|This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips.|
With the publication of the data of a their latest rodent study, the scientists have already taken the first step to a new, an "interactionist" perspective on the obesogenic effects of saturated vs.unsaturated and simple vs.complex carbohydrates and their interaction with another previously overlooked factor that has gotten quite some attention in the past months: The gut and its inhabitants.
Goodbye! Nutritional scapegoatism
It goes without saying that this model study is nothing but a first step on a long road we still have to travel, but the differential effects the four diets (see Table 1)...
Table 1: Composition of the diets.
- the lard-laden high cornstarch diet (LS),
- the soybean-powered high fructose diet (OF), and
- the lard-laden high fructose diet (LF)
World premiere! I know it sounds hilarious, but this is actually the first study I have seen that focused on nutrient interactions, instead of individual (macro-)nutrients in diets that are not even suitable to isolate the effects of the nutrient of interest - most prominent example the "high fat diet" which is high in fat (45% of the energy is the standard; there are yet also "high fat" diets with only 32% of the total energy from fat; Gajda. 2008) but leaves enough room for carbohydrates to complement, some would say "trigger" the obesogenic effects by providing a pro-insulinogenic stimulus that will blunt the oxidation of the dietary fat and help drive it into the cells.If you take a closer look at the actual study outcomes, you will see that the answer(s) the study provides are about as complex as its design.
In contrast to the dietary fat which had no independent effect on any of the measured markers of gut function, the carbohydrate source, i.e. cornstarch vs. fructose lead to significant differences in total small intestinal mass, mean pH of the ileal digesta and the mucosal activity of sucrase, all of which were increase on the high fructose diet.
|Figure 1: Serum lipid levels of the rodents after 4 weeks on obesogenic diets containing different forms of dietary fat and carbohydrate (Jurgoński. 2014)|
"Both the dietary fats and carbohydrates contributed to changes in the total SCFA concentration in the caecal digesta of rats (p < 0.05 and < 0 0.001, respectively). The highest total SCFA concentration was in group LS, while group OS had a significantly lower concentration (p ≤0.05). Similarly, the acetate concentration in the caecal digesta was influenced both by dietary fats and carbohydrates (p < 0.05 and p < 0.001, respectively) with a similar span of differences among particular groups (p ≤0.05). The type of dietary carbohydrate had significant influence on the propionate and isobutyrate concentrations in the caecal digesta (p < 0.001 and p < 0.05, respectively); however, both dietary factors had an interactive effect on their concentrations (p < 0.05). The highest propionate concentration was observed in the LS and OS group, whereas significantly lower concentration was found in the OF group. The lowest isobutyrate concentration was in group OF and it was significantly higher in group OS (p ≤0.05)." (Jurgoński. 2014)The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. What's particularly striking, here, is the nasty effects of a combined lard + fructose feeding on the triglyceride levels.
A similar fat-dependence as for the fructose induced triglyceride boost can be observed for the levels of total and HDL cholesterol, which were increased only by the combination of fructose + saturated fat. In the rodents that received soybean oil with their coke, ... ah, I mean with their fructose, the researchers observed the exact opposite trend and a 5x lower yet similarly increased artherosclerosis risk (as evidenced by the 5x higher atherogenic index).
- Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).