The potential nutritional strategies
to prevent or treat Alzheimer’s perhaps via the ApoE gene/protein is certainly
an interest of mine. One concern I have reading through the comments regards
recommendations for the intake of fat – namely that saturated fats should be
avoided and PUFA should be preferred. At risk of straying too far off
mainstream, my sense is that the unsaturated fats, given the higher likelihood
to be oxidized than saturated fats, can create some of the situations we are
seeing with Alzheimer’s pathology. From this article (1):
“ROS (reactive oxygen species) and RNS (reactive nitrogen species) can
substantially disrupt physiological processes through participation in
reduction–oxidation (redox) reactions involving the loss (oxidation) or
addition of electrons (reduction). Polyunsaturated
fatty acids (PUFAs), which are characterized by conjugated double carbon bonds
that can act as a source of electrons, are particularly susceptible to
oxidative damage. Cell membranes are rich in PUFAs, and free radical damage to
PUFAs can reduce the integrity of the membrane.”
In this summary piece on AD (2), these Harvard researchers state
that AD is caused by mitochondrial dysregulation due to oxidative damage. For
cellular structures made up of PUFA, the damage, it seems to me, will be much
greater than with saturated fats which are more resistant to oxidation.
(3) There are not many well designed
studies teasing out this issue/
(1)
Da Costa,
et al. Genetic Determinants of Dietary Antioxidant Status. Progress in
Molecular Biology and Translational Science Volume 108, 2012, Pages 179-200
(3)
Br J Nutr. 1987
May;57(3):383-93. Differential oxidation of saturated and unsaturated fatty
acids in vivo in the rat.
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