Friday, March 14, 2014

Scientists Probe the Interaction Between Saturated and Unsaturated High Fat Diets and Their Corresponding Carbohydrate Sources (Cornstarch vs. Fructose)

This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips.
Any hypothesis that tries to blame for our "fat misery" on a single nutrient is short-sighted. After years of fat-bashing, carbophobia and fructose hating in the course of which the situation progressively, we are now seeing the first studies which investigate what the Polish researchers, Adam Jurgoński, Jerzy Juśkiewicz and Zenon Zduńczyk from the Institute of Animal Reproduction and Food Research at the Polish Academy of  Sciences call the "biological interactions among these dietary factors" in their latest paper in the peer-reviewed open-source journal Nutrients (Jurgoński. 2014).

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 soybean powered high cornstarch diet (OS),
  • the lard-laden high cornstarch diet (LS), 
  • the soybean-powered high fructose diet (OF), and
  • the lard-laden high fructose diet (LF)
...had on the health, caecal short-chain fatty acid concentrations, cholesterol and triglyceride levels are revealing, to say the least.
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)
Interactive effects were observed for the mass of the cecum itself (the tissue) and the digesta with opposing effects of fructose on when it was administered in conjunction with lard (reductions) vs. soybean oil (increases in cecum mass). Slightly different effects were observed for the short-chain fatty acid composition (SCFA):
"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).
Suppversity Suggested Read: "EGGS - A Four-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport" | read more
The results are still difficult to place. The complementary increases in total and HDL cholesterol in the lard + fructose group for example could be interpreted as unproblematic in view of the contemporary social media trend to depict high cholesterol as absolutely irrelevant. In view of the concomitant 2.3x increase in the ratio of triglycerides to HDL-cholesterol, of which we do know for sure that it predicts extensive coronary disease (Luz. 2008), it is still warranted to conclude that the combination of fructose and saturated fats is even worse than the combination of a high fructose intake with unsaturated fats, which had almost no effect on the triglycerides to HDL ratio and left the rodents in the corresponding group with a trig:HDL ratio what was >2.5x lower than that of the lard + fructose rodents.

Yes, I know - that's only rodent data, there is no information on body weight, or the gut microbiome and even the impact on glucose metabolism wasn't measured (you can predict from the triglyceride levels, though, that the animals lard + fructose diet had the lowest insulin sensitivity), the reason I still spent a whole article on this paper is that this is the kind of study, we'd need if we actually want to understand "why we are fat" from the inexplicably popular (macro-)nutrient perspective... I mean, let's be honest: On the level of food items, the complexity is not a problem and we all know the food items that propel the obesity epidemic, don't we?
  • Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).