Monday, May 12, 2008

Whither BMI?

Body Mass Index is a much-maligned measure of fatness, yet it remains the standard measure of weight-related health risk among the medical and scientific community. In this post, I'm going to try to explain why this is the case.

Before BMI standards were widely adopted in the 1980s, fatness was largely determined by height/weight charts. Those early BMI standards considered men with a BMI >=27.8 and women with a BMI >=27.3 to be "overweight." Then in 1998, the National Institutes of Health lowered their BMI cutoffs to match the World Health Organization standards. Under the new guidelines, a BMI of 25 or more was considered "overweight," and 30 or more was considered "obese." It sounds a little convenient that these categories happen to fit such nice round numbers, doesn't it? But this is pretty much the basis for these categories:

And also, to a lesser extent, this:

(These images courtesy of Obesity Online).

The relative risk of diabetes and heart disease goes up at a BMI of 25, and the line of BMI vs. risk seems to change slope at around BMI = 30 (references are on the images). And BMI is cheap and easy to measure, all you need is a scale and a yardstick, or even just a telephone--you can just do a survey and ask people their height and weight. In contrast, to actually measure fat mass accurately, you need a machine called a DEXA scanner which costs $20K-$80K depending on how fancy your machine is.

So those are the main reasons why BMI is so popular among researchers and clinicians. Now, on to the criticisms.

The main criticism I hear of BMI is that it is simply a height/weight ratio and does not take into account muscle mass. While this is true, most people (women especially) are not going to be much affected by this unless they are body builders or professional-caliber athletes. Take, for example, Cruiserweight boxing champion David Haye, pictured here:

A very muscular guy, obviously, yet his fighting weight BMI clocks in right at 25, the border between normal and overweight (he's 6'3" and the Cruiserweight limit is 200 lbs. I chose a boxer for this example, because I figure their weights must be pretty accurate). The point here being that while muscle mass is one of the more common criticisms people have of BMI, I think that for the most part it's not that big a confounding factor in most cases.

One element that does seem to be a major confounding factor is race. Several studies have shown that people of Asian descent tend to be fatter than Caucasians with the same BMI, and consequently, they tend to develop weight-related illnesses at lower BMIs (1-4). Latinos also seem to be more susceptible to diabetes at lower weights, although less so than Asians (4). For this reason, some people now think that waist circumference is a better indicator of risk of overweight-associated illness, and other researchers suggest that using the two measurements in tandem provides the best estimate of risk (5-7).

In addition to racial differences, some investigators feel that BMI cutoffs should be different for women and men, as men tend to have more muscle mass due to their higher testosterone levels. As you can see in the graphs above, men have a lower relative risk of diabetes vs. BMI compared to women, but the risks for cardiovascular disease are similar.

Another major problem with using BMI as a determinant of health risk is the fact that several recent studies have shown that people with overweight BMIs have a lower risk of mortality than people with normal BMIs (8-9). (Of course, everyone's risk of mortality is 100% eventually, but this was as measured within the period of the study). This finding was perplexing to researchers, as it would seem to counteract the information in the graphs above, findings which had been replicated many times. Some have suggested that these findings could be a result of some people in the "normal" group experiencing weight loss due to undiagnosed illness that later contributed to death. Others pointed to the so-called "obesity" paradox: the finding that while overweight people are more likely to be diagnosed with heart disease and renal failure, they also have a survival advantage over normal-weight people with this disease (10). (There's a lot more to say about the obesity paradox, but I'll save it for another post!) At any rate, the overall picture is still quite murky.

In summary, I would say that BMI is a somewhat useful tool for determining whether a person is statistically at heightened risk for certain complications of obesity. But it should be kept in mind that this increased probability is not at all a predetermined fate. After all, even a 45-year old woman with a BMI of 30-35 still has less than a 50% chance of developing type II diabetes (11). So, as they say on the internet, YMMV.

1. WHO Expert Consultation.
Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. The Lancet. 363: 157-163, 2004.

2. Deurenberg-Yap M., Deurenberg P. Is a re-evaluation of WHO body mass index cut-off values needed? The case of Asians in Singapore. Nutrition Reviews 61:S80-S87, 2003.

3. Huxley R, James WP, Barzi F, Patel JV, Lear SA, Suriuawongpaisal P, Janus E, Caterson I, Zimmet P, Prabhakaran D, Reddy S, Woodward M, Obesity in Asia Collaboration. Ethnic comparisons of the cross-sectional relationships between measures of body size with diabetes and hypertension. Obesity Reviews 9:53-61, 2008.

4. Shai I, Jiang R, Manson JE, Stampfer MJ, Willett WC, Colditz GA, Hu FB. Ethnicity, obesity, and risk of type 2 diabetes in women: a 20-year follow-up study. Diabetes Care 29: 1585-1590, 2006.

5. McCarthy HD. Body fat measurements in children as predictors for the metabolic syndrome: focus on waist circumference. The Proceedings of the Nutrition Society 65: 385-392, 2006.

6. Deurenberg P, Deurenberg-Yap M. Validity of body composition methods across ethnic population groups. Forum of Nutrition 56: 299-301, 2003.

7. Koster A, Leitzmann MF, Schatzkin A, Mouw T, Adams KF, van Eijk JT, Hollenbeck AR, Harris TB. Waist Circumference and Mortality. American Journal of Epidemiology April 15 Epub ahead of print, 2008.

8. Flegal KM, Graubard BI, Williamson DF, Gail MH. Excess deaths associated with underweight, overweight, and obesity. Journal of the American Medical Association 293: 1861-1867, 2005.

9. Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific excess deaths associated with underweight, overweight, and obesity. Journal of the American Medical Association 298: 2028-2037, 2007.

10. Schmidt DS, Salahudeen AK. Obesity-survival paradox--still a controversy? Seminars in Dialysis 20: 486-492, 2007.

11. Narayan KMV, Boyle JP, Thompson TJ, Gregg EW, Williamson DF. Effect of BMI on Lifetime Risk for Diabetes in the U.S. Diabetes Care 30: 1562, 1566, 2007.

Monday, May 5, 2008

This blog is not dead

I know the last bunch of entries here garnered a lot of new traffic thanks to links from Big Fat Deal and Elastic Waist, so I've been feeling awfully guilty about not posting anything since then! But life has been hectic, and unfortunately, the blog has to take a back seat to things like my real job and eating and sleeping. But I am working on something new to go up hopefully later this week or possibly early next week about the history, utility and limitations of BMI. Thanks for sticking with me despite my inconsistent posting schedule!

