This post will be followed by a longer post on seed oils in the hopeful near future.
I shall try to show from "first principles" alone the likely negative health implications resulting from the generally recommended increased consumption of n-6 fats – with organizations like ADA and AHA being two of worst offenders.
All points in this post should be (bloody) obvious and indisputable for anybody slightly versed in the fields of chemistry, biology, evolution and medicine.
0. Linoleic acid is essential
As the human body can not produce linoleic acid, yet various functions in the body depend on it as precursors to other molecules, linoleic acid needs to be consumed.
(I think much of the confusion over the "healthyness" of seed oils stems from this fact. Water is by the same measure essential, yet the consumption of supranatural amounts of water can kill you, and given enough persistence will in fact kill you.)
1. An increased consumption of linoleic acid increases levels of said fats in the stomach, in the blood, and finally in the tissues.
Otherwise the recommendations of the ADA and AHA would be completely nonsensical.
2. The body has no mechanism to regulate the tissue levels of linoleic acid
It is always hard to prove a negative. I am however not aware of any mechanisms by which the body would regulate the levels of specific fatty acids.
Furthermore I think it should be obvious that no such mechanism was necessary in evolutionary past, as we see in the next point:
3. No other naturally occurring food besides seed oils enables to consume such large amounts of linoleic acid
Every other naturally food in this world contains comparatively low levels of linoleic acids.
Even if someone consumes seeds (and nothing but seeds) it is difficult to reach these amounts of linoleic acid that one can consume with seed oils (and should consume, according to the ADA and AHA).
Once more: Only with seed oils is it possible to massively increase the consumption linoleic acid – no other food in the world can do that.
(Furthermore seed oils makes it possible to consume massively more n-6 than n-3 fatty acids, unlike most other foods. Usually food contains – with pork and fish being two prominent exceptions – roughly equal amounts of n-3 and n-6 fatty acids. That will be important for the eicosanoid point further down the list.)
The proof for this point (the linoleic acid content of various foods) is left as exercise to the reader – the data is available. (E.g. I can recommend the very excellent German Bundeslebensmittelschlüssel BLS, which can be searched in German for free on this commercial website. The BLS data is even available in English.)
4. Consumption of seed oils in large amounts is only possible for about a century
Before the industrial production of seeds oils, it was simply not possible to consume linoleic acid in large amounts. I think this should be self evident.
5. The recommendations of the ADA and AHA should be considered as consumption of supranatural levels of linoleic acid
As far as I know no identified deficit is addressed by the the recommendation to consume supranatural levels of linoleic acid. As far as I know no mechanism is stated by which the need would arise to consume supranatural levels of linoleic acid. Supposedly n-6 fatty acids are more healthy than saturated fat, but no mechanism has been shown so far despite decades of research.
The practice of the ADA and AHA to recommend the consumption of supranatural levels of linoleic acid reminds me of those who recommend various supplements based on cherry-picked, slim and vague data – with arguably the volume of cherry-picked slim and vague data from the ADA and AHA being quite large.
6. There was not enough evolutionary time to adapt to the massively increased consumption of linoleic acids
Should be obvious for anybody with a little bit of experience with evolution that there was not enough evolutionary pressure and not enough time to adapt to a diet high in seed oils – if you dispute this fact, I'm afraid there is nothing I can do for you.
7. Supranatural amounts of linoleic acid in the tissue will lead to supranatural levels of series 2 prostaglandins in the tissue
So let me present my strongest evidence:
To summarize:
- Eicosanoids are signalling molecules derived from n-3 and n-6 fatty acids, involved in processes like inflammation.
- The left column is the n-3 cascade, the one on the right the n-6 cascade
- n-3 fatty acids are converted among others into PG3s (series 3 prostaglandins, a type of eicosanoids, the box to the right of EPA)
- n-6 fatty acids converted among others into PG1s and PG2s (series 1 and series 2 prostaglandins, the boxes to the left of DGLA and AA)
- Both the n-3 and n-6 fatty metabolism shares the same enzymes (e.g. delta6-desaturase, elongase, delta5-sesaturase, and so on) to produce their various eicosanoids.
- While it is considered that n-3 fatty acids have a greater "affinity" to these enzymes, if you massively increase the amount of linoleic acid (on the top of the right column) – through say the ADA and AHA recommended consumption of seed oils – this will massively increase the amount of PG1 (turquoise box) and PG2 (red box, uh-huh, red isn't good, is it?)
- PG3s (produced from n-3 fatty acids) are generally considered "less inflammatory"
- PG2s (produced from n-6 fatty acids) are generally considered "more inflammatory" (again, the red box) – seed oil, a bona fide candidate for a disease mechanism involved in heart disease. *
If you eat seed oils, you increase the levels of the pro-inflammatory series 2 prostaglandins above what would be considered "natural" – no other food can do that.
If you think this is good, then you might be an idiot.
People at the ADA and AHA think that the consumption of supranatural levels of seed oil is good.
People at the ADA and AHA might be idiots.
Further studies are warranted.
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* Be advised that this is not the only mechanism by which seed oils and the overconsumption of linoleic acid will cause disease – see here for a mechanism by which seed oils and the overconsumption of PUFAs could cause obesity and T2DM.
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