Diet seems to be all over the New York Times this week, with an oversell of the benefits of the Mediterranean diet, and now Mark Bittman, everyone’s favorite food scold, declaring sugar is the culprit for rising diabetes. His article is based on this interesting new article in PLoS One and begins with this wildly-inaccurate summary:
Sugar is indeed toxic. It may not be the only problem with the Standard American Diet, but it’s fast becoming clear that it’s the major one.
A study published in the Feb. 27 issue of the journal PLoS One links increased consumption of sugar with increased rates of diabetes by examining the data on sugar availability and the rate of diabetes in 175 countries over the past decade. And after accounting for many other factors, the researchers found that increased sugar in a population’s food supply was linked to higher diabetes rates independent of rates of obesity.
In other words, according to this study, obesity doesn’t cause diabetes: sugar does.
No! Not even close. I hate to repeat his misstatement, because I’d hate to reinforce this as a new myth, but it’s critical to see his full mistake here. This is a wildly inaccurate summary of the authors’ findings, and one they don’t even endorse in their discussion. Bittman has actually just said “obesity doesn’t cause diabetes”, and now has proven himself a deluded fool.
Let’s talk about this paper. This is what is called an “ecological study”, which means it studies populations as a whole, rather than individual patients. Using data from the United Nations Food and Agricultural Organization, the International Diabetes Federation, and various economic indicators from the World Bank, the authors compared populations of whole countries, in particular the prevalence of diabetes correlated to other factors such as GDP, urbanization, age, obesity, and availability of certain varieties of food like sugar, meat, fibers, cereals and oil. Using the rise, or fall, of diabetes prevalence over the last decade in various countries, they correlated this increase with increasing availability of sugar, obesity, urbanization, aging populations etc., and found a few interesting things. For one, increases in GDP, overweight and obesity, tracked significantly with increasing diabetes prevalence. But interestingly, when those factors were controlled for, increasing availability of sugar also tracked linearly with increasing diabetes prevalence, and the longer the duration of the exposure, the worse it got.
However, this does not mean that “obesity doesn’t cause” diabetes, if anything, it’s further support for the exact opposite. While a correlative study can’t be a “smoking gun” for anything, the data in this paper supports increasing modernization/GDP, obesity, and sugar availability are all correlated with higher diabetes prevalence. Even if the sugar relationship is causal, which is no guarantee, the increase in sugar availability could only explain 1/4 of the increase in diabetes prevalence. Obesity is still the main cause of diabetes, which can be demonstrated on an individual level by increases in weight resulting in loss of glycemic control, and subsequent weight loss results in return of euglycemia. In particular, the results of studies of bariatric surgery, in both restrictive and bypass procedures, weight loss is accompanied by improvement in diabetes. The attempts of toxin paranoids like Bittman to reclassify sugar as a diabetes-causing agent, and to dismiss obesity as a cause, are highly premature.
Mother Jones, has a slightly more balanced read, but it still oversells the results.
This is a correlation, of course, and correlation does not always equal causation. On the other hand, it’s an exceptionally strong correlation.
Well, that’s another overstatement. Want to see a picture?
I wonder what the R-squared is on that line fit. Now, consider a comparison with obesity rates by diabetes prevalence:
Hmm, they didn’t fit a line here, but I can bet the fit would be better. Diabetes strongly correlates with BMI, this has been shown time and again using national survey data like NHANES or SHIELD. And before people start whining about BMI as an imperfect measure of obesity, it is perfectly appropriate for studies at a population level, and other metrics such as waist size, hip/waist ratios etc., all show the same thing. Diabetes risk increases linearly with BMI, with as many as 30% of people with BMI > 40 having diabetes, and further, we know from cohort and interventional studies that weight loss results in decreased diabetes. Much of this data is correlative as well (with the exception of the weight-loss studies), and the study that would prove this for certain – dividing people into diets providing excess fat, vs sugar, vs mixed calories, vs controls, with resultant measurement of diabetes rates, would be unethical. Either way, declaring sugar the enemy is both incomplete, and premature. While this paper provides interesting correlative evidence for increased sugar availability increasing diabetes prevalence, it is still subject to risk of confounding errors, it is correlative, and the link does not explain away other known causes of type II diabetes such as obesity. It is a warning however, and we should dedicate more study towards determining if sugar consumption (rather than mere availability) is an independent risk factor for type II diabetes.
