The evolutionary roles of nutrition selection and dietary quality in the human brain size and encephalization
Roberto Carlos Burini, William R. Leonard
In addition to the energetic benefits associated with greater meat consumption, it appears that such a dietary shift would have also provided increased levels of key fatty acids necessary for supporting the rapid hominid brain evolution .
Half of human brain composition is fat, and 20% of its dry weight is long-chain polyunsaturated fatty acids (LCPUFAs). Consequently, improvements in consumption of dietary fat were a necessary condition for promoting encephalization [61, 62].
Mammalian brain growth is dependent upon sufficient amounts of two LCPUFAs: docosahexaenoic acid (DHA) and arachidonic acid (AA), and it appears that mammals have a limited capacity to synthesize these fatty acids from dietary precursors. Hence, species with higher levels of encephalization would have greater requirements for DHA and AA . Consequently, dietary sources of DHA and AA were likely limiting nutrients that constrained the evolution of larger brain size in many mammalian lineages .
Acides gras et fonctions cognitives
Association between maternal intake of n-6 to n-3 fatty acid ratio during pregnancy and infant neurodevelopment at 6 months of age: results of the MOCEH cohort study.
Kim H et al.
Nutrition journal, 2017
Cognitive and motor development of infants at 6 months of age was assessed by the Korean Bayley scales of infant development edition II (BSID-II) including the mental developmental index (MDI) and the psychomotor developmental index (PDI).
Maternal intakes of n-6/n-3 PUFAs and linoleic acid (LA)-to-α-linolenic acid (ALA) ratio (LA/ALA) were 9.7 ± 6.3 and 11.12 ± 6.9, respectively. Multiple regression analysis, after adjusting for covariates, showed that n-6/n-3 PUFAs was negatively associated with both the MDI (β = -0.1674, P = 0.0291) and PDI (β = -0.1947, P = 0.0380) at 6 months of age. These inverse associations were also observed between LA/ALA and both the MDI and PDI (MDI; β = -0.1567; P = 0.0310, PDI; β = -0.1855; P = 0.0367). Multiple logistic regression analysis, with the covariates, showed that infants whose mother’s LA/ALA were ranked in the 2nd, 3rd, and 4th quartile were at approximately twice the risk with more than twice the risk of delayed performance on the PDI compared to the lowest quartile (1st vs. 2nd; OR = 2.965; 95% CI = 1.376 - 6.390, 1st vs. 3rd; OR = 3.047; 95% CI = 1.374 - 6.756 and 1st vs. 4th; OR = 2.551; 95% CI = 1.160 - 5.607).
Both the maternal dietary n-6/n-3 PUFAs and LA/ALA intake were significantly associated with the mental and psychomotor development of infants at 6 months of age. Thus, maintaining low n-6/n-3 PUFAs and LA/ALA is encouraged for women during pregnancy.
When a wide range diets are evaluated in animal systems, it is possible to see that the level of DHA found in the blood of animals fed diets containing only LA and ALA can reach levels similar to that of animals fed diets rich in fish oil, but only when theALA:LA ratio is high and the total amount of dietary polyunsaturated fatty acids (PUFA) is low. Diets that are rich in either monounsaturates or saturates meet these requirements. Importantly, there are human infant studies that have tested such diets and demonstrated that human infants accumulate greater amounts of DHA than when diets are high in LA. It might be time to reconsider the dietary requirement of the two essential fatty acids LA and ALA in human infantsin terms of their ability to enhance endoge nous synthesis of DHA rather than moreadult biomarkers like cholesterol levels.
The dietary n6:n3 fatty acid ratio during pregnancy is inversely associated with child neurodevelopment in the EDEN mother-child cohort.
Bernard JY et al.
The journal of nutrition, 2013
This suggests that the ratio between maternal dietary n6 and n3 (LC)PUFA intake possibly influences the child’s brain development during fetal life but not during or by breastfeeding. However, breastfeeding might compensate for prenatal imbalance in maternal dietary n6:n3 fatty acid ratio.
Acides gras saturés
Dietary stearic acid regulates mitochondria in vivo in humans
Nature communication, 2018
This could explain part of the epidemiological differences between C16:0 and C18:0, whereby C16:0 increases cardiovascular and cancer risk whereas C18:0 decreases both.
Revisiting the diet-heart hypothesis: critical appraisal of the Minnesota Coronary Experiment
Tumas Beinortas et al.
Several articles have concluded that associations between high cholesterol and premature death are lacking and advocate revision of current guidance advising low consumption (<10%) of saturated fat.123 Ramsden and colleagues recovered 45 year old data from the Minnesota Coronary Experiment, a randomised controlled trial conducted in state psychiatric hospitals and nursing homes in Minnesota, USA, and reassessed the effect of a diet rich in linoleic acid on serum cholesterol and mortality.3 The authors found that the diet lowered total cholesterol but did not reduce the risk of premature mortality and might even have increased it.
Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)
Christopher E. Ramsden et al.
Results The intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001). Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27).
Conclusions Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.
The diet–heart hypothesis: a critique
Sylvan Lee Weinberg
Journal of the american college of cardiology, 2004
The low-fat “diet–heart hypothesis” has been controversial for nearly 100 years. The low-fat–high-carbohydrate diet, promulgated vigorously by the National Cholesterol Education Program, National Institutes of Health, and American Heart Association since the Lipid Research Clinics-Primary Prevention Program in 1984, and earlier by the U.S. Department of Agriculture food pyramid, may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate–high-protein diet may have a salutary effect on the epidemics in question.
Paul B. Pencharz, Rajavel Elango, Robert R. Wolfe, 2016