Tuesday, April 22, 2008

The politics of weight control

In doing research for my last post, I happened to come across an article written by Joanne Ikeda and her colleagues (1), critiquing the National Weight Control Registry program. Ikeda is a member of the board of directors of the Association for Size Diversity and Health, which promotes the Health at Every Size program. Their paper recycles the claim (twice) that 95% of persons who lose weight regain it (without providing any references), and basically makes the argument that since weight loss efforts are generally futile, HAES should be promoted instead of weight loss.

This is an argument that has been picked up by many in the Fat Acceptance movement, and I can understand their motivation. After all, if you say that significant permanent weight loss is impossible, then obese people are not "culpable" for their obesity, because it is utterly beyond their control. And if you say that it is possible, then you can rightfully accuse obese people of sloth and gluttony, right?

Obviously, I'm utilizing some hyperbole here, so you can probably tell that I personally don't agree with these viewpoints. I think the evidence strongly suggests that some people can lose weight permanently and others can't. It may even be the case that some people are able to lose weight at certain times in their lives and not at others. And it's impossible to make a judgement about any one individual's ability to lose weight.

So, I don't agree with the FA movement when they say that nobody should try to lose weight. And I don't agree with fat bashers who say that all obese people should try to lose weight. Having a "normal" BMI takes a different amount of effort for everyone, and people should be left to make their own decisions about how much energy to invest in regulating their body weight without being judged or criticized by others (except, obviously, in extreme cases involving eating disorders).

And I hope people will feel free to share their own views on the matter in the comments...

1. Ikeda J, Amy NK, Ernsberger P, Gaesser A, Berg FM, Clark CA, Parham ES, Peters P. The National Weight Control Registry: A Critique. Journal of nutrition education and behavior 37: 203-205, 2005.

Friday, April 18, 2008

Losing weight and keeping it off

As I mentioned in my last post, there is significant debate over the rate of success in losing weight and keeping it off without the use of surgery or drugs. However, it is definitely possible for some people, and there has been great interest in characterizing the behaviors of those people.

Many, but not all, of the studies I will mention in this post use subjects in the National Weight Control Registry (which I will refer to as the NWCR). They have a pretty detailed website, so if this subject is of interest, you might want to check it out. While this is a tremendously valuable resource in the study of successful weight loss maintenance, in general, I would say that the studies that come out of this cohort are slightly less reliable, because the analysis is retroactive in nature, meaning that the people's habits are being studied after they have lost weight and kept it off. Other studies, in contrast, have looked at people's habits immediately after losing weight and then looked to see what lifestyle factors ended up being associated with maintaining that loss. The former approach is more susceptible to something called recall bias, meaning that the fact that the people being studied have already successfully maintained their weight loss might affect their memories and perceptions of their own habits as compared to people who did not maintain weight loss. With that caveat (and you can tell which studies are NWCR-related by the authors...Rena Wing and James Hill are the founders of the registry), here is a summary of some of the major findings.

Diet--The following dietary habits have been found to be associated with successful maintenance of weight loss:
-Eating five or more servings of fruits and vegetables per day (1, 2)
-Not eating at fast food restaurants (as compared to those who eat fast food at least twice a week) (1)
-Using low-calorie pre-packaged meals (2-4)
-Practicing portion control (2, 11)
-Moderating intake of fat (2, 11)
-Eating breakfast (11)

Exercise: Multiple studies have found that exercise improves one's chances of maintaining weight loss (1,2, 5-8). There is some debate, however, over how much exercise is necessary. Several studies have suggested that an hour of exercise each day is needed to improve chances of weight loss maintenance (1, 2) but at least one other study found that any amount of exercise was beneficial (5)

Weight loss as a percentage of starting weight:
Multiple studies (5, 9, 10) have shown that basically, the more weight you lose, the harder it is to maintain. For this reason, many public health officials are now recommending that obese people strive to lose 10-15% of body weight and keep it off rather than trying to achieve a "normal" BMI and then rebound.

"Screen time": Television and computer use (outside of work) has been shown to be positively correlated with weight regain (5)

Consistent Monitoring of Weight: One of the characteristics identified in subjects in the NWCR was frequent weighing (11). 44% of these people said they weighed themselves daily and 31% weighed themselves weekly (11). A more detailed study also showed that subjects in the NWCR who started weighing themselves less frequently gained more weight than those who maintained their strict weighing schedule (14). However, it's not clear whether weighing itself somehow affected these people's motivation to maintain their weight or whether people who knew they'd "slipped" a bit had more trepidation about stepping on the scale regularly.

Online Support:
A recent study published in JAMA (12) looked at people who had lost weight through a 6-month program of monitored diet and exercise and then looked at the efficacy of three different types of counseling in helping them to maintain their weight loss over 30 months. Following the initial weight loss period, the "self directed" group were given some literature with recommendations for diet and exercise and met with a counselor after 12 months. An "interactive technology-based intervention" group was given unlimited access to a web site which assisted them in monitoring their weights, monitoring their caloric intake and physical activity and charting their progress, as well as giving them access to a message board where they could interact with other members of that group. The third group received monthly personal contact with a counselor either over the phone or in person. While all three groups regained some weight, they found that the technology-based intervention group regained less than the self-directed group, and the personal contact group regained the least.

While personal monitoring of weight maintenance may not be widely feasible, this does suggest that support provided through the internet may assist in weight loss maintenance. However, at least one other study (13) had different findings that a (different) website they set up to support maintenance of weight loss after a 4-month weight loss program did not make any difference in maintenance of weight loss. The authors attributed the lack of effect to the fact that many of the participants in the study were not comfortable using the internet.

Other: Interestingly, 2 found that unsuccessful maintainers were more likely to follow popular diet books than those who were successful at maintaining weight loss.

Anyway, I doubt any of these things are shockers, but it may be a helpful collection of information for some people!

1. Kruger J, Blanck HM, Gillespie C. Dietary Practices, Dining Out Behavior, and Physical Activity Correlates of Weight Loss Maintenance. Preventing Chronic Disease, 5:A11, 2008.

