ONLINE DRIVERS MEDIA

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 Jurgo?ski, Jerzy Ju?kiewicz and Zenon Zdu?czyk 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 (Jurgo?ski. 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.
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 (Jurgo?ski. 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)." (Jurgo?ski. 2014)

The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. Whats 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).
References:

• Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).

Red (meat) breast cancer alert!

Its not the first study and I am pretty sure its not going to be the last study to link red meat and cancer, but in view of the fact that I am pretty sure that the results Maryam S Farvid and colleagues present in their latest paper in the British Journal of Medicine are going to be all over the place this week, I feel that its worth to give you an unbiased overview of the results before you are confronted with the sensational press release celebrating the newest "Harvard science" - a source people trust, one that "propagates the truth" and one that is (ab-)used by press release writers to generate the impression that each and every word they write is true.

Well the truth is that we are dealing with yet another prospective epidemiological study which does not have the power to reveal causal links between parameter (a), in this case the dietary protein sources in early adulthood and parameter (b), which is the incidence of breast cancer.
The average ignoramus will still read the headlines as "red meat" causes cancer and think of poultry, fish, eggs, legumes, and nuts as "the cure". In contrast to the red meat intake which was associated with a 22% risk increase in the 2830 documented cases of breast cancer the scientists had been collecting and following for 20 years, the a higher intake of poultry, fish, eggs, legumes, and nuts was
not just unrelated to breast cancer, in postmenopausal women, a high poultry intake was even associated with a -27% reduced breast cancer risk.

Energy intake and cancer risk expressed relative to lowest intake quintile for red meat (Farvid. 2014)

The latter observation gives rise to one of the (imho) hilarious substitute this for that equations, where the "estimating the effects of exchanging different protein sources, substituting one serving/day of legumes for one serving/day of red meat was associated with a 15% lower risk of breast cancer among all women (0.85, 0.73 to 0.98) and a 19% lower risk among premenopausal women (0.81, 0.66 to 0.99). Substituting poultry for red meat was even associated with 17% and 24% lower breast cancer risk in all and postmenopausal women.

Unlike the fooled readers of the press release, the researchers are obviously aware of the weaknesses of the study, in the discussion of the results, Farvid et al. point out that "potential limitations need to be considered":

• participants were predominantly white, educated US adults, they cannot determine whether our findings are generalizable to other race or ethnic groups
• dietary intake was assessed by food frequency questionnaires, some degree of measurement error is inevitably present, and thus to reduce measurement error they used the cumulative average of
  multiple measurements in a sensitivity analysis
• residual confounders are always of concern in any observational studies; although they adjusted for a wide range of potential confounders for breast cancer, they still could not rule out the possibility that other unmeasured or inadequately measured factors have confounded the true association
• they only estimated the effects of substitution of legumes, poultry, and other protein sources for red meat on risk of breast cancer, when trials on dietary modification would be ideal to support these substitutions

In addition, the scientists made multiple comparisons (different food groups and nutrients, premenopausal and postmenopausal subgroups, and subtype of tumors) in this analysis, and can thus not exclude the possibility of type I errors. But (sarcasm) this is not so much of concern, "the central finding of an association with red meat was [after all] a prior hypothesis." (Farvid. 2014) - In other words: What do you want people, weve just made sure we confirm our hypothesis.
Reference:

• Farvid, et al. "Dietary protein sources in early adulthood and breast cancer incidence: prospective cohort study." BMJ 2014;348:g3437 doi: 10.1136/bmj.g3437