Todd Moody wrote:

>>>Perhaps, but it remains mysterious how it is possible for >people who eat
>>little or no EPA and DHA to avoid deficiencies.

Like me.  Zero DHA eaten for 18 years now, and I did the test on DHA.
It was quite high over the lower 5% levels (no standard is given).
It must have been synthesised all.

I took a closer look at the (a little cryptic) findings of the study
Theola cited.

Interesting was: 33% of the carbon was found in the breath.
That much has been used a fuel. Looks like "preferred fuel" is right.
Unfortunately it was not told how much had been given.

Then: only 6 subjects, on their habitual diet, only 21 days.
The LNA was not made into (blood plasma) DHA.
Very probable these people were eating meat (containing some DHA)
and probable were LNA deficient before, because the "usual" diets is
high in w-6 and low in w-3.

This would lead me to the following expectations:
1.LNA is a important part of cell walls (phospholipids).
The first LNA given would go into direct use of LNA to equal out
previous defficiencies (Erasmus estimates 2 years for the process).
Not much would be left for further elongation (in the first 21 days).

2.Why should the body make DHA, if DHA is already enough?
There *is* a enzyme to downgrade DHA to EPA.
If such a enzyme exists, then there must be a feedback loop in control
of the process. If DHA is already high, then the existing level control
should be steering towards *downregulation* of DHA instead of new
production.

3.DHA in cell walls of blood cells were measured and they didn't contain
new made DHA. How much percent of blood cells are made new within 21
days anyway?

In the short report about the study we don't see how much LA was eaten.
Much LA would result for increased competition for d5d on the w-3 way,
thus inhibiting the step before EPA and DHA making.

I think to be useful we should be able to know about the rest of the
"habitual" diet in the study.

>... Patricia
> Kane, a scientist who does extensive biochemical work with
> autistic children, has found that for some unknown reason they
> tend to have a massive *surplus* of DHA.

So, the downgrade mechanism DHA -> EPA isn't very active.
This could result in increased further elongation of DHA (and AA)
to even longer chain molecules.

This would lead into the problematic we know about since "Lorenzo's
oil". Brain function problems.

Cheers,

Amadeus