yana-notes

@Docosahexaenoic acid and arachidonic acid in infant development (Carlson 2002)

2022-02-10 links: DHA

@Docosahexaenoic acid and arachidonic acid in infant development (Carlson, 2002) #

We’ve got some references to peep… where to even start? Something to bear in mind is that these formula studies must give the infants ALA, but DHA is optional. Who knows what PUFA-free would look like in humans

  • DHA constitutes ~30% of the thanolamine and serine phosphoglycerides in Gray Matter and ~45% of them in the retina of all mammals.

    • Rhesus monkeys exposed to n-3 deficient diets had abnormal retinal function and visual acuity.
      • The visual system of newborn monkeys is more developed than that of term human infants
      • Rhesus monkeys which are n-3 deficient have been shown to have longer duration looks in tests of visual attention in comparison to monkeys with higher brain DHA… the investigators reported that the effects on look duration were unrelated to visual acuity.
        • Same results have been demonstrated in preterm human infants.
          • Infants who received the LCPUFA-containing formula had a higher novelty preference during the Fagan Test but did not find an effect on look duration
            • The availability of heart-rate information during exposure to visual stimuli permits looking to be parsed into three distinct phases:
              • ‘Orientation’ reflects a simple reaction to detection of the stimulus.
              • ‘Sustained attention’ includes the initial deceleration of heart rate and is presumed to reflect the maintenance of attention to the stimulus.
              • During the final phase, ‘attention termination’, heart rate begins to increase reflecting the end of processing.
                • There is evidence that at least some infants with longer visual fixations spend more time in ‘attention termination’ rather than in ‘active processing’
        • Higher levels of membrane DHA have also been associated with decreased apoptosis in both the retina and in cell systems. However, both apoptotoic and antiapoptotic functions of DHA have been reported, and some of the findings appear to be artifactual… it is likely that the apoptotic effect of DHA is the result of multiple regulations at various signaling stages, from the plasma membrane to nuclear events

  • During the last intrauterine trimester and the first 18 months of human postnatal life, DHA and AA accumulate rapidly in the CNS.

    • The accumulation occurs in part because of transfer of preformed DHA and AA from the mother to the fetus in utero.
      • Important point tbh.
    • Lower DHA accumulation occurs when human infants are born significantly before term (or fed diets free of DHA/AA after birth)
    • Rats receive most transfer of DHA to brain after birth. Brain development in rat pups is most analogous to development in human infants born at the beginning of the 3rd trimester of pregnancy.

  • Diets deficient in Linoleic Acid result in less n-6 LCPUFA in brain, but overall growth, including Brain growth, is less than in the absence of n-6 fatty acid deficiency. It is not surprising that behaviors are affected as has been shown previously for diets deficient in linoleic acids !!!

  • Diets deficient in α-linoleic acid but that contain linoleic acid do not result in less growth than normal, however, they do lead to lower accumulation of DHA in brain phospholipids.

    • Given the lesser accumulation of DHA, an increase in DPA is seen in cell membranes including brain.

  • DHA status of monkeys has not influenced performance on several kinds of learning tasks in monkey infants or adults, evidence against a primary effect of lower neural DHA accumulation on cognition

  • Three of the four studies that fed a source of n-3 LCPUFA without AA reported lower growth in the first year of life. (lower weight, length, and head circumference).

  • Two of the three studies measured developmental outcomes and found higher visual acuity in the first half of infancy, more mature attentional development late in infancy and one found higher performance on a scale of development, the Bayley Mental Developmental Index, at 12 months corrected age. These results were not seen in diets with AA+DHA.

Neurotransmitters #

  • A lower pool of dopamine in pre-synaptic vessels in both the meso-cortical and meso-limbic systems when DHA is replaced by DPA. These papers share many authors, all ω-3 shills.

  • Increases in dopamine, serotonin and their metabolites when DHA and AA are added to piglet feeds compared to a diet deficient in α-linolenic acid.

  • In a later study, they found newborn brain dopamine to be inversely related to DHA in brain phospholipids DHA but negatively related to AA, which were in turn related to the amount of α-linolenic acid in the diet

  • DHA status has been shown to reduce the GABA response and to increase ACh.

  • Piglets fed diets with DHA and AA have large increases of several biologically active acylethanolamide (Anandamide (arachidonoylethanolamide) is a cannabonoid receptor agonist; buffers dopamine overproduction, memory consolidation, et al) metabolites of these two fatty acids.

  • Dietary AA did not increase brain AA, but it did result in large increases in brain anandamide

The role of dietary n-6 and n-3 fatty acids in the developing brain (Innis, 2000) Readers interested in state-of-the-art discussion of the mechanisms of action that could underlie low DHA status in the central nervous system and retina, respectively, are referred to reviews by Salem et al. [110] and Politi [116].

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