About to go for a walk? Have fructose for breakfast to keep the hunger at bay. |
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"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."As you can see in Figure 1 the three test-meals initially had very similar effects on the subjects' appetite ratings, i.e. their desire to eat, hunger, fullness, and perceived ability to eat.
Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015). |
But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).
Irrespective of the previously mentioned methodological short-coming, it is, as the authors highlight, quite striking that "the increased fructose content in LGIF breakfast suppressed the appetite score, compared with isocaloric HGI and LGI breakfast" (Sun. 2015). Previously, scientists often argued that the satiety promoting effect of fructose must be mediated by the lower GI and correspondingly lower insulin spikes as well as reduced glucose excursions after fructose vs. glucose containing meals. The data in Figure 2, however, tells us that neither the insulin spikes (Figure 2, right) nor the glucose excursions (Figure 2, left) differed significantly between the LGI (low GI) and the LGIF (low GI + fructose) meals over the relevant last part of the study period - an observation which does by the way also show us that "[w]hen exercise is included as a co-intervention strategy, the effect of GI on appetite may be highly complex" (Sun. 2015) and in most cases relatively irrelevant."[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).In fact, scientists have previously speculated that fructose may affect appetite through slow and incomplete absorption. This effect, however, is eliminated when fructose is consumed with other CHOs (Anderson. 2003). As far as potential mechanisms are concerned, we are thus left with changes in satiety hormones and peptides like ghrelin, cholecystokinin, glucagon-like-peptide-1 and peptide-YY and/or direct or indirect effects on the gut-brain axis as potential mechanisms that would explain the results of Sun's study. Unfortunately, neither of these mechanism was assessed in their study.
There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.
In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!
- Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
- Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
- Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
- Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
- Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
- Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
- Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.