|Are the "good MUFAs" in olive oil not so "good" after all? Should you rather be eating SFAs all day?|
I mean, I was not surprised to hear that the gene-expression changes the scientists concluded revealed (we should rather say confirmed) that a high fat (HF) challenge in the course of which 18 lean and 18 obese male subjects between 50–70 years, who were non-smoking, normoglycemic (WHO criteria) and not diagnosed with any long-term medical condition, consumed milkshake with 95g of fat that were either high in saturated fat (SFA) or monounsaturated fat (MUFA).
Blood samples were collected before and 4 hours after shake consumption. Subjects were randomly assigned to a treatment order and a one-week washout period was the minimum between consecutive study days. On the day prior to each study day, subjects consumed a standardized low fat evening meal, were refrained from alcohol or strenuous exercise and were not allowed to eat or drink anything except water after 08.00 pm.
Both shakes had a volume of 500ml, were isocaloric and macronutrient composition differed only in fatty acid composition (Table 1). The SFA shake contained 95g palm oil and the MUFA shake contained 95g high-oleic acid sunflower oil. Vitamin E (165mg) was added to the shakes to match vitamin E present in the n-3 PUFA shake, that was used in the previously cited original study by the same research team (van Dijk. 2012).
"The design in the current study contains parts of a previously reported study . Six obese type 2 diabetic subjects were excluded because of the small number. Based on the more pronounced postprandial rise of TG after MUFA consumption, we selected the MUFA challenge for PBMCs transcriptome analysis. [...] Microarray analysis was performed for each individual at baseline and 4 hours after shake consumption, because we estimated that the observed effects after 4 hours are more pronounced compared to the 2 hour time point. For microarray analyses we therefore excluded samples after consumption of n3 PUFA shake and the 2h time point" (Esser. 2015). "
Table 1: Nutritional values of the intervention high fat shake (Esser. 2015).
What were the most important results of the original study? As you may have read in-between the lines, the previous study compared MUFA and N-3 and PUFA shakes. The results, however, were not much different from the ones that were observed in the study at hand: "MUFA and n-3 PUFA challenge, compared to the SFA challenge, induced higher changes in expression of inflammation genes MCP1 and IL1β in PBMCs" (an Dijk. 2012). So why would you do another study, anyway? Well, if you want to make a statement about the effects of different fat challenges in normal people, obese and obese diabetic subjects as they were recruited in the 2012 study are not the ideal object to study.While the overall results of this experiment are clear, the representation of the gene expressions in colorful gene maps is probably not really useful for 99% of you. Thus I've decided to stick to the overview of the results in Figure 1 and the verbalization of the implications of the differences the scientists observed.
|Figure 1: Graphical summary of the number of differences the scientists observed between (a - left) lean and obese subjects and (b - right) the MUFA and SFA shakes (Esser. 2015).|
That does certainly sound bad - at least for the Mediterranean MUFA lovers - in view of the epidemiological evidence that clearly indicates that high SFA and not high MUFA diets can have long-term negative consequences on your health (e.g. dementia (Kalmijn. 1997), chronically elevated insulin (Marshall. 1997), bone loss (Corwin. 2006), heart disease (Hu. 1999), etc.), it is yet questionable, if the allegedly "bad" increase in inflammatory genes is not fully compensated by the increase in PPARα which happens to be one of the main targets by which substances like fish oil act their anti-inflammatory magic.
"During fasting, 294 genes were significantly different expressed between lean and obese. The challenge increased differences to 607 genes after SFA and 2,516 genes after MUFA. [In that the SFA-induced changes in the lean vs. obese group appeared to be significantly more favorable | in the obese group, there were for example changes that suggest an increased risk of blood clots in the obese on SFA.]
Figure 2: Previous longer-term studies found sign. reductions in cholesterol w/ MUFA vs. SFA (Gillingham. 2011). So, maybe we should not overrate the gene essay - esp. in view of potentially increased "blood clogging" genes in the obese subjects of the study at hand.
In both groups, SFA decreased expression of cholesterol biosynthesis and uptake genes and increased cholesterol efflux genes. MUFA increased inflammatory genes and PPARα targets involved in β-oxidation" (Esser. 2015).
- Corwin, Rebecca L., et al. "Dietary saturated fat intake is inversely associated with bone density in humans: analysis of NHANES III." The Journal of nutrition 136.1 (2006): 159-165.
- Hu, Frank B., et al. "Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women." The American journal of clinical nutrition 70.6 (1999): 1001-1008.
- Kalmijn, Sandra, et al. "Dietary fat intake and the risk of incident dementia in the Rotterdam Study." Annals of neurology 42.5 (1997): 776-782.
- Marshall, J. A., D. H. Bessesen, and R. F. Hamman. "High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population: the San Luis Valley Diabetes Study." Diabetologia 40.4 (1997): 430-438.
- Piers, L. S., et al. "Substitution of saturated with monounsaturated fat in a 4-week diet affects body weight and composition of overweight and obese men." British Journal of Nutrition 90.03 (2003): 717-727.
- van Dijk, Susan J., et al. "Responses to high-fat challenges varying in fat type in subjects with different metabolic risk phenotypes: a randomized trial." PloS one 7.7 (2012): e41388.