2. Befort CA, Stewart EE, Smith BK, Gibson CA, Sullvan DK, Donnelly JE. Weight maintenance, behaviors and barriers among previous participants of a university-based weight control program. International Journal of Obesity, 32: 519-526, 2008.

3. Heymsfield SB, van Mierlo CA, van der Knaap HC, Heo M, Frier HI. Weight management using a meal replacement strategy: meta and pooling analysis from six studies. International Journal of Obesity and Related Metabolic Disorders 27: 537-549, 2003.

4. Ditschuneit HH, Flechtner-Mors, M. Value of structured meals for weight management: rsk factors and long-term weight maintenance. Obesity Research 9: 284S-289S, 2001.

5. Weiss EC, Galuska DA, Khan LK, Gillespie C, Serdula M. Weight Regain in Adults Who Experienced Substantial Weight Loss, 1999-2002. American Journal of Preventative Medicine, 33: 34-40, 2007.

6. Anderson JW, Konz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of U.S. studies. American Journal of Clinical Nutrition 74: 579-584, 2001.

7. Jeffery RW, Epstein LH, Wilson GT,
Drewnowski A, Stunkard AJ, Wing RR, Hill DR. Long-term maintenance of weight loss: Current status. Health Psychology 19 5-16, 2000.

8. Grodstein F, Levine R, Troy L, Spencer GA, Colditz GA, Stampfer MJ. Three-year follow-up of participants in a commercial weight loss program: can you keep it off? Archives of internal medicine 156: 1302-1306, 1996.

9. McGuire MT, Wing RR, Klem ML, Lang W, Hill JO. What predicts weight gain in a group of successful weight losers? Journal of Consulting Clinical Psychology, 67: 177-185, 1999.

10. Vogels N, Westerterp-Plantenga MS. Successful long-term weight maintenance: a 2-year follow-up. Obesity 15: 1258-1266, 2007.

11. Klem ML, Wing RR, McGuire MT, Seagle HM, Hill JO. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. American Journal of Clinical Nutrition, 66: 239-246, 1997.

12. Svetkey LA, Stevens VJ, Brantley PJ, Appel LJ, Hollis JF, Loria CM, Vollmer WM, Gullion CM, Funk K, Smith P, Samuel-Hodge C, Myers V, Lien LF, Laferriere D, Kennedy B, Jerome GJ, Heinith F, Harsha DW, Evans P, Erlinger TP, Dalcin AT, Coughlin J, Charleston J, Champagne CM, Bauck A, Ard JD, Aicher K for the Weight Loss Maintenance Collaborative Research Group. Comparison of Strategies for Sustaining Weight Loss. Journal of the American Medical Association, 299: 1139-1148, 2008.

13. Cussler EC, Teixeira PJ, Going SB, Houtkooper LB, Metcalfe LL, Blew RM, Ricketts JR, Lohman J, Stanford VA, Lohman TG. Maintenance of Weight Loss in Overweight Middle-aged Women Through the Internet. Obesity, advance online publication, 2008.

14. Butryn ML, Phelan S, Hill JO, Wing RR. Consistent Self-monitoring of Weight: A Key Component of Successful Weight Loss Maintenance. Obesity 15: 3091-3096, 2007.

Monday, April 14, 2008

Weight loss success: a teaser

In the "requests" posts, someone asked me to write about the issue of the success rate for weight loss maintenance. This is something I wondered about myself. I'd heard the factoid that "95% of dieters regain the weight within five years" but was not familiar with the actual scientific literature on the subject.

Now, having familiarized myself somewhat...I still have no idea what the success rate is for weight loss. The literature is a mess.

A big part of the problem is that different studies use different measures of "significant weight loss" and "long term." Is "significant weight loss" a certain number of pounds, maybe 20, or 30, or 50? Or a certain percentage of your starting body weight? And is "long term" one year, or two, or ten? There are also qualitative differences in studies looking at different kinds of weight loss. Some studies look at people who started out morbidly obese and others looked at weight loss in those who started out merely overweight. Some studies look at weight loss through diet alone, others through exercise alone, and some through a combination of the two. Some of the diets studied are moderate, and some actually involve medically-supervised fasting conditions. The weight loss interventions studied vary in their durations, as well.

So some studies say that the rate of long-term weight loss success is 2% (1) and others say it is 20% (2). At any rate, I think it's safe to say that the rate of success at long-term maintenance of significant weight loss is greater than 0% and less than 100% and instead of further dissecting the matter, I think it's more instructive to focus on studies looking at variables that predict success in long term maintenance of weight loss. Weight loss maintenance may truly not be feasible for all or even most people, but I still think dissecting out factors that can contribute to maintenance of long-term weight loss is useful.

And that's what I'm going to post about on Monday...

1. Stunkard AJ, McLaren-Hume M. The results of treatment for obesity. Archives of Internal Medicine 103: 79-85, 1985.

2. Wing RR and Phelan S. Long-term weight loss maintenance. American Journal of Clinical Nutrition, 82: 222S-225S, 2005.

Artificial sweeteners, part deux

I just wanted to post an update about artificial sweeteners, because one of the papers I mentioned in my earlier post on the subject was at that time still in press and now it has been published.

This article (1) is by a pair of researchers in the Department of Psychology at Purdue University, Susan Swithers and Terry Davidson. In their first experiment, they compared the weight gain of rats fed non-fat yogurt sweetened with glucose (a sweetener that has the same sweetness and number of calories as table sugar) vs. rats fed yogurt sweetened with saccharin. Each group got sweetened yogurt three days a week, unsweetened yogurt three days a week and chow one day a week. The rats stayed on the diets for 5 weeks while the researchers monitored their food intake and body weight. At the end of the study, they also measured the animals' body fat content.

The researchers found that all of the animals gained quite a bit of weight (about 20% over their starting weight) . However, they found that the animals which got saccharin yogurt gained slightly more weight than rats that got glucose yogurt in three out of the five weeks of testing, for an overall statistically significant effect*. They also found that the saccharin group had slightly more body fat. However, the researchers did not find a statistically significant difference in total calorie intake between the groups.

For a second experiment, the researchers sought to do a more detailed analysis of the effects of artificial sweetener on food intake. During a "training" period, rats were given normal chow along with yogurt for 14 days. On half of the days, each animal was given plain yogurt, and on the other half of the days one group of animals got glucose-sweetened yogurt and the other group got saccharin yogurt.