Bittman has wildly overstated the case made by this article. He should retract his claims, and the title and false claims should be corrected by the editors. This is a terrible misrepresentation of what this study shows.
42 thoughts on “No, It's Not the Sugar – Bittman and MotherJones have overinterpreted another study”
Have you considered that T2DM and obesity might share a common cause?
I wonder, is there something we eat that we didn’t have the evolutinary time to adapt to?
*Cough* Industrially produced seed oils *Cough* Omega-6 fatty acid over-consumption *Cough*
What do I know about n-6 metabolism that the good doctors don’t? It must be lust and gluttony, as your studies show.
Personally I think studies that ignore evolutionary changes in our nutrition and attribute diseases to christian sins are not to be trusted (probably a bit of confirmation bias in them) – but then again, you are the doctor, not me.
Forgot to through in heart disease for good measure:
I wonder, is it possible that the advise regarding healthy nutrition handed out by doctors is contra-factual to reality, and that the good doctors have a hard time adjusting to reality (read: being in denial of their deadly advises of the past)?
Of course, telling people to eat stuff that causes disease, and then telling people to try to eat less overall will help somewhat – if you eat less, you eat less of the stuff that causes disease.
So I call it a win for the medical industry and a win for the agricultural industry! Hey, who doesn’t love somebody who creates jobs!
“Have you considered that T2DM and obesity might share a common cause? ”
“I wonder, is there something we eat that we didn’t have the evolutinary time to adapt to?”
Yes, an overabundance of calories. And evolutionary adaptation is largely irrelevant. These diseases of obesity kill us largely after we’ve grown up and reproduced. There’s not going to be a strong pressure to prevent obesity or diabetes in your 40s in 50s from an evolutionary perspective. Your concern that I’m trying to punish Christian sin is absurd, and proposed evolutionary inputs to diseases of the middle aged and elderly – when the T2DM patients croak, aren’t meaningful. Evolution doesn’t care if you die after you’ve had and raised your kids.
Well, since it’s doctors doing these studies and uncovering these problems, this doesn’t make a whole lot of sense. This is an interesting study, and frankly, more compelling than the Mediterranean diet study from the NYT this week since it shows safflower oil rich in the lineloic acid increased all-cause mortality in a population of patients that had had previous cardiac events. This would actually make me change my practice before the NEJM paper would. Nutritional recommendations are hard, and there isn’t a lot of high-quality RCT data out there. Much of what we do is infer from epidemiologic evidence, and true, we often but not always, find errors, when advice is subsequently studied by RCT. I’m actually trying to discourage a similar mistake with overinterpretation of this paper here.
What does this have to do with sugar again? I’m confused.
At no point do I suggest people eat more sugar, or gain weight. People, do not eat more refined sugar or gain a bunch of weight. The dispute with Bittman here, is that he actually claims obesity doesn’t cause diabetes, on incredibly weak data about sugar availability. His claims are far in the excess of the data. Do I think people should shovel refined sugar into their maws? Of course not. But I still think, even considering the results of this study, the excess intake of sugar and obesity are related to diabetes because they both increase obesity rather than some direct “sugar toxicity”. These data are suggestive of a role of sugar availability independent of obesity on T2DM, but they are not proof of a direct link. Even if this were causal evidence, the sugar availability could only explain 1/4 of the increasing prevalence.
Relevant here: from the NIDDK website:
The Diabetes Prevention Program (DPP) was a major multicenter clinical research study aimed at discovering whether modest weight loss through dietary changes and increased physical activity or treatment with the oral diabetes drug metformin (Glucophage) could prevent or delay the onset of type 2 diabetes in study participants. At the beginning of the DPP, participants were all overweight and had blood glucose, also called blood sugar, levels higher than normal but not high enough for a diagnosis of diabetes—a condition called prediabetes.
