137 research outputs found
Fish and human brain evolution
Carlson and Kingston ([2007]: Am J Hum Biol 19:132â141) propose that
preformed dietary docosahexaenoic acid (an omega-3 fatty acid in fish) did not have a significant
role in hominin encephalization. Their position hinges on claiming that humans are able
to make sufficient docosahexaenoic acid from the plant-based \parent" omega-3 fatty acidâalinolenic acid. They also suggest that hominin fish consumption occurred too late to have materially influenced encephalization. The authors quantify here a summary of the published data
showing that humans cannot make sufficient docosahexaenoic acid to maintain normal infant
brain development. The authors also provide evidence that the fossil record shows that some of
the earliest hominins were regularly consuming fish. Hence, we reject Carlson and Kingstonâs
position and reiterate support for the concept that access to shore-based diets containing docosahexaenoic acid was necessary for hominin encephalization beyond the level seen in the great
apes. Am. J. Hum. Biol. 19:578â581, 2007
Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements
La communautĂ© scientifique accorde beaucoup dâintĂ©rĂȘt Ă plusieurs acides gras polyinsaturĂ©s (PUFA) et Ă leur attĂ©nuation potentielle du taux de mortalitĂ© et de morbiditĂ© causĂ©e par les maladies dĂ©gĂ©nĂ©ratives du systĂšme cardiovasculaire et du cerveau. Il nâen demeure pas moins que la confusion demeure au sujet du taux de conversion chez lâhumain des PUFA en amont â acide linolĂ©ique ou α-linolĂ©nique (ALA) â en des substances respectives Ă plus longue chaĂźne. On ne connaĂźt toujours pas les bienfaits potentiels de lâALA en amont de lâacide eicosapentaĂ©noĂŻque (EPA) ou de lâacide docosahexaĂ©noĂŻque (DHA). La confusion est en partie nĂ©e du fait que les mammifĂšres disposent des enzymes nĂ©cessaires pour synthĂ©tiser les PUFA Ă chaĂźne longue Ă partir des PUFA en amont alors que les Ă©tudes in vivo chez lâhumain rĂ©vĂšlent que â5 % de lâALA est converti en EPA et moins de 0,5 % de lâALA est converti en DHA. Du fait de la trĂšs faible capacitĂ© de cette voie de synthĂšse chez des humains en bonne santĂ© non vĂ©gĂ©tariens, mĂȘme un grand apport alimentaire dâALA a un effet nĂ©gligeable sur la concentration plasmatique de DHA ; on observe le mĂȘme phĂ©nomĂšne chez les PUFA omĂ©ga-6 : lâapport alimentaire dâacide linolĂ©ique a peu dâeffet sur la concentration plasmatique de lâacide arachidonique. Nonobstant cette conversion Ă faible rendement, lâALA et lâEPA ont potentiellement un rĂŽle Ă jouer au plan de la santĂ© chez lâhumain qui nâa rien Ă voir avec la conversion en DHA dans la voie de dĂ©saturation-Ă©longation des acides gras.Abstract: There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent PUFA, linoleic acid or alpha-linolenic acid (ALA), to their respective long-chain PUFA products. As a result, there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that asymptotically equal to 5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary ALA have a negligible effect on plasma DHA, an effect paralleled in the omega6 PUFA by a negligible effect of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the desaturation - chain elongation pathway
Survival of the fattest: fat babies were the key to evolution of the large human brain.
Abstract In the past 2 million years, the hominid lineage leading to modern humans evolved significantly larger and more sophisticated brains than other primates. We propose that the modern human brain was a product of having first evolved fat babies. Hence, the fattest (infants) became, mentally, the fittest adults. Human babies have brains and body fat each contributing to 11-14% of body weight, a situation which appears to be unique amongst terrestrial animals. Body fat in human babies provides three forms of insurance for brain development that are not available to other land-based species: (1) a large fuel store in the form of fatty acids in triglycerides; (2) the fatty acid precursors to ketone bodies which are key substrates for brain lipid synthesis; and (3) a store of long chain polyunsaturated fatty acids, particularly docosahexaenoic acid, needed for normal brain development. The triple combination of high fuel demands, inability to import cholesterol or saturated fatty acids, and dependence on docosahexaenoic acid puts the mammalian brain in a uniquely difficult situation compared with other organs and makes its expansion in early humans all the more remarkable. We believe that fresh-and salt-water shorelines provided a uniquely rich, abundant and accessible food supply, and the only viable environment for evolving both body fat and larger brains in human infants.