After the 14 day training period, they fed the animals chow and water for 1 day (presumably to "flush out" any short term effects of their yogurt diets), followed by an overnight fast (presumably to make the rats hungry...rats are nocturnal so they normally do most of their eating at night). Then half the rats in each group were given a "premeal" of Chocolate Ensure Plus** for 30 minutes, and then normal lab chow was given back to all the rats and their food intake was measured.

The researchers found that the rats that got the glucose yogurt ate slightly less during the 14-day training period than the rats that got saccharin yogurt. As in the first experiment, both groups gained weight, about 10% of their starting weight, but the saccharin group gained slightly more. During the testing period, they found that the glucose rats who got the premeal ate slightly less than those that didn't, but the saccharin rats ate the same amount, regardless of whether they ate a premeal. However, there does not appear to be an overall difference in chow intake in the testing period between the glucose and saccharin groups.

For their third and final experiment, the researchers sought to establish a physiological basis for the differences between the glucose and saccharin groups. In this experiment they look at the well established phenomenon of "postprandial thermogenesis,": when you eat food, it causes a small, temporary increase in body temperature. Studies have shown that when food is tasted, but not swallowed, it tends to cause a bigger increase in body temperature than if the food were actually eaten (2,3), whereas if food is delivered directly to the gut via a tube and not tasted, the increase in body temperature is smaller (2,4). The authors hypothesized here that since the saccharin rats have been trained to eat something that tastes sweet, but without the calories of sugar, that they might also see decreased body temperature in response to a meal compared with the rats whose bodies "expect" the calories associated with sugar. (n.b. Thanks to anonymous, who pointed out that my original interpretation of their hypothesis made no sense, and I have corrected this post accordingly. Sometimes I read stuff too fast!)

For this experiment, all the rats were surgically implanted with thermometers that transmitted temperature readings to a receiver, so the researchers were able to continuously monitor the temperature of each rat. Then they did the same 14-day training with glucose- or saccharin-sweetened yogurt as in the previous experiment. Then all rats were fasted overnight, and then given a premeal of chocolate Ensure, followed by ad lib access to chow.

They found that during the first hour of the 14-day training period that both the glucose and saccharin groups increased their body temperature after eating the yogurt, but the glucose group's temperature came down more slowly after the meal. Then during testing, they found that the glucose group's temperature went up slightly more in response to the Ensure than the saccharin group's, although both groups increased their body temperature.

Anyway, the authors' interpretation of this all is that there is a Pavlovian conditioning phenomenon occurring here. They believe that when rats eat yogurt sweetened with sugar, their bodies learn that sugary taste is associated with the intake of calories, and they adjust their diet accordingly when presented with things that are sweet. In contrast, rats that eat saccharin yogurt do not develop this association, and so when they are presented with sweet foods their bodies don't expect them to have any calories. They believe that the temperature differences following glucose- and saccharin-sweetened foods are part of the mechanism by which animals make these adaptations, but things get a little hand-wavy at this point for me.

This paper is kind of intriguing, but I think there are a few big leaps between the findings of the paper and the conclusions the authors draw. I think the biggest caveat is that they are assuming that saccharin's effects are due to the fact that it is an artificial sweetener and not due to some other possible effect of this chemical on the rats' bodies. A good way to test for this would be to look and see if other types of artificial sweeteners have the same effect.

Another big caveat is that the results in this study are mostly pretty subtle, and these studies were all done in rats that had been raised on a diet of lab other words, these experiments were the rats' first experience with sweet-tasting food. This makes me wonder about the applicability of the study in humans, since most people eat a combination of natural and artificial sweeteners, so we are not being "trained" in the same way as the rats.

A third caveat is the fact that their proposed mechanism is pretty vague. They don't identify an neural pathways or hormones or brain areas that might be implicated in this Pavlovian response. They merely show a difference in the effects on body temperature, which again, could be due to some specific effect of saccharin. I think a really interesting test of their hypothesis would be to train rats on glucose yogurt and then give them a pre-meal sweetened with saccharin and see if that caused them to eat less subsequently. Maybe that will be in their next paper.

In conclusion, I think this paper has some significant flaws (among which is the fact that they issued a press release about the paper before it was published so the results were reported in the media without any scrutiny). But I also think there might be something there. I think it's just not quite clear yet exactly what that is.

*These researchers do something I've never seen before with their statistics, which is that for the measures they say are statistically significant, they just say that the p-value is less than 0.05, they don't tell you what the p-value actually is. For the nonsignificant measures, they do tell you the actual p-value. Has anyone else ever heard of this? Is there any reason to do it other than my suspicion that these p-values were all very close to 0.05, and they wanted to downplay this by just called 0.05 the cutoff and then claiming that their data fit that criterion?

**Ensure is often used to fatten laboratory rats, and I used to work next door to a lab that did this a lot. As you can imagine, it definitely colored my view of those TV commercials for Ensure where people talk about how they give their senior citizen parents Ensure because they care about them so much.

1. Swithers SE, Davidson TL. A Role for Sweet Taste: Calorie Predictive Relations in Energy Regulation by Rats. Behavioral Neuroscience 122: 161-173, 2008.

2. Diamond P, Brondel L, LeBlanc J. Palatability and postprandial thermogenesis in dogs. American Journal of Physiology 248: E75-E79, 1985.

3. LeBlanc J, Cabanac M. Cephalic postprandial thermogenesis in human subjects. Physiology and Behavior 46: 479-482, 1989.

4. LeBlanc J, Cabanac M, Samson P. Reduced postprandial heat production with gavage as compared with meal feeding in human subjects. American Journal of Physiology 246: E95-E101, 1984.

Sunday, April 6, 2008

Book review: In Defense of Food

Michael Pollan's The Omnivore's Dilemma, which explores the moral, ecological and health impact of the food we choose to eat, was a life-altering book for me. So I was very excited to receive his follow-up book, In Defense of Food as a birthday gift. Unfortunately, as I read the book, I became gradually less thrilled, and now my Pollan-love has abated somewhat. But overall, I think Pollan and I come to the same conclusions, but perhaps for different reasons.

Pollan begins the book with his catchy new mantra: "Eat food. Not too much. Mostly plants" (I haven't seen this on a t-shirt yet, but fear that it is only a matter of time). Most of the first part of the book is devoted to his distinguishing food from what he calls "edible food-like substances," i.e. foods that have been heavily processed. I was with him this far, but he began to lose me with his forays into critique of food science.

