|Hard do believe, but the 10g from coke may actually do more harm than the same amount from cookies.|
It's certainly true that the exorbitant and mislead carbohydrate intake and the psyochological consequences ("Fat is bad, isn't it?") of the "low fat" decades from the 1970-1990s is part of the problem, but when we look closer, it's not as simple as to say "we don't eat enough fat".
As Yvonne Ritze and her colleagues from the University of Hohenheim, the Technische Universität München, and the Interdisciplinary Obesity Center in Rorschach (Switzerland) write in their latest paper in PLoS One, it's rather the unhealthy conglomerate of "changes in dietary and eating behavior such as preferring sugar-sweetened beverages and sugar-rich processed food, in addition to a sedentary life style", which is to blame form the "sharp rise in obesity" (Ritze. 2014).
In said paper, Ritze and her colleagues present data from rodent and human experiments they conducted which highlight the fact the "form of sugar intake (liquid versus solid) is presumably more important than the type of sugar" (Ritze. 2014), when it comes to its ability to disturb our appetite regulation, increase the fat accumulation in the liver and promote the development of type II diabetes.
In mice, Ritze et al. observe a liquid high-sucrose diet caused an enhancement of total caloric intake which was not comparable to the effects the solid variety of the high sucrose diet had.
|Figure 1: Diet (left) and energy (right) intake in the five diet groups (Ritze. 2014)|
- Group 1 (controls, C) received water and mouse breeding (MZ)-diet (standard diet from Sniff, Soest, Germany) containing 10% (g/g) sugars.
- Groups 2 (fructose liquid, Fl) and 3 (sucrose liquid, Sl) received water supplemented with fructose or sucrose at 30% (vol/vol), respectively, and enriched MZ-diet to compensate for reduced food uptake.
- Groups 4 (fructose solid, Fs) and 5 (sucrose solid, Ss) received water and the high-fructose or -sucrose diet containing 65% (g/g) sugars, which equals the sugar amount per day that mice ingested when offered sugar water at 30%.
- The sugar intake in groups 2-4 was significantly higher than in group 1 - obviously a simple and necessary consequence of the composition of the diet
- The mice on the liquid diets consumed significantly more energy, sugar, liquid and food - distinct evidence that the rodent equivalent of sugar-sweetened beverages leads to overeating
- The fructose diets were not by any means worse than the sucrose diets - an observation that confirms what I have been preaching to the choir: The fructose bashing as "lustig" (engl. "funny") as some experts believe it was, is based on a shortsighted prejudice
- The weight increase in the solid high-sucrose groups was small compared to that of the mice in groups 2 & 3 who were fed sucrose or fructose in their water - this is the logical consequence of the increased energy intake
- When the scientists compared the obesogenic effects (weight gain per food intake) of the diets, they found a significant difference between the liquid and solid sugars but not the sugar types - more evidence we cannot simply blame everything on fructose
- Interestingly, all four high sugar-diets caused an increase in blood glucose and in tendency some increase in liver weight, which was more pronounced if the sugars were administered in solid form.
"Similar results were obtained for GLUT5 mRNA expression. Comparing sugar form and type we showed a significant difference between liquid and solid sugar form for GLUT2 and GLUT5 (P < 0.001) as well as a significant difference of sugar type (fructose versus sucrose) for GLUT5 (P < 0.05) within the different dietetic groups." (Ritze. 2014)Whether these difference in glucose transporter activity are actually relevant (they would simply speed up the uptake of glucose / fructose) is questionable.
Is absorption speed all that matters?
|Figure 2: Suspiciously similar changes in glut-2 & 5 expression in the two groups fed liquid diets (top) and obese vs. lean human (bottom)|
Whether the speed of the sugar influx is also responsible for the slightly up-regulated ghrelin mRNA levels in mice who were fed the liquid diet compared to the solid diet (P < 0.05) is something, I cannot tell. What I can tell you though is that (a) elevated or rather not appropriately reduced ghrelin levels after a meal are characteristic of obese vs. lean humans, too (Le Roux. 2005) and that (b) there was once again no difference between fructose and sucrose diet.
Did you ever notice that none of the "fructose is bad studies" was conducted with a solid diet? The fructose was always provided on top of a solid diet with the liquid, just like the the surcose and fructose in the diet at hand. And if we are honest, it does not look like fructose was by any means significantly worse than simple sugar (which obviously is a 1:1 glucose : fructose mixture).
The endotoxin concentration in the portal vein (see Figure 3, C), on the other hand, are the highest (yet not significantly elevated!) in the fructose groups. In conjunction with the relatively low triglyceride levels in the liver this goes against a theory by Bergheim et al. which revolves around the idea that fructose induced changes in the gut microbiome would lead to an increased endotoximia (this is true) and consequent fatty liver disease (this is at least less severe that with sucrose in the study at hand).
- Bergheim, Ina, et al. "Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin." Journal of hepatology 48.6 (2008): 983-992.
- Le Roux, C. W., et al. "Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects." The Journal of Clinical Endocrinology & Metabolism 90.2 (2005): 1068-1071.
- Pan, An, et al. "Changes in water and beverage intake and long-term weight changes: results from three prospective cohort studies." International journal of obesity 37.10 (2013): 1378-1385.
- Ritze, Yvonne, et al. "Effect of High Sugar Intake on Glucose Transporter and Weight Regulating Hormones in Mice and Humans." PloS one 9.7 (2014): e101702.