The DPP found that participants who lost a modest amount of weight through dietary changes and increased physical activity sharply reduced their chances of developing diabetes. Taking metformin also reduced risk, although less dramatically. The DPP resolved its research questions earlier than projected and, following the recommendation of an external monitoring board, the study was halted a year early. The researchers published their findings in the February 7, 2002, issue of the New England Journal of Medicine.
While Bittman may have used words that weren’t in the paper, I’m sure study author Robert Lustig was more than happy to see it happen. He’s made a living out of demonizing sugar, and like a Tea Party politician being more beloved the more he gets criticized by everyone else, the more Dr. Lustig is criticized is (to him and his followers), more proof that he is right.
He’s offered studies of sugar in rats, despite known metabolic differences between rats and humans. He’s offered humans ingesting astronomical amounts of sugar which he extrapolated to demonize any amount of sugar for the entire population, and now it’s a population-wide correlation study that lends itself perfectly to overgeneralization by people like Bittman.
In fact, here’s Lustig himself in the Huffington Post:
“Up until now, scientists have shown that sugar is ‘assoicated’ or ‘correlated’ with various chronic metabolic diseases…But correlation is not causation.
Which direction do the data go? Does sugar cause obesity and metabolic disease? Or do obese people with metabolic disease drink soda? You can’t tell, because you only have one point in time – the snapshot, not the movie. In the February 27 issue of the journal PLoS One, my colleagues…and I put this issue to rest, because we now have the movie.
Bottom line – only changes in sugar availability explained changes in diabetes prevalence worldwide, nothing else mattered”.
Hmmm, sounds suspiciously like “sugar causes diabetes”. If this is what the author of the study is going to write about it, are you really surprised that a journalist like Bittman is going to echo it? Lustig should be the one retracting his claims.
Wow. That is also an overstatement. This is by no means “put to…rest”, nor did “nothing else matter”. Obesity mattered. GDP mattered. Other factors were in play in their own data. It is interesting that sugar availability correlated, but it wasn’t consumption.
This needs to be followed by a real cohort study showing sugar reduction, and not calorie reduction, creates a difference in diabetes development in an at-risk or overweight population.
And thanks for that reference Jane, it’s another good one.
> Bittman has actually just said “obesity doesn’t cause diabetes”, and now has proven himself a deluded fool.
Wouldn’t it be a bit hasty as a generalization?
While I can understand that overeating causes diabetes, I am not sure how obesity can. Overeating is an activity, while obesity is a state. Something’s amiss at the conceptual level, the level where talk about causality is supposed to be.
Besides, Lustig’s more general point is that eating sugar will make you overeat. Isn’t that obvious enough?
Why can’t a state cause diabetes?
The state of obesity is one of hyperinflammation, endocrine changes, dyslipidemia, etc., if you eat a ton of calories, and exercise at a level to consume that energy, you don’t get diabetes. It’s not the intake, it’s the imbalance, over a prolonged time, that creates a disease state.
If you’re obese, and you lose weight, your diabetes gets better, ceases to progress etc. Obesity is the overwhelming cause of the majority of cases of diabetes. To say otherwise is to ignore an extensive scientific literature, as well as the results of the paper he cites in the article.
It is foolish. It’s irresponsible. It’s factually incorrect.
> Why can’t a state cause diabetes?
Because the state is not enough to guarantee a mechanism. Hence the need to add something like:
(1) It’s not the intake, it’s the imbalance, over a prolonged time, that creates a disease state.
Notwithstanding the overselling and the moral castigation from all sides, I believe everyone can agree on (1). It’s easier to debate the metabolic stuff (i.e. how the imbalance plays a role) when putting (1) on the table. Sticking to “obesity causes diabetes” ain’t even correct, since not all obeses get diabetes. Causality is best left as a bait for the concern troll industry, specialized in dismissing any evidence as inconclusive and demanding more data.