Pollan is often sloppy or unclear in his treatment of the subject. On page 69, in talking about the placebo effect, he says "About a third of Americans are what researchers call responders–people who will respond to a treatment or intervention regardless of whether they've actually received it." I cringed when I read this, for several reasons. For one thing, he makes it sound as though responders are a fixed (and apparently highly suggestible) segment of the population that will respond to anything. This is not the case, nor is it the case that people respond equally to all placebos. He unfortunately does not provide a citation for this particular factoid. The book throughout is rather poorly sourced, with only a few of his claims having more than one citation to back them up.

His main critique of nutrition science is that research in that field has focused on the effects of single nutrients. This, he argues, is problematic because we do not eat nutrients, we eat foods with different combinations of nutrients that may interact with one another and thereby affect our health in ways that would not be predicted from single-nutrient studies. This is a fair enough criticism, but uses this argument to basically reject the entire field of nutrition science (except for those studies which back up his conclusions). In rejecting nutrition science as overly reductionist, he also neglects to acknowledge that the most important discoveries of nutrition science and those which have arguably had the greatest health impact were the identification and treatment of diseases resulting from deficiencies of single nutrients, such as scurvy, rickets, and beriberi.

I do agree with Pollan that nutrition science is not sufficiently advanced that we ought to eat food which has been stripped of its nutritional content through processing and then re-fortified with vitamins, or that we can depend on vitamin supplementation to balance out a diet that is not nutritionally sound. But I imagine most nutrition scientists would also agree with this...unless they work for Frito-Lay, maybe.

Interestingly, for all his talk about reductionism, Pollan does seem to be convinced as to the miraculous health properties of one nutrient: omega-3 fatty acids. He does not attempt to address the apparent contradiction between his criticism of studies that look at single nutrients, and his belief in those exact types of studies about omega-3s. He even manages to sneak in a little anti-science jab when he writes "I have been specifically warned by scientists allied with the carbohydrate camp not to 'fall under the spell of the omega-3 cult.' Cult? There is a lot more religion in science than you might expect." Sounds to me like an advanced case of the pot calling the kettle black!

Another of Pollan's main claims is that the "Western" diet is inherently unhealthy (I agree with him here) and that virtually all "traditional" diets are superior in their health effects. Here, he relies heavily on the work of a dentist, Weston Price, who conducted studies in the 1930s of traditional diets and dental health. Pollan acknowledges that Price "could sometimes come across as a bit of a crackpot," but embraces his conclusions nonetheless.

To be fair, he also looks at other studies of traditional diets, in each case finding that people eating the diets their ancestors had consumed over the past several hundred years were healthier than people who had changed their traditional diets. Even the Masai people, whose diet consisted of meat, blood, milk and virtually no plant foods were deemed to be healthier than people eating a modern Western diet. He quotes one nutritionist as saying "Just don't eat anything your Neolithic ancestors wouldn't have recognized and you'll be OK."

The obvious (to me, anyway) problem with this philosophy is that like most Americans, my Neolithic ancestors were scattered (in my case around Europe) and likely ate vastly different diets from one another. If traditional diets are truly healthier, it seems to me that we much accept one of two explanations: either various cultures were able, through trial and error, to develop optimally healthy diets from the available foods over a period of hundreds of years, OR alternatively, people may have genetically adapted to the diets to which they had access over those hundreds of years to get optimum health out of the foods available to them. Neither of these hypotheses is proven, but given the tremendous variation of the content of healthy traditional diets, the latter seems vastly more likely to me.

Pollan does talk about people adapting to their diets a few times, saying, for example, that "our bodies have a long-standing and sustainable relationship to corn that they do not have to high-fructose corn syrup. Such a relationship with corn sytrup might develop someday (as people evolve superhuman insulin systems to cope with regular floods of pure fructose and glucose)." But he never makes the leap to confront the politically incorrect notion that if people have to adapt to their diets over centuries, the ethnically heterogeneous among us might just be screwed.

That being said, while I disagree with some of Pollan's reasoning and analysis, in the end, we pretty much arrive at the same place. I found the dietary principles he espouses at the end of the book to be sound. In fact, in that part of the book, I felt the flame of Pollan-love starting to come back to life. Overall, I think the book is worth a read...with a bit of skepticism reserved.

Friday, April 4, 2008

No new post this week

It's been a hectic week, but I'll be back on Monday with a book report on Michael Pollan's In Defense of Food.

Wednesday, March 26, 2008

The environmental scourge of obesity

Last month, I was reading an article in The New Yorker about calculating carbon footprints. The article referenced an article in the New Scientist which they said "suggested that the biggest problem arising from the epidemic of obesity is the additional carbon burden that fat people—who tend to eat a lot of meat and travel mostly in cars—place on the environment." The article, which appeared in the June 30, 2007 issue of the magazine, is by Ian Roberts, a professor of public health at the London School of Hygiene and Tropical Medicine. It is only available online to subscribers to the magazine, but I think it's just as well, as it is a truly shameful excuse for science "journalism."

Here are Roberts's key points (please note that he does not cite any sources for any of this information, and much of it is either highly suspect, or I know it to be incorrect):

-The U.S. has the world's highest rate of obesity and also has the highest per capita carbon emissions, and this shows that obesity and carbon emissions are linked.

-Obese people eat 40% more calories than lean people, and food production accounts for 20% of greenhouse gas emissions

-I was going to summarize this next part, but realized that I could not possibly convey its awfulness by doing so, and so I will just reproduce it:

Consider what happens to someone on the path to obesity. It might start when he (or she, of course) decides to drive rather than walk the half mile to the office, just to get there a few minutes earlier. A year on he might have gained a kilogram of fat, and as the weight continues to pile on he eventually finds it harder to move around and is loath to walk or cycle anywhere[...]By now he'll be suffering low self-esteem, which leads to comfort eating and perhaps heavier drinking, too. He'll even notice a load on his household energy bills: his greater bulk and higher metabolic rate will cause him to feel the heat more in the globally warmed summers, and he'll be the first to turn on the energy-intensive air conditioning.