Plasma Ketone and Medium Chain Fatty Acid Response in Humans Consuming Different Medium Chain Triglycerides During a Metabolic Study Day
Background: Medium chain triglycerides (MCT) are ketogenic but the relationship between the change in plasma ketones and the change plasma medium chain fatty acids (MCFA)âoctanoate, decanoate, or dodecanoateâafter an oral dose of MCT is not well-known. An 8 h metabolic study day is a suitable model to assess the acute effects on plasma ketones and MCFA after a dose of tricaprylin (C8), tricaprin (C10), trilaurin (C12) or mixed MCT (C8C10).Objective: To assess in healthy humans the relationship between the change in plasma ketones, and octanoate, decanoate and dodecanoate in plasma total lipids during an 8 h metabolic study day in which a first 20 ml dose of the homogenized test oil is taken with breakfast and a second 20 ml dose is taken 4 h later without an accompanying meal.Results: The change in plasma acetoacetate, ÎČ-hydroxybutyrate and total ketones was highest after C8 (0.5 to 3 h post-dose) and was lower during tests in which octanoate was absent or was diluted by C10 in the test oil. The plasma ketone response was also about 2 fold higher without an accompanying meal (P = 0.012). However, except during the pure C10 test, the response of octanoate, decanoate or dodecanoate in plasma total lipids to the test oils was not affected by consuming an accompanying meal. Except with C12, the 4 h area-under-the-curve of plasma ÎČ-hydroxybutyrate/acetoacetate was 2â3 fold higher when no meal was consumed (P < 0.04).Conclusion: C8 was about three times more ketogenic than C10 and about six times more ketogenic than C12 under these acute metabolic test conditions, an effect related to the post-dose increase in octanoate in plasma total lipids
Plasma n-3 fatty acid response to an n-3 fatty acid supplement is modulated by apoE É4 but not by the common PPAR-α L162V polymorphism in men
The risk of Alzheimer's disease is increased for carriers of apoE4 (E4) or the PPAR-α L162V polymorphism (L162V), but it is decreased in fish and seafood consumers. The link between high fish intake and reduced risk of cognitive decline in the elderly appears not to hold in carriers of E4, possibly because better cognition is linked to EPA+DHA in the blood, but only in non-carriers of E4. As yet, no such studies exist in carriers of L162V. Our objective was to determine whether the plasma fatty acid response to a dietary supplement of EPA+DHA was altered in carriers of L162V and/or E4. This was an add-on project; in the original study, men were selected based on whether or not they were carriers of L162V (n 14 per group). E4 status was determined afterwards. All subjects received an EPA+DHA supplement for 6 weeks. L162V polymorphism did not interact with the supplement in a way to alter EPA and DHA incorporation into plasma lipids. However, when the groups were separated based on the presence of E4, baseline EPA and DHA in plasma TAG were 67 and 60 % higher, respectively, in E4 carriers. After the supplementation, there were significant gene à diet interactions in which only non-carriers had increased EPA and DHA in plasma NEFA and TAG, respectively
Does aging change docosahexaenoic acid homeostasis? Implications for the challenge to cognitive health in the elderly
Epidemiological studies fairly convincingly suggest that higher intake of fish and omega-3 fatty acids present in fish is associated with reduced risk for age-related cognitive decline (ARCD). Normally, docosahexaenoic acid (DHA) in plasma is positively associated with DHA intake. However, despite being associated with lower fish and DHA intake, unexpectedly, ARCD is not consistently associated with lower plasma DHA. Furthermore, DHA is often slightly but significantly higher in plasma and erythrocytes in the elderly without ARCD compared to young adults. Higher plasma DHA in the elderly may be a sign that their fish or DHA intake is higher but we show here that various aspects of DHA homeostasis also change with age. Our supplementation and tracer studies show that DHA metabolism, e.g. transit through the plasma and apparent retroconversion but not beta-oxidation, is different in healthy elderly compared to healthy young adults. Apolipoprotein E4 increases the risk of ARCD, possibly in part because it changes DHA homeostasis. Therefore, independent of differences in fish intake, changing DHA homeostasis may contribute to making the elderly more susceptible to cognitive decline despite them having similar or sometimes higher plasma DHA than in younger adults. Key words: aging, cognitive decline, dietary, docosahexaenoic acid, omega-3 fatty aci
Can nutrition support healthy cognitive ageing and reduce dementia risk?
