allDiseases & Conditions

Sugar and Metabolic Syndrome

sugarObviously, things have changed since then. Taubes writes that as Americans have gotten fatter and the incidence of diabetes has increased, “physicians and medical authorities have come to accept the idea that a condition known as the Metabolic Syndrome is a major, if not the major risk factor for heart disease and diabetes.” Taubes points to data from the Center for Disease Control and Prevention that estimate that 75 million Americans now have metabolic syndrome. This is a staggering number.

Taubes explains the symptoms and pathology of metabolic syndrome. Typically evidenced by an “expanding waistline,” metabolic syndrome has been associated with insulin resistance, where insulin isn’t working as effectively as it should within the body. This means that as we eat, more insulin is required than usual to keep blood sugar normal after a meal. In time, as these elevated insulin levels continue to be secreted, the pancreas fails to “keep up” in terms of demand, or “pancreatic exhaustion” occurs. When blood sugar rises incredibly, we get diabetes. For those who do not get diabetes, other conditions may develop. Heart disease is one, where triglycerides and blood pressure levels increase and HDL cholesterol decreases, farther fueling insulin resistance. In fact, according to Scott Grundy, a nutritionist interviewed by Taubes, metabolic syndrome is now the stronger predictor for heart disease than dietary fat ever was.

What then causes metabolic syndrome, or rather the insulin resistance that causes metabolic syndrome? Taubes explains that one of the prominent hypotheses among researchers in the field points to the accumulation of fat in the liver. Taubes quotes Varman Samuel, a researcher studying insulin resistance at The Yale School of Medicine, who observes that in the study of the link between liver fat and insulin resistance in humans, whether lean or obese, the correlation is “remarkably strong…. When you deposit fat in the liver, that’s when you become insulin resistant.” Although it is easy to suppose that a fatty liver stems from getting fatter, it is not that simple. According to Taubes, some cases of fatty liver can be traced back to “genetic predisposition,” but there is a very strong possibility that Lustig is right, that it can be caused by sugar.

Apparently, the study of metabolic syndrome and insulin resistance are what lead many of the scientists currently studying fructose to become engrossed in the subject. According to Gerald Reaven, a Stanford University diabetologist whom Taubes references, fructose is one of the easiest ways to cause insulin resistance in rats, creating a “very obvious, very dramatic” effect. In the early 2000s researchers had “established findings” and “well-established biochemical explanations” for what was happening. Taubes phrases it as such: “Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat – the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol.” According to Michael Pagliasotti, a Colorado State University biochemist involved in many of the animal studies in the field, changes in the liver can happen within the span of a week if animals consume 60-70% fructose/sugar diets. If they consume the 20% levels of sugar/fructose found in American diets, the process expands to several months. As soon as the sugar is removed from the diets, the liver normalizes, and insulin resistance ceases to occur.

Taubes claims effects are similar in humans; however, studies in this area typically involve the use of pure fructose—as with Luc Tappy in Switzerland and Peter Havel and Kimber Stanhope at the University of California, Davis. The problem here is that pure fructose is not sugar or high fructose corn syrup. In Luc Tappy’s experiments, Taubes reports, patients were fed the fructose equivalent of 8-10 cans of coke a day, “a pretty high dose” according to Tappy himself. At this dose, Taubes notes, their livers began to be insulin resistant and triglycerides would shoot up in a matter of days. At lower doses, the same results would appear but after a longer period of time.

Despite all the research, Taubes acknowledges that the evidence is far from definitive; the studies conducted on rodents do not really apply to humans. On the other hand, studies that were conducted on humans done by Tappy, Havel and Stanhope do not reflect actual human standards and experiences and thus do not apply; humans consume fructose with glucose, most commonly through sucrose or HFCS. Furthermore, our actual consumption of fructose is nowhere near the levels administered during these tests. Inconclusive results such as these are the reason why research reviews on the subject matter, such as those performed by the FDA, almost always claim that more research is essential, particularly research that attempts to determine at what dosage sucrose and high fructose corn syrup become “toxic.” “There is clearly a need for intervention studies,” Taubes quotes Tappy as saying, “in which the fructose intake of high-fructose customers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term intervention studies, however, suggest that a high-fructose intake consisting of soft drinks, sweetened juices or bakery products can increase the risk of metabolic and cardiovascular diseases.” Unfortunately, without long-term studies, definitive results are nowhere in sight. According to Taubes, it doesn’t help that fructose is, as Lustig mentions, a “chronic toxin” and not an “acute toxin,” “not toxic after one meal, but after 1000 meals.”

Luckily, as Taubes mentions, there are several clinical trials currently running that are supported by the National Institutes of Health, all of which are small and short-term, lasting a little over several months. Lustig himself, together with Jean-Marc Schwarz, one of the best fructose scientists in the world, and their peers at UCSF are conducting one of these, studying the effects in obese teenagers of the consumption of fructose only from fruits and vegetables. Another study with the same consumption parameters will look for effects on pregnant women to see if healthier and leaner offspring are produced. To answer the main concern about levels where fructose becomes toxic, only one study is being conducted by Havel and Stanhope at the University of California, Davis, where healthy people are given three sugar/HFCS-sweetened beverages a day and to measure their impact on the body. However, the study’s subjects are only observed for a maximum of two weeks, essentially covering only “42 of the 1000 meals,” Taubes points out. Despite

this, Taubes reports that the team is quite confident that the time period is enough to observe some symptoms of metabolic syndrome.