If we really wish to pay due diligence to overstatements, I’d like you to retract your bit on Bittman on “proving himself a deluded fool” on the grounds of parsing one sentence from an op-ed. This has not been addressed, and this seems to matter to those who’d invoke foolishness, irresponsibility, and factual incorrectness.
No, I am not asking you to retract anything. I’m just showing the absurdity of such editorial stance.
It’s only absurd if you ignore everything we know about obesity.
Fat is an endocrine organ. A hypertrophy of that organ has specific metabolic effects. To dismiss it as a “state” and therefore not responsible for physiologic effects makes no sense. Obesity is a cause of negative physiologic effects. Just because it doesn’t cause diabetes 100% of the time, doesn’t mean it isn’t a cause. Cigarettes don’t cause cancer 100% of the time, but they are a cause.
Your arguments don’t make sense. Bittman is a fool.
Update: It should be noted Bittman has changed (or the editors have changed) his statement from the foolish “obesity doesn’t cause diabetes” to “obesity also is a cause”, although it would have been better to say it’s the main cause. I won’t be retracting my statement calling him a fool any time soon, as it looks as though the NYT editors have backed me up, and posted a correction on his misstatement.
Lovely article, Mark.
I think the data of sugar on visceral fat is very clear as explained on the first sentence of the paper:
“While experimental and observational studies suggest that sugar intake is associated with the development of type 2 diabetes, independent of its role in obesity”
> Fat is an endocrine organ.
We can admit “adipose tissue is an endocrine organ”  without reaching to a concept of obesity defined by a measure which is, as you yourself admit, more appropriate “for studies at a population level”. At the population **level**, we don’t have access to the adipose tissue of the individuals: all we have some abstract measure defined by the BMI, which should be revised according to the authors according to ethnicity.
In any case, I’m not dismissing the information that provide such abstract states. What I’m saying is that it can only **indicate** the drivers at the individual level, which might never be subject to a decisive inference, since, as you say:
> [T]he study that would prove this [Diabetes risk increases linearly with BMI, I gather] for certain – dividing people into diets providing excess fat, vs sugar, vs mixed calories, vs controls, with resultant measurement of diabetes rates, would be unethical
In other words, to talk about causality is a double-edge sword here, a point I don’t think Bittman’s alleged delusion won’t dispel.
But to return to Bittman’s delusion, I believe the topic his claim is introduced in the first sentence of the article’s abstract (with emphasis):
> While experimental and observational studies suggest that sugar intake is associated with the development of type 2 diabetes, **independent of its role in obesity**, it is unclear whether alterations in sugar intake can account for differences in diabetes prevalence among overall populations.
Bittman does seem to misread the article, as the emphasized text shows. But one has to admit that every sentence from the abstract hints at the fact that they’re saying that people’s size of their “fat organ” might not be the main driver of diabetes at the population level. And it continues all along the text of the article, for instance:
> In countries like the Philippines, Romania, Sri Lanka, Georgia and Bangladesh, where high and rising diabetes rates were observed in the context of low obesity rates, sugar availability rose by over 20% during the study period.
Of course, this is only at the population level, but the authors also mention that, at the individual level:
> About 20% of obese individuals appear to have normal insulin regulation and normal metabolic indices (no indication of diabetes) and normal longevity , while up to 40% of normal weight people in some populations manifest aspects of the “metabolic syndrome” –.
Perhaps this does not mean that obesity does not cause diabetes, and only that it is not the main driver, at least according to these authors. The last quote should at least raise some issue about the confidence by which one can claim that obesity causes diabetes. Perhaps we should take a bite at the references being handwaved by the authors (their 8-12) instead of biting a foodist.
I don’t think Bittman’s punchline provides sufficient evidence to conclude delusion, and even if it did, I don’t think it would justify having to read more bloggers with bad attitudes.
Then these authors would be wrong, and in conflict with the overwhelming majority of the literature, and their own paper. Sugar availability, after all, only explained 1/4th of the excess diabetes prevalence, making it a minority driver.
Obesity is the main cause of diabetes. I’m sorry if you think that my attitude is bad, but given the wildly incorrect position Bittman initially staked out, I saw it not only as wrong, but dangerous. It appears the NYT editors agreed it was worth correction.