In looking for the New Scientist article, I had come across some other media reports on the environmental impact of obesity, most of them referencing this study by a University of Illinois Computer Science professor and a graduate student. Unfortunately, I wasn't able to read the original article, as none of the libraries I have access to subscribe to The Engineering Economist, but according to that press release, the study showed that weight gain by Americans since 1960 now causes us to consume an additional 938 million gallons of gasoline per year. That sounds pretty bad, right? But maybe not so much when you consider that that represents only a 0.7% increase in fuel consumption over what it would cost if Americans weighed the same now as in 1960. As the authors, McLay and Jacobson, write in the paper, "the amount of fuel consumed as a result of the rising prevalence of obesity is small compared to the increase in the amount of fuel consumed stemming from other factors such as increased car reliance and an increase in the number of drivers
" (not to mention the fact that people still opt to drive heavier and less fuel-efficient vehicles). And yet still, the article was widely reported on with headlines like "Expanding waistlines lead to pain at the pump."

It also occurs to me that even if obesity did have a significant impact on fuel consumption and carbon emissions, what would be the logical response to such a finding? Forced weight loss surgeries? Food rationing for fat people? Forcing people to pay for carbon offsets for their fat? Obviously these are all ridiculous ideas, particularly in light of the fact that there are many factors which we can control that also contribute to fuel consumption and global warming.

Although there may indeed be a link between our high-carbon lifestyle and obesity, it seems to me that we ought to be looking at this issue from the perspective of those things we can change. This study for example, finds that taking public transit is associated with an additional 8.3 minutes per day of walking, which if applied to people who now commute in their cars could dramatically reduce obesity rates (in addition to the carbon savings associated with public transit). This is a theoretical model, so its validity is not established, but if it's true, increased funding and use of public transit will result in both decreased pollution and increased health, which sounds like a win-win situation to me.

Tuesday, March 18, 2008

Can gastric banding cure diabetes? Part II.

As I mentioned in the last entry, in 1995, Pories et al. found that Roux-en-Y gastric bypass surgery normalized blood glucose in some type II diabetics within days of the operation (1). This immediate improvement in blood glucose, which preceded any significant weight loss, led some to speculate that the blood glucose changes were a result of the effects of surgery on the gut rather than a consequence of weight loss. The gastrointestinal tract has been shown to secrete a number of hormones that can influence glucose and insulin levels and insulin sensitivity (2), and people theorized that changes in the levels of those hormones following absorptive surgery might be the mechanism by which those surgeries caused improvements in diabetes (1). Indeed, a number of papers showed that absorptive weight loss surgeries caused changes in levels of many of these gut hormones, and that these changes persisted even 20 years after the surgeries (3-5).

Other studies showed that while gastric bypass surgery altered the levels of these hormones, gastric banding surgery did not (4, 6). This makes sense, as the absorptive surgeries work by physically disconnecting some parts of the gastrointestinal tract that make the hormones, whereas the gastric banding, which is only restrictive, does not.

So, if gastric banding doesn't abate diabetes by altering gut hormone levels, how does it work? In the recent JAMA paper showing dramatic levels of diabetes remission with gastric banding, the authors found that weight loss was strongly correlated with diabetes remission, both in the gastric banding group and in the traditional diabetes therapy group (7). They conclude that "degree of weight loss, not the method, appears to be the major driver of glycemic improvement and diabetes remission in obese participants. This has important implications, as it suggests that intensive weight-loss therapy may be a more effective first step in the management of diabetes than simple lifestyle changes."

So, it seems that while gastric banding's effects on diabetes are primarily a result of its effects on weight loss, gastric bypass surgery also improves diabetes by altering levels of gut hormones that are involved in regulation of glucose and insulin. While gastric bypass surgery is generally more effective against diabetes and has a dual mechanism, the recent JAMA paper serves as evidence that with the right surgical team, gastric banding can also be very effective against diabetes in newly diagnosed patients, at least in the short term. This has generated a lot of excitement in the medical community, with some proposing gastric banding as the standard treatment for type II diabetes. However, until longer-term results have been shown, I think that assessment is a bit premature.

1. Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, Barakat HA, deRamon RA, Israel G, Dolezal JM. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Annals of Surgery 222: 339-352, 1995.

2. Drucker DJ. The role of gut hormones in glucose homeostasis. Journal of Clinical Investigations 117: 24-32, 2007.

3. Naslund E, Gryback P, Hellstrom PM, Hacobsson H, Holst JJ, Theodorsson E, Backman L. Gastrointestinal hormones and gastric emptying 20 years after jejeunoileal bypass for massive obesity. International Journal of Obesity and Related Metabolic Disorders 21: 387-392, 1997.

4. Kellum JM, Kuemmerle JF, ODorisio TM, Rayford P, Martin D, Engle K, Wolf L, Sugerman HJ. Gastrointestinal hormone responses to meals before and after gastric bypass and vertical banded gastroplasty. Annals of Surgery 211: 763-771, 1990.

5. Wilson P, Welch NT, Hinder RA, Anselmino M, Herrington MK, DeMeester TR, Adrian TE. Abnormal plasma gut hormones in pathologic duodenogastric reflux and their response to surgery. American Journal of Surgery 165: 169-177, 1993.

6. Korner J, Inabnet W, Conwell IM, Taveras C, Daud A, Olivero-Rivera L, Restuccia NL, Bessler M. Differential effects of gastric bypass and banding on circulating gut hormone and leptin levels. Obesity (Silver Spring), 14: 1553-1561, 2006.

Dixon JB, O'Brien PE, Playfair J, Chapman L, Schachter LM, Skinner S, Proietto J, Bailey M, Anderson M. Adjustable Gastric Banding and Conventional Therapy for Type 2 Diabetes. JAMA 299: 316-323, 2008.

Monday, March 17, 2008

Can gastric banding cure diabetes? Part I.

A couple of months ago, a paper published in the Journal of the American Medical Association made headlines with the claim that gastric banding surgery resulted in remission of type II diabetes in 73% of patients who had the surgery (as opposed to only 13% remission in controls).

A few obvious questions come to mind here: is it true? And if so, is the remission from diabetes just a consequence of weight loss, or does the surgery result in some other physiological change that results in diabetes remission? In this post, I'm going to write about the validity of these studies. And in Part II, which I'll post on Friday, I'll talk about the mechanisms by which weight loss surgeries are believed to affect diabetes.