â Global prevalence of dementia is predicted to almost triple by 2050 â There are currently no effective drugs to prevent or treat dementia â Improved eating behaviour holds significant potential to reduce the risk and population prevalence â Owing to its multifactorial aetiology, multiple dietary components which target several physiological pathways and risk factors simultaneously are needed. Therefore dietary patterns and foods (rather than single dietary components), hold the most promise to meaningfully improve cognition in the medium term â Randomised controlled trials with robust validated cognitive outcomes or, ideally, change in dementia or mild cognitive impairment incidence are needed in order to support the prospective cohort evidence, establish efficacy and effect size, and inform public health polic
Plasma incorporation, apparent retroconversion and ÎČ-oxidation of 13C-docosahexaenoic acid in the elderly
<p>Abstract</p> <p>Background</p> <p>Higher fish or higher docosahexaenoic acid (DHA) intake normally correlates positively with higher plasma DHA level, but recent evidence suggests that the positive relationship between intake and plasma levels of DHA is less clear in the elderly.</p> <p>Methods</p> <p>We compared the metabolism of <sup>13</sup>C-DHA in six healthy elderly (mean - 77 y old) and six young adults (mean - 27 y old). All participants were given a single oral dose of 50 mg of uniformly labelled <sup>13</sup>C-DHA. Tracer incorporation into fatty acids of plasma triglycerides, free fatty acids, cholesteryl esters and phospholipids, as well as apparent retroconversion and ÎČ-oxidation of <sup>13</sup>C-DHA were evaluated 4 h, 24 h, 7d and 28d later.</p> <p>Results</p> <p>Plasma incorporation and ÎČ-oxidation of <sup>13</sup>C-DHA reached a maximum within 4 h in both groups, but <sup>13</sup>C-DHA was transiently higher in all plasma lipids of the elderly 4 h to 28d later. At 4 h post-dose, <sup>13</sup>C-DHA ÎČ-oxidation was 1.9 times higher in the elderly, but over 7d, cumulative ÎČ-oxidation of <sup>13</sup>C-DHA was not different in the two groups (35% in the elderly and 38% in the young). Apparent retroconversion of <sup>13</sup>C-DHA was well below 10% of <sup>13</sup>C-DHA recovered in plasma at all time points, and was 2.1 times higher in the elderly 24 h and 7d after tracer intake.</p> <p>Conclusions</p> <p>We conclude that <sup>13</sup>C-DHA metabolism changes significantly during healthy aging. Since DHA is a potentially important molecule in neuro-protection, these changes may be relevant to the higher vulnerability of the elderly to cognitive decline.</p
Eicosapentaenoic acid decreases postprandial beta-hydroxybutyrate and free fatty acid responses in healthy young and elderly
Objectives:
We investigated whether a dietary supplement rich in eicosapentaenoic acid (EPA) increases fasting plasma ketones or postprandial ketone responses in healthy young and elderly subjects.
Methods:
Ten young (22 ± 1 y old) and 10 elderly (75 ± 1 y old) subjects were recruited and participated in two identical study days, one before and one 6 wk after providing an EPA-enriched supplement (1.4 g/d of EPA and 0.2 g/d of docosahexaenoic acid). On the study days, blood samples were collected at fasting and every hour for 6 h after giving a breakfast. Fasting and postprandial plasma ÎČ-hydroxybutyrate (ÎČ-OHB), free fatty acid (FFA), triacylglycerol, glucose, and insulin responses were measured. Fatty acid profiles were assessed in fasting plasma samples before and after the EPA supplement.
Results:
After the EPA supplement, postprandial plasma ÎČ-OHB responses decreased by 44% in the young and by 24% in the elderly subjects, in addition to 20% and 34% lower FFA responses in the young and elderly adults, respectively. ÎČ-OHB and FFAs were positively and significantly correlated in young but not in elderly subjects before and after the EPA supplement. In both groups, postprandial plasma triacylglycerols, glucose, and insulin were not significantly different after the intake of the EPA supplement. Before and after the EPA supplement, fasting plasma EPA was 50% higher in the elderly but increased by about five times in both groups after intake of the EPA supplement.
Conclusion:
Contrary to our expectations, EPA supplementation lowered postprandial ÎČ-OHB response and, in the elderly subjects, the concentration of postprandial ÎČ-OHB was not lowered after intake of the EPA supplement
Image-derived input function in dynamic human PET/CT: methodology and validation with 11C-acetate and 18F-fluorothioheptadecanoic acid in muscle and 18F-fluorodeoxyglucose in brain
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