A good review in the Lancet I think summarizes most of what we know of the pathogenesis of type II diabetes. It’s a combination of genetic and lifestyle factors, and there is an extensive literature on the effects of excess adipose tissue on creating a hyperinflammatory state, secretion of cytokines, insulin resistance, and even direct “adipotoxicity” with adipose tissue secreting factors directly inhibiting pancreatic b cell function. The cornerstone of diabetes prevention, however, remains the prevention of obesity, as we know that patients who are obese that increase exercise and decrease weight are able to improve insulin resistance, delay progression of disease as well as diabetic comorbidities such as diabetic retinopathy and nephropathy.
It could be that ready availability of sugar, in addition to increasing weight gain, also worsens incipient type II diabetes, as we know that improved hyperglycemic control is key to preventing diabetic comorbidity and progression of disease. I’m not ruling out that sugar aggravates type II diabetes at all, the PLoS paper is quite suggestive that having too much sugar around is worsening the disease, and it’s another warning sign we need to avoid excessive sugar intake such as with sugary beverages. But to suggest that obesity and obesity prevention should be anything but the central goal of diabetes prevention is unfounded, and contradictory to the literature.
You left out “glucose toxicity” as discussed in the Lancet paper that you cite.
“You left out “glucose toxicity” as discussed in the Lancet paper that you cite.”
The glucose toxity referred to is not exogenous glucose but ones’ own hyperglycemia causing damage itself. And I actually didn’t leave it out, I just didn’t call it by name when I said:
I think a hypothesis that could make the two factors fit is that increasing sugar availability could also aggravate the progression of diabetes and make it more apparent.
Glad to see that Bittman corrected his op-ed.
Here’s how the authors set up the quandary:
> The issue of whether added sugars may be a population-level driver of the diabetes pandemic is of importance to global health policy. If obesity is a primary driver of diabetes, then measures to reduce calorie consumption and increase physical activity should be prioritized. However, if added sugar consumption is a primary driver, then public health policies to reduce sugar consumption warrant investigation as diabetes prevention proposals—especially for developing countries where diabetes rates are rising dramatically, irrespective of obesity.
Regarding that issue, here’s what the authors conclude:
> We found that obesity appeared to exacerbate, but not confound, the impact of sugar availability on diabetes prevalence, strengthening the argument for targeted public health approaches to excessive sugar consumption.
Putting the two together and applying modus tollens does seem to make us infer that the main driver of diabetes, at the population level, might not be obesity. This might not be what the authors should conclude from their own study, but it does look to me that it’s what they are conveying.
Even if they were right in saying so, I don’t think the issue should be phrased like a dichotomy. Both eating too much sugar and overeating in general are important causes for diabetes on the personal level. Obesity is still a good predictor for diabetes at the population level, even if sugar availability may be seen (by some) as a more appropriate indicator in the end. My own opinion on this is that, instead of focusing on the alternative, I’d rather welcome a way to integrate both lines of investigation, i.e. how eating too much sugar can lead to overeating, while trying to make sure that the personal and the population levels are not confused, which was my point about causality.
Thank you for the Lancet reference.
PS: Sorry about the typos and all — first life keeps getting in the way.
Mark, interesting column. I personally agree that Bittman overstated the significance of this study, relying way too heavily on observational evidence to make his case — a rookie mistake. Personally I prefer to wait for all the evidence to come in before making any bold claims.
But I have a question for you. You state that “obesity is the overwhelming cause of the majority of cases of diabetes,” and that losing weight reverses the disease. But research on obese diabetics who undergo bariatric surgery shows that in many cases, the resolution of their diabetes precedes their weight loss. These subjects also show rapid changes in their levels of gut hormones — caused very likely by the radical rearrangement of their bowels.
I’m curious, what do you make of these findings. How do they fit in with what you’ve written above? Thank you, and as I said before, great blog.
“Even if they were right in saying so, I don’t think the issue should be phrased like a dichotomy.”
Exactly. I don’t know how you can separate sugar over consumption from obesity since the former almost always leads to the other.
