On Jul 1, 9:45 pm, MattLB <mat...@angelfire.com> wrote:
> Well done on posting something that's suggests EFA are actually
> required for health, but you've done your usual thing of giving the
> post a completely misleading title. It wasn't an excess of omega 6
> that caused the DHA deficiency, it was a linolenic acid deficiency
> that caused a DHA deficiency.
The title concerns the Blog I found interesting rather than the cited
paper. It's suggested in the Blog that in the presence of "enough" AA
the desaturase-elongase apparatus is inhibited leading to the
deficiency in the manufacture of the other LC-PUFAs such as DHA and of
course Mead acid. There are many claims about the poor conversion of
ALA to the LC-PUFAs such as EPA/DHA in humans (and non-pregnant women
especially) these days (justifying the consumption of fish oil
supplements) but the researchers are missing the possibility that the
molecular machinery manufacturing LC-PUFAs is inducible. And what
else can induce it than a mild "deficiency" of its end products.
Because the same machinery is used for the production of all Omega-3,
Omega-6 and Omega-9 series of LC-PUFAs, any of them would inhibit its
expression. The cited Abstract and some other papers you may have
also mentioned in the past suggest that the Omega-3 LC-PUFAs such as
DHA are required during the development of brain and eyes. So it may
be wiser to stay in a mild EFAD state rather than supplement any of
the "EFAs" risking an improper balance leading to e.g. DHA (or Mead
acid) deficiency due to its suppressed manufacture from the shorter
PUFAs.
Interestingly, both the Blogger (feeling better at 52 than during his
teenage years) and Monty (cured from a wasting disorder) restrict the
consumption of dietary PUFAs ...
Taka
MattLB
