Dissonant Discourse

This is just an excerpt from an interview conducted by Robert Crayhon, MS talking about the Paleolithic diet and its modern implications with Loren Cordain, PhD. There was a little section on arachidonic acid I thought was interesting.

Robert Crayhon: This brings us to the enormous topic of the shift in the kinds of fats in the Paleolithic even through the last centuries favoring the Omega-6’s…safflower, sunflower, corn oil, and arachidonic acid rich meats devoid of EPA/DHA as opposed to…

Loren Cordain: This shift has only occurred in the last 80 years or so.

Robert Crayhon: And what has happened because of that shift?

Loren Cordain: The types of fats that you eat influence the type of fats that are incorporated in the cell membrane. They can also influence hormonal profiles, and eicosanoid function. We tend to see a more inflammatory eicosanoid profile with elevated levels of Omega-6 fats.

Robert Crayhon: And also arachidonic acids?

Loren Cordain: The information is equivocal on arachidonic acid. Initial experiments indicated that arachidonic acid had mainly deleterious effects. A recent metabolic ward study of arachidonic acid indicates otherwise (Nelson GJ, et al. A human dietary arachidonic acid supplementation study conducted in a metabolic research unit: rationale and design. Lipids. 1997; 32: 415-420).

Arachidonic acid is an essential fatty acid in virtually every cell of the body, and it is an important precursor for prostanoid synthesis and tissue function.

More recent data suggests that the balance of arachidonic acid to long chain Omega-3 fatty acid may be more important in influencing health than absolute dietary intakes of arachidonic acid.

Germ-line epigenetic modification of the murine Avy allele by nutritional supplementation

Jennifer E. Cropley*,{dagger}, Catherine M. Suter*,{ddagger}, Kenneth B. Beckman{dagger}, and David I. K. Martin*,{dagger},§,¶

*Victor Chang Cardiac Research Institute, 384 Victoria Street, Darlinghurst 2010, Sydney, Australia; §School of Biotechnology and Biomolecular Sciences and {ddagger}Faculty of Medicine, University of New South Wales, Anzac Parade, Kensington 2033, Sydney, Australia; and {dagger}Children’s Hospital Oakland Research Institute, 5700 Martin Luther King Junior Way, Oakland, CA 94609

Edited by Mark T. Groudine, Fred Hutchinson Cancer Research Center, Seattle, WA, and approved September 27, 2006 (received for review August 16, 2006)

Environmental effects on phenotype can be mediated by epigenetic modifications. The epigenetic state of the murine Avy allele is highly variable, and determines phenotypic effects that vary in a mosaic spectrum that can be shifted by in utero exposure to methyl donor supplementation. We have asked if methyl donor supplementation affects the germ-line epigenetic state of the Avy allele. We find that the somatic epigenetic state of Avy is affected by in utero methyl donor supplementation only when the allele is paternally contributed. Exposure to methyl donor supplementation during midgestation shifts Avy phenotypes not only in the mice exposed as fetuses, but in their offspring. This finding indicates that methyl donors can change the epigenetic state of the Avy allele in the germ line, and that the altered state is retained through the epigenetic resetting that takes place in gametogenesis and embryogenesis. Thus a mother’s diet may have an enduring influence on succeeding generations, independent of later changes in diet. Although other reports have suggested such heritable epigenetic changes, this study demonstrates that a specific mammalian gene can be subjected to germ-line epigenetic change.

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