Gastric banding is a "restrictive" surgery involving the placement of a band around the stomach, restricting food intake by limiting the capacity of the stomach (1). Some other types of weight loss surgery are "absorptive" and work by limiting absorption from the gastrointestinal tract by physically bypassing parts of the gastrointestinal tract (1). And some surgical procedures are both restrictive and absorptive.

There are different advantages and disadvantages to different types of surgeries. Patients who undergo gastric banding tend to lose less weight than those who have other types of weight loss surgeries (an average of 47.5% of excess weight loss with gastric banding vs. an average 70.1% of excess weight with the duodenal switch procedure, a restrictive and absorptive surgery), however, the gastric banding procedure is faster, less invasive, and has a lower risk of complications than more invasive surgeries (1). It also has the advantage of being reversible.

Two studies in the 1990s had demonstrated that the Roux-en-Y gastric bypass surgery (which is both restrictive and malabsorptive) reduced pre-diabetic patients' risk of developing type II diabetes (2) and normalized blood glucose in some type II diabetics within days of the surgery (3) (in fact, some patients experienced an "overnormalization" of blood glucose and suffered occasional attacks of hypoglycemia).

In 2004, Ponce et al. (4) set out to see if gastric banding (ahem, excuse me, Lap-Banding ® which is just a specific brand of gastric band) produced similar results. They measured HbA1c levels, an indicator of average blood glucose over the past couple of months, in patients 12, 18, and 24 months after their surgeries. They found that glucose levels improved following surgery and maintained that improvement at 24 months. They also found that type II diabetes was resolved in a majority of patients who had been diabetic for less than 5 years prior to their surgery, but in only about a third of those who had been diabetic for more than 5 years prior to surgery.

Last year, Korenkov et al. (5), set out to look at a slightly longer follow-up period, but unfortunately, because the patients varied in their followup durations from 2 to 8 years (with an average of 5 years) it is not possible to determine based on their results if the health improvements they saw were truly stable over this period. They found that the prevalence of type II diabetes decreased from 10% pre-surgery to 4% at followup. However, they do not say how many (if any) of these patients were still diabetes free 8 years out. Another short-term study published last year (6) compared gastric band and Roux-en-Y gastric bypass surgeries and found that at 13 months post-surgery, 50% of diabetic gastric band patients and 95% of gastric bypass patients had improvements in their diabetes. However, again, it is not clear whether these effects persisted over the long term.

So the JAMA study which received so much media attention recently was really not so revolutionary. The study's subjects were all patients with a BMI <40* style="font-style: italic;">JAMA explain the discrepancy by pointing out that the surgical team participating in the study "is among the most experienced groups in the world using LAGB, and their excellent results may not be reproducible elsewhere. Their reported post-LAGB weight loss often exceeds that observed by other investigators" (8). I hope that longer-term findings will be published in the coming years, but the results this far look pretty promising. But of course, weighing the risks and benefits of any surgical procedure is something that should be the sole prerogative of patients themselves.

*The authors explain that they "believed it inappropriate to recruit those with a BMI greater than 40 into the study, because a number of observational studies have shown effectiveness of bariatric surgery in these patients." I think they're missing a "not" in there somewhere...

1. Korenkov M, Sauerland S, Junginger T. Surgery for Obesity. Current Opinions in Gastroenterology 21: 679-683, 2005.

2. Long SD, O'Brien K, MacDonald KG Jr., Leggett-Frazier N, Swanson MS, Pories WJ, Caro JF. Weight loss in severely obese subjects prevents the progression of impaired glucose tolerance to type II diabetes: a longitudinal interventional study. Diabetes Care 17: 372-275, 1994.

3. Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, Barakat HA, deRamon RA, Israel G, Dolezal JM. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Annals of Surgery 222: 339-352, 1995.

4. Ponce J, Haynes B, Paynter S, Fromm R, Lindsey B, Shafer A, Manahan E, Sutterfield C. Effect of Lap-Band®-Induced Weight Loss on Type 2 Diabetes Mellitus and Hypertension. Obesity Surgery 14:1335-1342, 2004.

5. Korenkov M, Shah S, Sauerland S, Duenschede F, Junginger T. Impact of Laparoscopic Adjustable Gastric Banding on Obesity Co-morbidities in the Medium- and Long-Term. Obesity Surgery, 17: 679-683, 2007.

6. Gan SSH, Talbot ML, Jorgensen JO. Efficacy of Surgery in the Management of Obesity-Related Type 2 Diabetes Mellitus. ANZ Journal of Surgery, 77:958-962, 2007.

7. Dixon JB, O'Brien PE, Playfair J, Chapman L, Schachter LM, Skinner S, Proietto J, Bailey M, Anderson M. Adjustable Gastric Banding and Conventional Therapy for Type 2 Diabetes. JAMA 299: 316-323, 2008.

8. Cummings DE, Flum DR. Gastrointestinal Surgery as a Treatment for Diabetes. JAMA 299: 341-343, 2008.

Sunday, March 16, 2008

Health at Every Size

The "Health at Every Size" (HAES) program has attracted a lot of positive attention among fat acceptance groups, and has been touted as an alternative to weight loss programs for obese people. The program was developed by the Association for Size Diversity and Health (ASDAH), a non-profit self-described "international professional organization." I put that phrase in quotes not to be snarky, but because the board of directors is comprised of a mix of people, some of whom have professional training in psychology and nutrition, and some of whom don't, and membership in the organization is open to anyone who is willing to pay for it. The program is based around five basic principles:
  1. Accepting and respecting the diversity of body shapes and sizes
  2. Recognizing that health and well-being are multi-dimensional and that they include physical, social, spiritual, occupational, emotional, and intellectual aspects
  3. Promoting all aspects of health and well-being for people of all sizes
  4. Promoting eating in a manner which balances individual nutritional needs, hunger, satiety, appetite, and pleasure
  5. Promoting individually appropriate, enjoyable, life-enhancing physical activity, rather than exercise that is focused on a goal of weight loss
HAES is a relatively new program, and as a result, the published research about this program per se is still fairly scant. However, there are a few studies of non-dieting psychological interventions in obese patients dating back to the 1990s that likely formed the basis for this program. Ciliska (1) looked at the effects of "education intervention" and "psychoeducational intervention" in obese women (the "education" group had classroom-style lectures about the etiology and health consequences of obesity and the "psychoeducation" group had small discussion group-format meetings about HAES principles). While weight and blood pressure did not change in either of these groups, the psychoeducation group improved in measures of "self-esteem, restraint, and body dissatisfaction." The education intervention group showed no change. Another study (2) looked at the effects of "cognitive treatment" and "behavioural treatment" in obese binge eaters and obese non-binge-eaters. They found that both treatments had statistically significant positive effects on "shape concern, weight concern and eating concern, binge eating, self-esteem, and depression." However, there was little effect on weight loss with those in the behavior treatment group losing 3 kg (6.6 lbs) at the 1 year followup and those in the cognitive treatment group losing 0.3 kg (0.66 lbs). Interestingly, they found that participants who gained weight had equal improvement in their psychological well-being as those who lost weight.