In response to Mark’s comment #19. Glucose is glucose. The body does not distinguish from dietary glucose spikes endogenously synthesized.
Here’s a piece from a few years ago (complete with 400 comments, and a link to a recap of the comments in case you don’t want to read all of them) that dives into claims made by Dr. Lustig (and widely repeated by people like Bittman, Gary Taubes, Mother Jones, etc)
“In response to Mark’s comment #19. Glucose is glucose. The body does not distinguish from dietary glucose spikes endogenously synthesized.”
Yes, but in the absence of insulin resistance, glucose levels in the body are tightly regulated. Even if you eat a big dose of sugar, that is rapidly stored into tissues by insulin release. Glucose toxicity will not occur just because you eat some sugar, because the healthy body will manage it just fine. In the diabetic, however, either type I or type II, you no longer respond to glucose effectively, and the levels rise in blood. Elevated blood glucose then creates a variety of responses in tissues, from immune suppression (inhibition of macrophage function for instance) to the direct b-cell toxicity described in those papers, to acidosis and ketosis as seen at the extreme end of “glucose toxicity”.
This, of course, doesn’t mean that glucose that you ingest is toxic. Far from it, it’s a molecule your body uses every day, synthesizes itself, etc., for energy, and the predominant source of energy for the human brain. And in a healthy person, glucose ingestion is handled without harm. It’s only in the context of absence of insulin, or insulin insensitivity that levels of glucose are dysregulated, with subsequent injury to tissues and altered physiology.
This effect is interesting, and is limited to the Roux-en-Y gastric bypass where the stomach is basically separated from the duodenum, so there isn’t direct gastric emptying into the part of the duodenum where the pancreas excretes it’s enzymes etc. There is some interruption of the normal signalling that has a beneficial effect, very rapidly after surgery, without weight loss. We don’t understand exactly what’s happening yet.
However, other procedures, such as restrictive procedures (lap bands) that simply constrict the stomach without actually rearranging the bowels also result in improved glucose tolerance with concomitant weight loss. Patients undergoing these procedures typically lose a large fraction of their total body weight, and the effects this has in terms of risk modification make it worthwhile in terms of improved diabetes, dyslipidema etc., and in some of the time series now showing the effects out 10 and 15 years, a decreased mortality rate in the surgerized cohorts.
So both types of bariatric surgery work on diabetes, but we don’t know exactly where the immediate effects in the Roux-en-Y come from. It’s certainly not from prevention of sugar intake, if anything, that’s the one way patients can sabotage these surgeries and maintain their weight – drinking lots of sugary beverages…
Sam Wang puts it best:
@SamWangPhD: True causation indicated by strong correlation: across 175 nations, sugar intake predicts diabetes as no other food http://t.co/woXjBbeMxt
Wow, another idiotic statement, good find. “True causation indicated by strong correlation” might be the stupidest thing I’ve heard in this thread. It’s also not that strong a correlation (please take another look at figure 2 and tell me what the statistics are on that line) , and it’s not even consumption, merely availability. We have no idea on an individual basis what’s happening here. Just repeating yourself over and over again, doesn’t make you right.
“The state of obesity is one of hyperinflammation, endocrine changes, dyslipidemia, etc.”
Er no. Obesity is having too much body fat, with BMI as a popular measure. What you describe seems to be a state of metabolic disorder which is measured with indicators taken with blood tests. Obesity is clearly a symptom—but a cause? In the way a rash or a fever isn’t usually considered a cause when trying to cure an illness, I don’t see why obesity should be.
Why don’t you read the review Cvrai, rather than just drive-by dumping on all science about obesity? There is a significant amount of science behind the effect of obesity on health, and excess fat is like hypertrophy of a great big endocrine organ. On it’s own it has specific physiologic effects. Read first, then try again.
Why not dump on all science about obesity? If anything what needs to be appreciated is how poor it is relative to where it should be and where most people would probably expect it to be. Aside from an insipid generality like “one should try to avoid being obese” what well-grounded advice does the scientific literature offer?
