly, the 10% weight loss groups decreased their energy expenditure by 15%. The authors' interpretation of this study was that these changes in energy expenditure represent an attempt by the body to return to its "setpoint" weight.
So, changes in body weight do seem to result in changes in energy expenditure. But do repeated changes in body weight permanently affect your metabolism?
A number of researchers set out to answer this question using animal studies in the 1980s and 1990s. Ernsberger et al. (5) looked at rats with a specific genetic mutation making them prone to obesity and mimicked yo-yo dieting by putting half of the rats through a process of "weight cycling." The weight cycled rats were fed ad lib for 4-6 weeks, and then switched to a very low calorie diet (16.7% of baseline calories) for 12 days. This cycling of ad lib and restricted feeding was done three times. The researchers found that the cycled rats had a higher final body weight than controls which were fed ad lib throughout the study. They also found that the cycled rats lost slightly less weight each successive time they were put on the very low calorie diet. Similarly, Lim et al. (6) found that weight cycled rats had a lower resting metabolic rate than rats that were consistently food restricted (both groups were restricted to 70% of the food control rats ate), but that exercise on a treadmill eliminated that difference. These studies seemed to validate the hypothesis that yo-yo dieting had lasting effects on metabolism. However, Lu et al. (7) found that weight cycling of rats facilitated the development of insulin resistance, but didn't have any effect on body weight.
In humans, the story appears to be somewhat more consistent. While one paper (8) found that adolescent male wrestlers who engaged in yo-yo dieting had lower energy expenditure than those that didn't, subsequent studies of humans have repeatedly failed to see any permanent effects of yo-yo dieting on weight or metabolism in either obese or lean individuals (9-16).
So why the differing results in the human and animal studies? I can think of a few possible explanations. One possibility is that humans and rats may simply differ physiologically with respect to the effects of repeated weight cycling. Another possibility is that since the rat studies tended to involve a greater degree of restriction, there may be effects of weight cycling that don't kick in until the person or animal is in a severely hypocaloric state. This might also explain why the one human paper that did show an effect of yo-yo dieting was in adolescent male wrestlers...adolescent males have tremendous caloric needs so severe dieting may have more of an impact on this group. A third possibility is that rats exposed to involuntary food restriction with no knowledge of when their food access will return to normal may differ physiologically from people who voluntarily restrict their food intake, knowing that food is available to them if they need it.
The upshot is that while weight loss can decrease your metabolic rate, this change appears to be reversible with a return to "normal" weight.
1. Ravussin E, Burnand B, Schutz Y, Jéquier E. Energy expenditure before and during energy restriction in obese patients. The American Journal of Clinical Nutrition 41(4): 753-759, 1985.
2. Weigle DS, Sande KJ, Iverius PH, Monsen ER, Brunzell, JD. Weight loss leads to a marked decrease in nonresting energy expenditure in ambulatory human subjects. Metabolism 37(10): 930-936, 1988.
3. Keesey RE, Hirvonen MD. Body weight set-points: determination and adjustment. The Journal of Nutrition 127(9): 1875S-1883S, 1997.
4. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. The New England Journal of Medicine 332(10): 621-628, 1995.
5. Ernsberger P, Koletsky RJ, Baskin JS, Collins LA. Consquences of weight cycling in obese spontaneously hyperactive rats. American Journal of Physiology--Regulatory, Integrative and Comparative Physiology 270(4): R864-R872, 1996.
6. Lim K, Murakami E, Lee S, Shimomura Y, Suzuki M. Effects of intermittent food restriction and refeeding on energy efficiency and body fat deposition in sedentary and exercised rats. Journal of Nutritional Science and vitaminology 42(5): 449-468, 1996.
7. Lu H, Buison A, Uhley V, Jen KL. Long-term weight cycling in female Wistar rats: effects on metabolism. Obesity Research 3(6): 521-530, 1995.
8. Steen SN, Oppliger RA, Brownell KD. Metabolic effects of repeated weight loss and regain in adolescent wrestlers. Journal of the American Medical Association 260(1): 47-50, 1988.
9. Jebb SA, Goldberg GR, Coward WA, Murgatroyd PR, Prentice AM. Effects of weight cycling caused by intermittent dieting on metabolic rate and body composition in obese women. International Journal of Obesity 15(5): 367-374, 1991.
10. Nitzke SA, Voichick SJ, Olson D. Weight Cycling Practices and Long-term Health Conditions in a Sample of Former Wrestlers and Other Collegiate Athletes. Journal of Ath
11. Wadden TA, Bartlett S, Letizia KA, Foster GD, Stunkard AJ, Conill A. Relationship of dieting history to resting metabolic rate, behavior, and subsequent weight loss. American Journal of Clinical Nutrition 56: 203S-208S, 1992.
