Science and Law
19th March 2013

The Science of Sugar and Obesity

Is sugar making America fat? It seems that this is a rampant theme in the popular media, and thus, deserves a close inspection of the science. After all, even scientists appear to agree that obesity is a complex disease, with a multitude of factors contributing to its etiology.

The Science of Sugar and Obesity

Is sugar making America fat? It seems that this is a rampant theme in the popular media, and thus, deserves a close inspection of the science. After all, even scientists appear to agree that obesity is a complex disease, with a multitude of factors contributing to its etiology. And the magnitude of the problem cannot be ignored – according to The WHO, in 2008 more than 1.4 billion adults, 20 and older, were overweight (of these over 200 million men and nearly 300 million women were obese), and more than 40 million children under the age of five were overweight in 2011.

It is also useful to lay out some basic definitions related to sugar. Sucrose (commonly referred to as table sugar) and high fructose corn syrup (HFCS) consist of 2 molecules, glucose and fructose. When linked together in a chain (polymerized), glucose forms starch (which is not considered very sweet), and has a high glycemic index and generates an insulin response. Fructose on the other hand, is present in fruits, and does not generate an insulin response.

ETIOLOGIES OF OBESITY

Regrettably, distilling the obesity epidemic down to one component – sugar – may not give this topic the serious attention it requires. As noted, one only needs to scratch the surface to get lost in the complexity of obesity. It is driven by a number of factors, including genetics (single genes or polygenic), lifestyle choices, psychological (e.g. stress), exposure to environmental chemicals, and socioeconomic factors, among others.

Overall, it is not clear that the scientific community understands the underlying causes of obesity. Nevertheless, when one assesses the history of obesity, the one factor that is consistently linked to weight gain is total caloric intake, and not simply to “sugar”. Indeed, as a percentage of total calories, “added sugar” consumption has been flat or decreasing in the US during the obesity epidemic.  A recent study by Welsh and colleagues demonstrates that older trends of increased added sugar intake have since leveled off and dramatically declined.  Welsh and colleagues report that the absolute intake of added sugars in the US decreased from 100.1 g in 1999-2000 to 76.7 g in 2007-2008, a decline of 24%.

Indeed, according to an assessment by White (and consistent with the data from Welsh and colleagues), added sugar as a per cent of total calories has been declining for quite some time. In a recent article by Hill, the concept of energy balance was discussed, whereby the author notes that “reducing obesity requires modifying both energy intake and energy expenditure, not simply focusing on either alone. Food restriction alone will not be effective in reducing obesity if human physiology is biased toward achieving energy balance at a high energy flux (i.e. at a high level of energy intake and expenditure).”

MECHANISTIC CONSIDERATIONS

At a very high level, a primary role of adipocytes (fat cells) is to store energy and release it when needed, whereby the energy storage occurs in the form of triglycerides (fat molecules). But how has sugar been posited to set the foundation for obesity? A number of theoretical mechanisms have been forwarded (both on regulation of appetite and biochemical):

1) Fructose may not cause the level of satiety equivalent of a glucose-based meal

2) The sweetness of fructose or sucrose makes food more palatable

3) Fructose may slow the basal metabolic rate, as well as generate excess fat molecules, increased oxidative stress, and uric acid levels.

In a recent publication by Tappy and Le, the authors review two potential mechanisms for why fructose may elicit lower-short-term satiation than equivalent doses of glucose (or starches): 1) fructose has a 5x lower glycemic index compared to glucose, and therefore fructose will elicit a lower glycemic response compared to an equivalent amount of glucose ingested; and 2) a meal with fructose stimulates less suppression of the hormone ghrelin, and less increase in the satiety hormone leptin than a meal containing an equivalent amount of glucose.

With respect to palatability, this has long been discussed in the literature, including Dr. John Yudkin in his 1967 American Journal of Clinical Nutrition publication. Yudkin noted that once man learned how to separate  nutrition from palatability in foods, it gave way to “greater availability of naturally preferred foods coincided with the ability of man to make quite new foods that were also highly palatable”; the extraction of sugar being an example he uses.

As for a biochemical mechanism, a vast number of studies exist, with an equally large number of proposed mechanisms including increased oxidative stress, uric acid levels, mitochondrial effects, and increased fat generation, to name a few. In a recent review article by Lustig, a researcher that has called on the government to regulate sugar in a similar fashion to alcohol, he compares the metabolic actions of fructose with those of glucose and alcohol to try to illustrate his thesis that fructose is “alcohol without the buzz.” And it is commonly thought the fate of glucose is decided in the liver (i.e. for storage, use it for energy, or convert it to triglycerides), whereas fructose enters the liver, and is preferentially metabolized to fat (See Elliott et al.). For a good review of some of these mechanisms, please refer to the Tappy article.

Importantly however, these proposed mechanisms remain in the theoretical domain. Despite the vast research activities that have been ongoing in this area for decades, the greatest limitation has been that the effects of fructose have almost been exclusively conducted in animals, and even as Lustig concedes: “… mechanistic data in humans are difficult to obtain….”

RECENT SCIENTIFIC FINDINGS

If these theories are correct, shouldn’t we see a direct effect on obesity? In fact, when tested, sugar does not appear to explain obesity alone. In addition to the complexity of obesity (as described earlier), in a recent blog post, we noted new data by Lustig (also reviewed in the NYTimes) that suggests “…sugar should be investigated for its role in diabetes pathogenesis apart from its contributions to obesity,” since he describes his data as showing an effect from sugar on diabetes, independent of obesity. But of course the ecological nature of the study renders it susceptible to multiple limitations that are discussed in the article.

In regard to obesity, a very recent systematic review and meta-analyses of cohort studies and randomized trials, the authors conclude that intake of sugars is a determinant of body weight (in free living people consuming ad libitum diets), and “The data suggest that the change in body fatness that occurs with modifying intake of sugars results from an alteration in energy balance rather than a physiological or metabolic consequence of monosaccharides or disaccharides. Owing to the multifactorial causes of obesity, it is unsurprising that the effect of reducing intake is relatively small.” Another meta-analysis found no effect on reducing BMI from sweetened beverages. The authors note: “The current evidence does not demonstrate conclusively that NSB [Nutritively sweetened beverage] consumption has uniquely contributed to obesity or that reducing NSB consumption will reduce BMI levels in general.”

Overall, Lustig’s certainty notwithstanding, we clearly have a long way to go before we can find a single, well defined culprit for the obesity epidemic and the health sequela related to that epidemic. Rather, many fingers seem to point to energy imbalances as an important consideration for the obesity epidemic.

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