You take Bittman to task for over-interpreting the effects of sugar but your own comments on obesity lack precision. You describe obesity as a host of symptoms yet there is another term in use: metabolic syndrome. Why have the term metabolic syndrome if obesity fully captures the same meaning? Perhaps in casual conversation the distinction need not be made but it is made in the journals because there is one. Considering how dietary advice has repeatedly gotten ahead of itself I will take issue with any supposed negative assertion of the “effect of obesity on health” absent clear reference and context. Do you already forget the study a short time ago showing that slightly greater BMI than normal was actually beneficial?
Obesity certainly remains a risk factor for T2D and Bittman certainly shouldn’t have said that it doesn’t. However, in addition to epidemiological data to support the idea that sugar intake is a risk factor independent of obesity/overweight, we also have data from animal studies and cell and molecular biology. And as I understand it, these data do support the idea that excessive fructose consumption appears to have uniquely terrible effects on plasma TGs, fatty liver, and insulin resistance vs. a high-calorie diet alone. I agree (and the authors of the study appear to as well: see http://epianalysis.wordpress.com/2013/02/27/sugardiabetes/) that a RCT is really what’s needed here, but I also think at this point in time there is already a pretty strong argument that fructose-containing sugars help to precipitate (or have a synergistic effect on) what we think of as “metabolic syndrome.”
Metabolic syndrome and obesity are not the same and the effects are not the same. Obesity is certainly a risk factor for metabolic syndrome but many patients have metabolic syndrome despite a normal body weight/body fat. The effects I described in the Lancet article linked above are specific to excessive adipose tissue. They are the direct effects of adipose tissue on the body, and they present a plausible mechanism for excess adiposity to predispose an individual to diabetes, metabolic syndrome, etc. They do not capture the same meaning at all. Further, we have specifically discussed those BMI studies here at denialism blog, and they are not relevant. Being a higher-than-normal BMI was indeed, not that different to a normal BMI, but being obese (BMI > 30) unquestionably increased risk, and with a dose-response relationship linearly showing increasing risk with increasing obesity after that point. The mistake being made here is assuming excess adiposity, on it’s own, does not have a negative physiologic effect. The data is pretty clear, adipose tissue is not inert, and an excess has specific, and negative, impacts on the physiology of multiple tissues.
There is no evidence that obesity (BMI > 30) is healthful, even if overweight (BMI 25-30) isn’t worse than normal (BMI 18-25). Granted, a physician and a patient may need to determine in an individual case if a high BMI appropriately describes the individuals state, as some people people can have a BMI despite very low bodyfat (body-builders, atheletes, etc.), but on a population level, and for most people, the measure is appropriate. The relation of BMI to mortality is a J-shaped curve, increasing on the extreme low end, and on the high end. Anorexia, is very dangerous, BMI about 22-27 captures the majority of the bottom of the J, with linearly increasing mortality with BMI higher than 30.
Since we know that most diets don’t work, weight loss is extremely difficult, and bariatric surgery (the one reliably effective intervention) is both risky and expensive, the best advice to give is prevention, and public health measures to avoid the development of obesity in the youth.
This, of course, could reasonably include measures against the availability of highly-refined sugars, sugary beverages and high calorie snacks directed at children, sold in schools, advertised on tv etc. I don’t entirely disagree with Bloomberg’s campaign against refined sugars period. These foods have the potential to cause wildly increased calorie consumption and really are a public health menace. I don’t drink them, and I wouldn’t let my kids drink them. But I think the main goal should be increasing funding for programs designed to prevent obesity at a young age, teaching kids how to eat healthy, and incorporating exercise into their daily regimen. Kind of what Michelle Obama travels around doing, it’s important, and the awareness of child obesity may be having an effect as we are starting to see a decline in child obesity in some locations. Primary prevention is the most important strategy, just like preventing people for starting smoking is one of the most important strategies for preventing lung cancer. Get them while they’re young.
