Monday, March 11, 2013

The 2013 PLoS ONE sugar and diabetes study: Sugar from fruits is harmless


A new study linking sugar consumption with diabetes prevalence has gained significant media attention recently. The study was published in February 2013 in the journal PLoS ONE (). The authors are Sanjay Basu, Paula Yoffe, Nancy Hills and Robert H. Lustig.

Among the claims made by the media is that “… sugar consumption — independent of obesity — is a major factor behind the recent global pandemic of type 2 diabetes” (). As it turns out, the effects revealed by the study seem to be very small, which may actually be a side effect of data aggregation; I will discuss this further below.

Fruits are exonerated

Let me start by saying that this study also included in the analysis the main natural source of sugar, fruit, as a competing variable (competing with the effects of sugar itself), and found it to be unrelated to diabetes. As the authors note: “None of the other food categories — including fiber-containing foods (pulses, nuts, vegetables, roots, tubers), fruits, meats, cereals, and oils — had a significant association with diabetes prevalence rates”.

This should not surprise anyone who has actually met and talked with Dr. Lustig, the senior author of the study and a very accessible man who has been reaching out to the public in a way that few in his position do. He is a clinician and senior researcher affiliated with a major university; public outreach, in the highly visible way that he does it, is probably something that he does primarily (if not solely) to help people. Dr. Lustig was at the 2012 Ancestral Health Symposium, and he told me, and anyone who asked him, that sugar in industrialized foods was his target, not sugar in fruits.

As I noted here before, the sugar combination of fruits, in their natural package, may in fact be health-promoting (). The natural package probably promotes enough satiety to prevent overconsumption.

Both (unnatural) sugar and obesity have effects, but they are tiny in this study

The Diabetes Report Card 2012 () provides a wealth of information that can be useful as a background for our discussion here.

In the USA, general diabetes prevalence varies depending on state, with some states having higher prevalence than others. The vast majority of diabetes cases are of type 2 diabetes, which is widely believed to be strongly associated with obesity.

In 2012, the diabetes prevalence among adults (aged 20 years or older) in Texas was 9.8 percent. This rate is relatively high compared to other states, although lower than in some. So, among a random group of 1,000 adult Texans, you would find approximately 98 with diabetes.

Prevalence increases with age. Among USA adults in general, prevalence of diabetes is 2.6 percent within ages 20–44, 11.7 percent within ages 45–64, and 18.9 percent at age 64 or older. So the numbers above for Texas, and prevalence in almost any population, are also a reflection of age distribution in the population.

According to the 2013 study published in PLoS ONE, a 1 percent increase in obesity prevalence is associated with a 0.081 percent increase in diabetes prevalence. This comes directly from the table below, fifth column on the right. That is the column for the model that includes all of the variables listed on the left.



We can translate the findings above in more meaningful terms by referring to hypothetical groups of 1,000 people. Let us say we have two groups of 1,000 people. In one of them we have 200 obese people (20 percent); and no obese person in the other. We would find only between 1 and 2 people with diabetes in the group with 200 obese people.

The authors also considered overweight prevalence as a cause of diabetes prevalence. A section of the table with the corresponding results in included below. They also found a significant effect, of smaller size than for obesity – which itself is a small effect.



The study also suggests that consumption of the sugar equivalent of a 12 oz. can of regular soft drink per person per day was associated with a 1.1 percent rise in diabetes prevalence. The effect here is about the same as that of a 1 percent increase in obesity.

That is, let us say we have two groups of 1,000 people. In one of them we have 200 people (20 percent) consuming one 12 oz. can of soft drink per day; and no one consuming sugar in the other. (Sugar from fruits is not considered here.) We would find only about 2 people with diabetes in the group with 200 sugary soda drinkers.

In other words, the effects revealed by this study are very small. They are so small that their corresponding effect sizes make them borderline irrelevant for predictions at the individual level. Based on this study, obesity and sugar consumption combined would account for no more than 5 out of each 100 cases of diabetes (a generous estimate, based on the results discussed above).

Even being weak, the effects revealed by this study are not irrelevant for policy-making, because policies tend to influence the behavior of very large numbers of people. For example, if the number of people that could be influenced by policies to curb consumption of refined sugar were 100 million, the number of cases of diabetes that could be prevented would be 200 thousand, notwithstanding the weak effects revealed by this study.

Why are the effects so small?

The effects in this study are based on data aggregated by country. When data is aggregated by population, the level of variation in the data is reduced; sometimes dramatically, a problem that is proportional to the level of aggregation (e.g., the problem is greater for country aggregation than for city aggregation).

Because there can be no association without correlation, and no correlation without variation, coefficients of association tend to be reduced when data aggregation occurs. This is, in my view, the real problem behind what statisticians often refer to, in “statospeech”, as “ecological fallacy”. The effects in aggregated data are weaker than the effects one would get without aggregation.

So, I suspect that the effects in this study, which are fairly weak at the level of aggregation used (the country level), reflect much stronger effects at the individual level of analysis.

Bottom line

Should you avoid getting obese? Should you avoid consuming industrialized products with added sugar? I think so, and I would still have recommended these without this study. There seems to be no problem with natural foods containing sugar, such as fruits.

This study shows evidence that sugar in industrialized foods is associated with diabetes, independently from obesity, but it does not provide evidence that obesity doesn’t matter. It shows that both matter, independently of one another, which is an interesting finding that backs up Dr. Lustig’s calls for policies to specifically curb refined sugar consumption.

