Let me clarify: Inefficient conversion of dietary ALA to DHA is neither correlated nor causative to anything.
My point is that ALA provides adequate, not elevated levels of DHA, and there's no evidence to the contrary.
Now let's examine the actual context of my quote:
> ALA is adequately converted to DHA
I think it's worth mentioning where you make a false statement, directly after citing inefficient conversion rates in humans.
>It specifically states that ALA->DHA is only a phenomena that occurs in rats and not humans.
Which is it, inefficient or non-existent in humans?
This statement:
>It is not enough to assume that ALA exerts effects through conversion to EPA and DHA, as the process is highly inefficient in humans.
... Says exactly nothing about healthy levels of DHA. It is non sequitur. It skirts the issue, it avoids the topic, the statement tries to make a huge jump in unreasonable unproven logic. This paper shows nothing but the therapeutic effect of DHA/EPA on diseased people.
There is no evidence to suggest inadequate DHA is produced from dietary ALA in otherwise healthy humans. Not in this paper, nor any I've seen.
> Inefficient conversion of dietary ALA to DHA is neither correlated nor causative to anything
It's correlated with being a human, but the significance of very inefficient conversion versus trivial conversion is simply that it prevents us from claiming they are metabolically identical goods.
>Which is it, inefficient or non-existent in humans?
Inefficient. 'ALA->DHA' shorthand was meant to token the previous idea of "efficient endogenous ALA to DHA conversion" and not initialize a new false one.
>no evidence to suggest inadequate DHA
I think you're missing the point by intentionally or unintentionally rephrasing this in terms of avoiding a negative. Let me requote the initial context by jeremymims:
> Just for the record, fish consumption is linked to increased IQ in children because of the presence of Omega-3 Fatty Acids. Did you know though that both Flaxseed and Walnuts are both better, cheaper, and less environmentally damaging sources of Omega 3s than fish?
My primary point is that one cannot rationally assert that the numerous positive IQ benefits scientific literature attributes to consumption of fish and fish oil are somehow equally or better attributable to walnut and flax consumption. The evidence indicates differing methods of action and a need to consider their health benefits independently.
My point is that ALA provides adequate, not elevated levels of DHA, and there's no evidence to the contrary.
Now let's examine the actual context of my quote:
> ALA is adequately converted to DHA
I think it's worth mentioning where you make a false statement, directly after citing inefficient conversion rates in humans.
>It specifically states that ALA->DHA is only a phenomena that occurs in rats and not humans.
Which is it, inefficient or non-existent in humans?
This statement: >It is not enough to assume that ALA exerts effects through conversion to EPA and DHA, as the process is highly inefficient in humans.
... Says exactly nothing about healthy levels of DHA. It is non sequitur. It skirts the issue, it avoids the topic, the statement tries to make a huge jump in unreasonable unproven logic. This paper shows nothing but the therapeutic effect of DHA/EPA on diseased people.
There is no evidence to suggest inadequate DHA is produced from dietary ALA in otherwise healthy humans. Not in this paper, nor any I've seen.