For those that are already obese, the focus should be on risk-modification, control of hypertension, hyperglycemia, dyslipidemia, exercise, and ideally a weight-loss regimen. It should be emphasized that exercise, even without weight loss, can be beneficial. For the morbidly obese, and extremely obese (BMI > 45 for instance), interventions like bariatric surgery should probably be considered if a weight loss regimen is not successful, and the patient has significant morbidity as a result of their excess weight.
Is that more complete?
Patrick, I agree but statements like “it remains a risk factor” are still misleading. Obesity is the primary risk factor. We have data from plenty of animal studies, whole human studies, physiology etc., creating a direct link between adipose tissue and endocrine dysfunction. Don’t get me wrong, I don’t think we should be eating refined sugars except in extremely limited amounts. No one should be living on deserts or treats. And we should accept that food items like sugary-beverages are a public-health disaster. That doesn’t change the fact that the primary prevention of type 2 diabetes must remain obesity. I don’t disagree with the goals of the anti-sugar people, since I think these foods are wildly overconsumed, but if your BMI is 40, and you cut out the sugary sweets, don’t expect to avoid diabetes, dyslipidemia, hypertension, etc.
The graph in the article shows the U.S. with an obesity prevalence (BMI >= 30) of 46%. The correct number is 36% according to WHO and the CDC. The 11% diabetes prevalence shown in the graph is correct.
You’ve got a sharp eye Mark, I left a comment at PLoS asking for a clarification. It actually appears several of the obesity rates for those countries are skewed higher, and I’m not sure why. I queried the database they used as the source for several countries and got a different result every time. Maybe they have a more updated source? Maybe they’re looking a subgroup that wasn’t clear from the methods? I’m sure they’ll let me know, I hope I’m not misreading it, but I agree, those figures are way off.
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Mark Caplan. After an extensive back-and-forth with the lead author I figured out why there is such a discrepancy between the CDC numbers and the reported obesity on the x-axis. The authors used WHO estimates of obesity, which appear to be calculated based on previous survey results. There is a 2005 citation attached to the database that supposedly explains the estimates, but I can’t find the actual citation in pubmed. So I have no idea how they came up with them. But yes, US obesity is closer to 36%, not 45%, as the figure would suggest. In general the estimates are a great deal higher or lower than measured values from surveys, and in some cases appear to be extrapolated from some truly ancient data, so their use, to me at least, is strange. Those trying to make sense of the y-axis, by the way, would be better served using an older IDF atlas (4th edition) as the updated edition shows wildly different values for many of the data points, including Sri Lanka and New Zealand, the examples used by the authors in their introduction to suggest a divergence between diabetes and obesity.
In other words, because they used estimates and an old atlas they found Sri Lanka’s obesity to be 0.1%, and diabetes rate to be 10%. Using survey data and newer atlas data these values become 4% and 7%, much more reasonable frankly. Similarly, New Zealand, their other example has an increase in obesity from about 17-24% with a slight increase in their diabetes rate from 8-9%, rather than a decrease from 8 to 5%. I think this kind of turns over their “divergence” examples.
Ive taken another look at portions of the data used in the analysis. While the sugar correlation holds up, it is somewhat sensitive to which measure of diabetes is used, whether data are weighted, and whether population size is controlled. It also depends on whether you look at only mean effects or at other points in the distribution http://jaysonlusk.com/blog/2013/3/6/does-sugar-consumption-drive-diabetes
That’s really interesting Jason. Between your analysis and a closer examination of the starting data set – these “estimates” which appear totally invalid when compared to actual survey data of obesity – I might have to just totally dismiss the importance of this paper. Depending how you weight x, y, or z, the effect is either up or down, depending on which comparative estimate the effect exists or not. I think I might just have to conclude GIGO on this one.
There are some glaring examples that the findings in the PLoS study are meaningless. Australians have seen a tripling of diabetes prevalence over the past 30 years. Over the same timeframe, added sugars intake actually went down substantially according to FAO/WHO per capita food consumption statistics (the same database used by the authors of the article).
Nice article…Regarding obesity rates, based on state assessments in the U.S., the mean obesity rate is less than 30% I think, with only about 12 states having rates > 30%. Cheers — Mark
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