Again, what the study refers to as sugar, as availability but implying consumption, seems to refer mostly to industrialized foods where sugar was added to make them more enticing. Fruit consumption was also included in the study, and found to have no significant effect on diabetes prevalence.

Here is a more interesting question. If a group of people have a predisposition toward developing diabetes, due to any reason (genetic, epigenetic, environmental), what would be the probability that they would develop diabetes if they became obese and/or consumed unnatural sugar-added foods?

This type of question can be answered with a moderating effects analysis, but as I noted here before (), moderating effects analyses are not conducted in health research.

16 comments:

Gretchen said...

Ned, Thanks for this.

1. Could you expand on the comment that "there can be no association without correlation" in a way that nonstatistics people like me can understand? Examples would be nice. Some people use the terms as synonyms.

2. Could you expand on the comment that "The effects in this study are based on data aggregated by country. When data is aggregated by population, the level of variation in the data is reduced."

I value your expertise, but I'm not a statistician and need simplified explanations.

3. The small effect of obesity is surprising. But in worldwide data, many things might explain this.

In the US, the fasting BG threshold for a diagnosis was reduced from 140 to 126 about a decade ago, thus suddenly increasing the incidence of diabetes. I suspect, although I haven't researched it, that in some countries diabetes is not diagnosed until it becomes obvious, as limited medical resources focus on other diseases like schistosomiasis, AIDS, and malaria. So there would be more cases of undiagnosed diabetes than in the US.

Also, in some countries like India, diabetes occurs at lower BMIs, where fat seems to accumulate internally without a large increase in weight.

Ned Kock said...

Hi Gretchen. On the issue of variation-correlation- association, the best example I can give is the strange “case” of the chain smokers:

http://bit.ly/a0fgep

Gretchen said...

Ned, I understand correlation vs causation. I don't understand correlation vs association. Was that a typo?

Ned Kock said...

I indeed meant to say association, because coefficients of association (such as path coefficients) rely on at least some correlation existing among variables. The former are usually lower in magnitude than the latter, but sometimes are be amplified due to competing effects.

George Henderson said...

Extrinsic and intrinsic sugars are the terms often used to differentiate added sugars from those in fruit and veges.

Ugur Gundogmus said...

It seems that sugar in fruits and vegetables are not problem. I wish there was a research about sugar in honey and maple syrup:)

Ned Kock said...

Another term that has recently been proposed, more commonly used in the context of carbohydrates in general, is “acellular”. So, you could have sources of sugar that are acellular and cellular, roughly corresponding to extrinsic and intrinsic, respectively.

If the sugar comes inside a cell, likely it will be from a natural source, such as fruit. At least for the time being.

dearieme said...

" I suspect, although I haven't researched it, that in some countries diabetes is not diagnosed until it becomes obvious": and in the UK my endocrinologist tells me that I am on the verge of being diagnosed as diabetic whereas in the US I would be firmly non-diabetic.

As you might guess, the UK diagnostic threshold was lowered a few years ago and GPs were given financial incentives to diagnose diabetes. So any diabetic stats coming out of Britain may safely be ignored unless you can be confident that both effects have been properly allowed for. Fat chance!

Ned Kock said...

Hi Ugur. I am not sure about maple syrup, but there is research on honey:

http://www.jacn.org/content/29/5/482.short

Gretchen said...

"If the sugar comes inside a cell, likely it will be from a natural source, such as fruit."

??? Fructose is fructose and glucose is glucose, regardless of where they come from. All sugars have to come inside intestinal cells in order to get into the bloodstream.

Gretchen said...

@Dearieme. What numbers were you given in the UK?

In the US, 100-125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes and 126 (7) and above is considered diabetes.

Note that numbers vary from day to day; a person could test 95 one day and 110 the next.

Ugur Gundogmus said...

Thank you very much for the link, Ned.

I always thought organic honey should not have the same negative effects of table sugar on our bodies.

Of course, we need more researches in order to have solid conclusions, but this research is good news for me.

dearieme said...

"I always thought organic honey should not have the same negative effects of table sugar on our bodies."

That is surely very unlikely?

What about fruit juice? Without the accompanying fibre of the fruit, it must presumably be as pernicious as table sugar? Which is to say, only a little pernicious.

Gretchen: my readings have wandered up and down from below 5.6 up to a highest of 6.5. There's a possibility that the recent readings are partly a side effect of a drug I'm taking for a different condition. (Whether or not it matters that a reading is partly a side effect I have no idea.)

Gretchen said...

@Dearieme. What numbers were you given in the UK?

What I meant was, what are the current UK cutoffs.

According to your own numbers, you'd be classified as prediabetic in the US, so either your endo is wrong or he didn't make clear what he meant.

dearieme said...

We don't have a class of "pre-diabetic" though he told me that was how I'd be classified in the US. He also said he thought it was a bogus classification, or at least a mislabelled classification, in the sense that most "pre-diabetic" patients do not go on to develop diabetes.

In Britain you go from non-diabetic to diabetic at 6.5. If you touch 6.5 and then fall away again (as has happened to me) your doctor will classify you as diabetic. It is popularly alleged that if you want to become non-diabetic you move to a different doctors' practice and hope that the medical records aren't forwarded properly.

You end up with the madness of my GP telling me "Formally you are diabetic and therefore always will be, although of course you're not really diabetic at all." I trust that is clear?

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