It is possible that the MS group was already functioning at its lowest biological limit, and was unresponsive to the deficiency in our study. Another possibility is that we are observing more the effects of the early-life stress itself, rather than a diet X stress interaction per se in this result. Interestingly, animals exposed to MS and to the dietary deficiency in n-3 PUFAs demonstrated increased palmitoleic acid in our study. Palmitoleic acid is associated with increased insulin concentrations and resistance, type II diabetes, metabolic LEE011 CDK inhibitor syndrome, heart failure and coronary heart disease. Plasma palmitoleic acid content is an independent marker of both triglyceridemia and abdominal adiposity in men, which agrees with the positive correlation between this fatty acid peripheral level and the amount of abdominal fat deposition found in this study. In addition, it has been shown to induce hepatic steatosis and increase fatty acid synthase expression in mice, corroborating to the idea of hepatic lipotoxicity in MS_deficient animals, as PI-103 discussed above. Our findings also agree with the literature regarding the negative correlations between stearic acid and HOMA index as well as insulin levels. Despite the fact that the n-3 PUFAs deficient diet used in this study ultimately increased the peripheral levels of DHA, the groups had no difference in other n-3 PUFAs indices such as the Omega-3 Index and total n-3 PUFAs in blood. One possible explanation for the increased peripheral DHA levels is based on the very mild deficiency imposed by the diet that we used. A study using different dietary content of a-linolenic acid demonstrates that, at such level of deficiency, DHA in plasma was not affected by the diet. Another study shows that DHA levels decrease more 
slowly than EPA subsequent to n-3 PUFAs reduction, indicating some type of docosahexaenoic acid retention. In the serum, the effects of a low n-3 PUFAs diet are less severe than in other tissues. In addition, it seems that the blood compartmental metabolism of DHA differs substantially depending on the type of the diet, both in terms of bioavailability in plasma and accumulation in target tissues. As plasma and erythrocyte EPA, DHA, Omega-3 Index and total n-3 PUFAs have weaker correlations with the corresponding fatty acid content in the brain compared with other tissues, the animals receiving the deficient diet in our study could still be experiencing low levels of essential n-3 PUFAs in target tissues, especially the brain, and this could explain the metabolic effects seen especially in the MS group. Finally, our deficient diet is more closely related to mild n-3 PUFAs deficiencies that can be easily found in human populations, therefore one could argue that our results have the potential of being more readily translatable to the human conditions. The modern Western diet can reach n-6/n-3 ratio as high as 30:1, when the desirable vary between 2:1 to 5:1. The ratio in our deficient diet was 5:1 – again, a mild deficiency. This is of added significance to our findings, considering that possibly the interactions between early life stress and nutritional deficiency in n-3 PUFAs could have impacted even more the metabolic outcomes if the dietary deficiency imposed were to be more intense. It remains to be established to what extend our findings are applicable to humans.