12. McCargar L, Taunton J, Birmingham CL, Paré S, Simmons D. Metabolic and anthropometric changes in female weight cyclers and controls over a 1-year period. Journal of the American Dietetic Association 93(9): 1025-1030, 1993.
13. Brownell KD, Rodin J. Medical, metabolic, and psychological effects of weight cycling. Archives of Internal Medicine 154(12): 1325-1330, 1994.
14. Muls E, Kempen K, Vansant G, Saris W. Is weight cycling detrimental to health? A review of the literature in humans. International Journal of Obesity and Related Metabolic Disorders 19(Suppl ): S46-S50, 1995.
15. Platte P, Wurmser H, Wade SE, Mercheril A, Pirke KM. Resting metabolic rate and diet-induced thermogenesis in restrained and unrestrained eaters. International Journal of Eating Disorders 20(1): 33-41, 1996.
16. Li Z, Wong E, Maxwell M, Heber D. Weight cycling in a very low-calorie diet programme has no effect on weight loss velocity, blood pressure and serum lipid profile. Diabetes, Obesity and Metabolism 9(3): 379-385, 2007.
Introduction
Who am I? I'm a 35-year-old postdoctoral fellow working at an academic diabetes research center. I've spent the last 12 years working in labs studying various aspects of the biology of obesity and type II diabetes.
What is this blog all about? Everybody knows that what we eat is one of the most important determinants of our overall health. But navigating the tremendous amount of diet and fitness advice we have available to us can be overwhelming. The goal of this blog is to try to give people an impartial assessment of current scientific findings on food, fitness, obesity, and type II diabetes as well as to look at the scientific basis for the "conventional wisdom" on these topics. I will always provide full citations for any scientific papers discussed here, and I strongly encourage readers to seek out these papers for themselves (most state-funded medical schools have libraries of scientific journals that are available to the general public) and post your own interpretations in the comments.
I will not accept any advertising on this blog, and you won't see any links to industry advocacy groups. Unfortunately, special interests in the food and diet industries have played far too big a role in the dissemination of information about health and fitness, and I hope this blog will be one small step against that. Everyone has biases, including me, but I will be doing everything I can to minimize the extent to which mine can be said to be financial. One negative consequence of my lack of financial interest in this blog, though, is that I can't promise how regularly I will be able to update it. I'm hoping to shoot for once a week.
Why am I doing this? I really enjoy talking about what I do and sharing the major findings in my field with people. Scientists in general have a somewhat isolated existence...we spend all day in research labs, we tend to speak in a language that most people can't understand, and we communicate our findings through journals that are read pretty much only by other scientists (save for the tiny percentage of papers whose existence is picked up on by science journalists). As a consequence, even many physicians are not aware of current developments in biology. We all have bodies and we all want to do what we can to keep them healthy. Unfortunately, with so many conflicting sources of information out there, this is not always an easy task. Science doesn't have all the answers, but it can help us navigate through the messages that are presented to us. And my hope is that I can facilitate that navigation.
What is this blog all about? Everybody knows that what we eat is one of the most important determinants of our overall health. But navigating the tremendous amount of diet and fitness advice we have available to us can be overwhelming. The goal of this blog is to try to give people an impartial assessment of current scientific findings on food, fitness, obesity, and type II diabetes as well as to look at the scientific basis for the "conventional wisdom" on these topics. I will always provide full citations for any scientific papers discussed here, and I strongly encourage readers to seek out these papers for themselves (most state-funded medical schools have libraries of scientific journals that are available to the general public) and post your own interpretations in the comments.
I will not accept any advertising on this blog, and you won't see any links to industry advocacy groups. Unfortunately, special interests in the food and diet industries have played far too big a role in the dissemination of information about health and fitness, and I hope this blog will be one small step against that. Everyone has biases, including me, but I will be doing everything I can to minimize the extent to which mine can be said to be financial. One negative consequence of my lack of financial interest in this blog, though, is that I can't promise how regularly I will be able to update it. I'm hoping to shoot for once a week.
Why am I doing this? I really enjoy talking about what I do and sharing the major findings in my field with people. Scientists in general have a somewhat isolated existence...we spend all day in research labs, we tend to speak in a language that most people can't understand, and we communicate our findings through journals that are read pretty much only by other scientists (save for the tiny percentage of papers whose existence is picked up on by science journalists). As a consequence, even many physicians are not aware of current developments in biology. We all have bodies and we all want to do what we can to keep them healthy. Unfortunately, with so many conflicting sources of information out there, this is not always an easy task. Science doesn't have all the answers, but it can help us navigate through the messages that are presented to us. And my hope is that I can facilitate that navigation.
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