In 2002, Bacon et al. (3) did the first study comparing a HAES-type program to a traditional weight-loss-centered diet program. They looked at subjects they described as "Obese, Caucasian, female, chronic dieters, ages 30-45." These women were divided into two groups, one of which participated in a HAES-type program, with the others following a traditional diet program. Both groups received 6 months of weekly group intervention followed by 6 months of monthly after-care group support. After this year, they found that both groups had demonstrated significant improvements in metabolic fitness, psychological variables and eating behaviors. While they reported that attrition was high in the diet group (41%) compared to the HAES group (8%), the diet group showed significant weight loss (5.8 kg or 13 pounds) the HAES group did not. The authors concluded from this that the main advantage of HAES over traditional dieting is the lack of attrition.

In 2005 Bacon's group at Davis published another study, the first one to actually use the term "Health at Every Size" (4). While this study was very similar in methodology to the first one they had published, the results were quite different. While the HAES group did not show any significant change in weight throughout the study period, members of the diet group lost an average of 5.8 kg in the initial six months, however, in the six month followup period they gained back some of that weight, and they found the net change in weight (3.2 kg, or 7 pounds) to be statistically insignificant. They found that the HAES group improved their total cholesterol, HDL, LDL and systolic blood pressure scores, whereas the diet group did not. They also found that the HAES group had significant long-term improvement (this was measured 2 years out) in a number of measures of psychological well being and eating disordered behavior, whereas the diet group showed long-term improvement in only a couple of these measures.

So how should these conflicting findings be interpreted? The papers by Bacon's group at UC Davis seem particularly confusing, as their two studies were carried out under very similar conditions but had quite different results. This may have been a result of their small sample size (after attrition, there were only 19 women left in the diet group in their second study). It also may have been a result of demographic differences between the two groups in that second study. While the authors do not mention this explicitly, a table in the paper shows that in the HAES group, 89.5% of women were married or in a domestic partnership, whereas only 68% of the women in the diet group were in such relationships. The two groups also differed in their education levels: 53% of the HAES group were college graduates, whereas 63% of the diet group were. These disparities may have resulted from the attrition in the diet group, but they are probably an important factor to consider in assessing the results of this study.

Another problem with studying interventions like HAES counseling is that it is subject to significant observer bias. If you are studying, say, a drug, you can do a double-blind study where both the doctors who are scoring the outcomes of the study and the subjects themselves are unaware whether they are being treated with the drug in question or a placebo. If you are comparing two types of counseling that is obviously not possible. In these studies, it is possible that the HAES counselors were simply better or more enthusiastic than the counselors leading the control groups.

Clearly, many questions remain about HAES. A few things do seem to be consistent from study to study, though. There seems to be reasonable evidence that HAES improves self-esteem. Its effects on weight loss, binge eating, and other physical measures are less clear.

1. Ciliska D. Evaluation of two nondieting interventions for obese women. Western Journal of Nursing Research 20: 119-135, 1998.

2. Nauta H, Hospers H, Jansen A. One-year follow-up effects of two obesity treatments on psychological well-being and weight. British Journal of Health Psychology 6: 271-284, 2001.

3. Bacon L, Keim NL, Van Loan MD, Derricote M, Gale B, Kazaks A, Stern JS. Evaluating a "non-diet" wellness intervention for improvement of metabolic fitness, psychological well-being and eating and activity behaviors. International Journal of Obesity and Related Metabolic Disorders, 26: 854-865, 2002.

4. Bacon L, Stern JS, Van Loan MD, Keim NL. Size Acceptance and Intuitive Eating Improve Health for Obese, Female Chronic Dieters. Journal of the American Dietetic Association 105: 929-936, 2005.

Thursday, March 6, 2008

I take requests...

Just wanted to mention that while I do have a list of topics I eventually hope to cover here, I am also happy to write about things that people are curious about. So please feel free to post to the comments if there's something you have in mind!

John Godfrey Saxe neatly summarizes scientific inquiry

I've always thought that the John Godfrey Saxe poem Six Blind Men & the Elephant was a great metaphor for scientific inquiry.

You are probably familiar with the poem, but to summarize it, six blind men go to visit an elephant and each explores a different part of the elephant with his hands and comes to a different conclusion about what the elephant looks like. The first man feels the elephant's side and concludes that the elephant is like a wall. The second feels a tusk and concludes that the elephant is like a spear. The third feels the trunk and declares than the elephant is like a snake. The fourth feels the elephant's knee and declares the creature to be tree-like. The fifth touches the elephant's ear and says it is like a fan. And the sixth feels the tail and says it is like a rope.

Of course, they are all partially right and yet also wrong. Ideally, the next step would be for all six men to discuss their findings and to thereby collectively come to a broader understanding of the elephant. That obviously doesn't happen in the poem and it doesn't always happen in science, either. I think it also doesn't help that media accounts of science tend to focus on single studies rather than on the body of knowledge in a given field (news report: Elephants are like spears!).

I guess what I am really trying to say here is that while every study is limited in its scope, those limitations don't necessarily make a study "wrong." One particular example I encounter a lot in reading blogs is that people frequently critique epidemiologic studies (studies looking at behavioral and disease trends in large populations) by pointing out that correlation and causation are not the same thing. That is a fair enough point, but that doesn't mean that correlation is not a useful piece of information. It's often a great jumping-off point for further studies that may establish causation.

So, basically, it's a good thing to be aware of any study's limitations. But a limitation doesn't necessarily mean that the findings are invalid.

Friday, February 22, 2008

Recommended reading

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

I don't agree with absolutely everything Friedman says in the interview, but we're definitely on the same page with the quote above.

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'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.

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.

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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.