Isocaloric substitution studies can be interesting if they are rigorously controlled and care is taken to eliminate confounding variables. However, all too often the studies change more than one variable and this obfuscates the cause and effect of the changes. A recent study published in the American Journal of Clinical Nutrition investigated the effects of a high saturated fatty acid diet and a high monounsaturated fatty acid diet on the physical activity, resting energy expenditure and mood of young healthy adults1. The authors reported that the high oleic acid diet was effective at increasing physical activity, resting metabolic rate and lowering of anger and hostility, and concluded that replacement of the high palmitic acid (PA, C16:)) acid diet with a high oleic acid (OA, C18:1 (n-9)) diet may increase the propensity for participating in physical activity. Indeed, the involvement of saturated fatty acids in the development of insulin resistance suggest that high saturated fatty acid diets may be detrimental to energy production.
However, care needs to be exercised when interpreting such studies as exact isocaloric substitution of macronutrients is difficult. In fact a closer look at the methodology of this study shows that the two diets contained different compositions of fatty acids, some of which were refined oils and some of which were unrefined. The high PA diet for example was made up of 89 % refined palm oil, 6.75 % refined peanut oil and 4.25 % extra virgin olive oil. However, the high OA diet consisted of just refined hazelnut oil. Comparison of these diets is already problematic because a number of variables have changed and therefore the effects of these diets cannot be ascribed to the fatty acids. All subjects consumed both of these diets in a random order for 3 weeks before switching to the other diet. However, before this treatment phase, all subjects consumed a diet consisting of 36.9% palm oil, 19.3 % high oleic sunflower oil and 43.8 % hazelnut oil for 7 days, which was higher in OA (15.9% of energy) compared to PA acid (5.3 % of energy).
Therefore the results from this study are confounded because the diets differed in more than one variables, and because the control diet was higher in monounsaturated oil than saturated oil and was also artificially low in fat (19.7, 51.6 and 28.4 % of energy from protein, carbohydrate and fat respectively). Also, because a true baseline reading was not taken, it is unclear as to the physiological parameters of the subjects before their diets were artificially manipulated. For example, both the high OA and the high PA diets could have both caused weight gain, detrimental mood changes and a lowering of metabolic rate from the subjects habitual free-living diet. However, we do not know as these baseline readings were not reported. Further, the details of the rest of the diet are not fully disclosed, other than the fact that they were a ‘habitual’ diet. This suggest the diet was likely a Western style diet with carbohydrates coming from refined grains and sugar, and this may have had modified the effects of the changes to fatty acids.
Another interesting component of this study was the fact that both the resting energy expenditure and physical activity levels increased significantly in the high OA diet compared to the high PA diet. The authors suggested that this may related to an upregulation of the mitochondrial oxidation capacity, which has its merits. However, because the authors did not take a true baseline reading for these parameters it is difficult to know whether either of the diets were actually beneficial. Both may have been detrimental, but the high OA diet may just have been less detrimental than the high PA diet. Another aspect to this discussion is the fact that the body weights of the subjects did not change with any of the treatments. This is interesting because the results showed an increase in physical activity as measured by an accelerometer that was carried by the subjects. That resting metabolic rate and physical activity levels increased, but they did not lose weight is therefore problematic for those that believe that physical activity is a cause of weight loss.
Of course the subjects could have gained muscle and lost fat but we do not know as it was not measured, and this omission is a common feature of many studies. The changes in the mood of the subjects may have indicated a change in hormonal conditions within the subjects. The results showed a decrease in anger and hostility in the high OA diet compared to the high PA diet. Again we do not have a true baseline reading and so both of these diets may have caused detrimental changes compared to the subjects habitual diet. The reduction in aggression and anger suggests that either changes to eicosanoid synthesis, or a change in testosterone levels, occurred in the subjects. If the testosterone levels of the subjects changed, a measure of lean mass may have been enlightening. However, as with much of this study, the cause of the effects are difficult to address because so many parameters have changed. Therefore although interesting, no real conclusions can be drawn from this study, and as such it is of questionable value.
RdB
