No correlation between dietary linoleic acid (omega-6) and inflammation

Too much linoleic acid promotes inflammation-doesn't it?
Fritsche KL.
Source

University of Missouri, Columbia, MO, USA. fritschek@missouri.edu
Abstract

Controversy exists over how much linoleic acid (LA) should be consumed in a healthy diet. Some claim that high LA intake promotes inflammation through accumulation of tissue arachidonic acid (AA) and subsequent production of pro-inflammatory lipid mediators. Here the author reviews the current available evidence from human studies that address this issue. The data indicate that high LA in the diet or circulation is not associated with higher in vivo or ex vivo pro-inflammatory responses. Surprisingly, several studies showed that those individuals consuming the highest level of LA had the lowest inflammatory status. Recent findings suggest that LA and AA are involved in both pro- and anti-inflammatory signaling pathways. Thus, within the ranges of intake that are achievable for most human populations, the evidence do not support reducing LA intake below current consumption levels.

imprisoned-radical wrote:I hate it when i find information which contradicts what I believe, but here it is:

Too much linoleic acid promotes inflammation-doesn't it?
Fritsche KL.
Source

University of Missouri, Columbia, MO, USA. fritschek@missouri.edu
Abstract

Controversy exists over how much linoleic acid (LA) should be consumed in a healthy diet. Some claim that high LA intake promotes inflammation through accumulation of tissue arachidonic acid (AA) and subsequent production of pro-inflammatory lipid mediators. Here the author reviews the current available evidence from human studies that address this issue. The data indicate that high LA in the diet or circulation is not associated with higher in vivo or ex vivo pro-inflammatory responses. Surprisingly, several studies showed that those individuals consuming the highest level of LA had the lowest inflammatory status. Recent findings suggest that LA and AA are involved in both pro- and anti-inflammatory signaling pathways. Thus, within the ranges of intake that are achievable for most human populations, the evidence do not support reducing LA intake below current consumption levels.

I'm very open to the idea that peat is on an unjustified PUFA witch hunt, but what can you gleam from this?

imprisoned-radical wrote:Well, it's vague but I don't think it's useless. Hopefully I'll be able to find the actual review, and that way I can look through the studies which were used. There are factors to consider before jumping to conclusions. For example, increasing intake of linoleic acid by adding nuts to one's diet is not the same as adding refined vegetable oils.

I'm very open to the idea that peat is on an unjustified PUFA witch hunt, but what can you gleam from this?

Sometimes I feel like Ray Peat has an intellectual grudge against certain foods (anything containing PUFA), and a bias favoring others (caffeine/coffee, coconut oil, dairy). Even though he presents some sophisticated arguments, it could be that he just really likes how some foods taste. When you like a particular food and it's not undeniably terrible for your health (ie., donuts and chips), you can do a pretty good job producing arguments suggesting that the food is great for your health. Especially if you have some knowledge of important biology concepts.

He promotes coffee, coconut oil, and dairy as if they were the foods of Gods, but I've seen plenty of studies suggesting otherwise. In particular excessive intake of caffeine has been linked to disregulation of sugar metabolism and spikes in cortisol.

I just had some iced coffee first thing in the morning and it really hit the spot. Based on this positive experience I'm more likely to think about the health-promoting effects of coffee than the bad stuff I mentioned above.

Summary
Evidence from in vitro studies shows that increased intake of polyunsaturated fatty acids leads to increased oxidative stress, which may be associated with endothelial damage. We measured the urinary levels of 8-iso-PGF2~ and nitric oxide metabolites as well as plasma slCAM-1 levels from healthy subjects after strictly controlled diets rich in either linoleic acid (LA, C18:2 n-6) or oleic acid (OA, C18:1 n-9).

Thirty-eight volunteers (20 women and 18 men, mean age 27 years) consumed a baseline diet rich in saturated fatty acids (SFA) for 4 weeks and were then switched to either a high LA diet (11.5 en%) or a high OA diet (18.0 en%) also for 4 weeks. During the LA and OA diets, nearly all food was provided for the whole day. A control group of 13 subjects consumed their habitual diet throughout the study.

Urinary excretion of 8-iso-PGF2~ was significantly increased after the LA diet (170 vs 241 ng/mmol creatinine, P=0.04), whereas the urinary concentration of nitric oxide metabolites decreased (4.2 vs 2.6 mg/mmol creatinine, P=0.03). No significant changes were seen in the OA group. Significant differences between the LA and control group were found for both 8-oxo-PGF2~ (P=0.03) and NO (P=0.02), whereas the OA and LA groups did not differ with respect to any parameter. Also plasma slCAM-1 remained unchanged in both groups throughout the study. In conclusion, the high-LA diet increased oxidative stress and affected endothelial function in a way which may in the long-term predispose to endothelial dysfunction.

Abstract
Recent studies primarily in man have shown that cod fish oil rich in polyunsaturated fatty acids (PUFA) are beneficial to certain inflammatory diseases such as ulcerative colitis. This study was undertaken to observe any change in intestinal secretion where the tissues have been treated with cod fish and sunflower oils. Male Sprague Dawley rats weighing 200 gms were fed omega-3 fatty acids for 50 days. Changes in colonic secretion (fed with PUFA) were studied in-vitro in an Ussing chamber. Rat colon which were not fed with PUFA served as controls. Basal intestinal short circuit in PUFA group were comparable with control group in stripped rat colon. The results showed significant high short circuit current in cod fish oil and sunflower oil treated tissues. When stripped colonic tissues (fed with PUFA) were stimulated by EC50 of carbachol, bradykinin and prostaglandin; there was no significant changes in Short circuit current. PGE2 and LTB4 levels were measured in rat colon fed with PUFA by using radioimmunoassay. Biochemical changes in PGE2 and LTB4 levels showed LTB4 were significantly raised in both cod fish oil group and sunflower oil group. This study reveals that intestinal permeability increases in the rat colon (fed with PUFA) as indicated by high short circuit current. The high levels of leukotriene in colonic tissues also explains the high basal short circuit current in the present study.