OBJECTIVE: To determine the interaction between a high fructose diet and PA levels on postprandial lipidemia and inflammation in normal weight, recreationally active individuals.
METHODS: Twenty-two men and women (age: 21.2 ± 0.6 yrs; BMI = 22.5 ± 0.6 kg/m) consumed an additional 75 g of fructose for 14 days on two separate occasions: high physical activity (∼12,500 steps/day: FR+Active) and low PA (∼ 4,500 steps/day; FR+Inactive). A fructose-rich test meal was given prior to and at the end of each intervention. Blood was sampled at baseline and for 6 h after the meal for triglycerides (TG), very-low density lipoproteins (VLDL), total cholesterol (TC), glucose, insulin, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and c-reactive protein (CRP).
RESULTS: Log transformed TG AUC significantly increased from pre (10.1 ± 0.1 mg/dL x min for 6 h) to post (10.3 ± 0.08 mg/dL x min for 6 h; p = 0.04) in the FR+Inactive intervention with an 88% increase in Δpeak[TG] (p=0.009) and an 84% increase in Δpeak[VLDL] (p=0.002). Δpeak[IL-6] also increased by 116% after FR+Inactive intervention (p=0.009). Insulin tAUC significantly decreased after FR+Active intervention (p=0.04) with no change in AUC after the FR+Inactive intervention. No changes were observed in glucose, TNF-α and CRP concentrations (p>0.05).
CONCLUSIONS: Low physical activity during a period of high fructose intake augments fructose-induced postprandial lipidemia and inflammation while high PA minimizes these fructose-induced metabolic disturbances. Even within a young healthy population, maintenance of high PA (>12500 steps/day) decreases susceptibility to cardiovascular risk factors associated with elevated fructose consumption.
Alex’s Notes: We have all heard the arguments about the evils of fructose. People drink soda that has high-fructose corn syrup in it and health authorities blame the health consequences on fructose, which then gets extended to all fructose including that found in fruit, which then begins to encompass carbohydrates as evil in general, and so on. To be frank, it’s annoying. But before I get ahead of myself, let’s explore the theoretical basis for the demonization of this nutrient.
Fructose is metabolized almost exclusively in the liver without dependence on insulin and is almost immediately converted into a metabolite of the glycotic pathway, making the majority of its metabolism identical to that of glucose. Indeed, 50% of ingested fructose is converted into glucose, 25% into lactate, at least 15% into liver glycogen, and the remainder is oxidized directly. Aside from directly contributing to liver glycogen, fructose also enhances glycogenesis of co-ingested glucose. However, fructose may also be metabolized into acetyl CoA which in large enough quantities can stimulate de novo lipogenesis (DNL; creation of fat) while simultaneously inhibiting fat breakdown, leading to insulin resistance, fatty liver, dyslipidemia, and low-grade inflammation. This is a misconception. In actuality, perhaps only 2-3% of ingested fructose is converted into triglycerides, and overfeeding studies show that there is no difference in lipogenesis between glucose and sucrose – which is half fructose. This makes sense when looking at basic physiology, since fructose is metabolized in the same manner as glucose.
Moreover, virtually all the studies looking at the negative effects of fructose are either in animal models and/or use unrealistically high amounts of fructose that make the study’s clinical relevance completely obsolete. For example, one study in obese humans (which adds another confounding variable because these people are already metabolically unhealthy) concluded that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral fat. Okay, but these people consumed 25% of their total calories from fructose in addition to their normal unrestricted diets. To put that in perspective, it is the equivalent of adding just over six 12 ounce sodas to a normal 2,000 kcal diet. In another study, things get even more atrocious. Although this study used lean and healthy males, it also supplied them with an additional 234 grams of fructose (almost 12 cans of soda) per day for a week. And these are the studies that people refer to when they say fructose is evil. I hope you can see why I get so annoyed about this topic and the demonization of nutrients in general.
Like everything, context is another critical aspect. The first flawed study mentioned above was in obese & sedentary persons for instance. Completely ignoring the unrealistic doses of fructose consumption, it is known that physical activity changes our metabolisms for the better. A physical culturist or athlete consuming six cans of soda daily will not respond in the same manner as a fat couch potato. This finally brings us to the study at hand, which aimed to examine the effects of fructose consumption during a time of increased physical activity to its effects when coupled with inactivity.
22 healthy lean college students who were engaged in moderate to vigorous activity for at least 20-60 minutes per day, 3-4 days per week were recruited for this study. Importantly, none of the subjects regularly consumed a “high-fructose” drink (i.e. a 12 ounce can of soda). The subjects underwent a control week to establish baseline dietary habits and activity levels, followed by a two-week intervention in which they supplemented their diets with an additional 75g of fructose per day via a provided 40 ounce soda beverage. Although this amount is also ridiculously high, it does reflect a more accurate intake of the typical Westerner when you consider sugar intake from beverages, snacks, and candies. For comparative purposes, since us Super Humans don’t eat or drink that crap, this is about 6-7 medium apples or ten bananas; pretty unrealistic. Anyways, during this time the subjects were also randomized to perform either low or high levels of activity and to refrain from any additional exercise throughout the study duration. Then they did a two-week washout period and repeated the intervention with the opposing activity level.
Extremely importantly, the activity levels were based on steps. The low-active (LA) group took around 4,500 steps daily, while the high-active (HA) group took about 13,000 steps per day. I’ll make a big deal of this again later on. As for the results, the first interesting note is that during the interventions total energy intake and body weight did not change. Despite adding 40 ounces of soda (500 kcal) to their diets, the participants compensated for this additional intake by reducing intake of other dietary carbohydrates and some fat. This occurred in both LA and HA interventions.
As for the effects on health markers, in the LA group the fructose beverage lead to an 88% increase in triglycerides, an 84% increase in VLDL, and a 116% increase in IL-6 (an inflammatory marker). In the HA group, the rise in VLDL was only 33% and the subjects actually reduced their triglycerides by 5% and IL-6 by 30%. The HA intervention also reduced the insulin response to a test meal by 19%, and neither intervention differed in their effects on glucose or cholesterol. As the authors nicely state,
“In conclusion, in a population of young, healthy individuals, being physically inactive (~4200 steps/day) while consuming an addition of 75 grams of fructose resulted in increased postprandial lipidemia and signs of potential low-grade inflammation, independent of energy intake, in as few as two weeks. However, an increased physical activity level (~13000 steps/day) seems to protect against these adverse changes.”
And back to the extremely important point, this was by simply moving around more! Now imagine what happens when you engage in structure resistance training or athletic events. There is absolutely ZERO reason to fear fructose, especially when you avoid all the added sugars of the typical Western diet.