PUFA Deficiency Highly Protective Against Endoxotin

[haidut]

Something Ray has written about. Unfortunately, there are only animal studies but I think they are still indicative of the synergy between endotoxin and PUFA. The proposed mechanism of action is reduced prostaglandins in PUFA deficient organisms.

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability - PubMed
Resistance of essential fatty acid-deficient rats to endotoxic shock - PubMed

"...Intravenous administration of S. Salmonella enteritidis endotoxin (1 mg/100 gm) in normal male Long-Evans rats (7--8 weeks old) produced severe shock with an 88% mortality. In marked contrast, injection of this dose of endotoxin in EFA-deficient rats of the same age resulted in only an 18% mortality. The deficient state afforded significant protection to even supralethal doses of endotoxin (2 mg/100 gm). Evaluation of reticuloendothelial (RE) phagocytic activity with colloidal carbon did not reveal significant differences in RE clearance rates. Within five hours after induction of shock, however, plasma acid hydrolase activity of shocked control rats was approximately double that of the EFA-deficient group. Likewise, the endotoxin induced hypoglycemic response was milder in the EFA-deficient rats. The lower plasma glutamic-oxaloacetic transaminase activity and glutamic-pyruvic transaminase activity of the EFA-deficient group also indicated a maintenance of hepatic integrity. These observations suggest that essential fatty acids of their products (ie, prostaglandins) contribute to the pathogenesis of endotoxic shock."

 

[Such_Saturation]

I think Mead's acid can block some prostaglandin production, so that might be involved.

 

[narouz]

This whole "PUFA deficiency" series has been great, haidut.
And you are inscribing the Peat ironic way of naming it each time,
which I enjoy.

 

[andvanwyk]

Amazing, great studies. Thanks for posting.

 

[haidut]

This whole "PUFA deficiency" series has been great, haidut.
And you are inscribing the Peat ironic way of naming it each time,
which I enjoy.

Thanks and also thanks to "burtlancast"! His request for study showing PUFA are not needed for human cells to grow in vitro is what led to these findings and posts.

 

[narouz]

I remember Peat, in an interview, offering a specific criticism of Chris Masterjohn (sp?)
on the question of the essentiality of PUFA.
He generally had high praise for Masterjohn,
but did criticize him gently for still subscribing to the idea that they are, to some extent, essential.

 

[Such_Saturation]

But they can just keep splitting the "requirements" down to the last molecule, so it will take a while before they give up.

 

[Xemnoraq]

Is anybody aware of PUFA depletion taking longer than 4 years? That was always the number I gathered but the I read Ray's quote a little more and he said "significant amount of oils will still be present up in the tissues even after 4 years", so is PUFA depletion something that you can still see improvements on 4+ years?

 

[cedric]

Mead acid inhibits the growth of KPL-1 human breast cancer cells in vitro and in vivo

Mead acid inhibits the growth of KPL-1 human breast cancer cells in vitro and in vivo
Authors: Yuichi Kinoshita Katsuhiko Yoshizawa Kei Hamazaki Yuko Emoto Takashi Yuri Michiko Yuki Nobuaki Shikata Hiroshi Kawashima Airo Tsubura


"Mead acid (MA; also referred to as 5,8,11-eicosatrienoic acid), which was first characterized by James F. Mead, is a carboxylic acid with a 20-carbon chain and three methylene-interrupted cis double bonds, in which the first double bond is located at the ninth carbon from the terminal methyl group of a fatty acid (20:3n-9; Fig. 1). MA is a minor constituent of plasma and tissue in adult mammals. Elongation and desaturation of OA take place to form MA when n-6 and n-3 essential fatty acids, particularly LA, are deficient. Therefore, MA elevation in the blood is an indication of essential fatty acid deficiency. MA is found in large quantities in cartilage; MA decreases osteoblastic activity for the maintenance of cartilage to prevent ossification and suppresses angiogenesis to maintain avascular status (16,17). Angiogenesis plays an important role in the growth of breast cancer (18), and anti-angiogenic agents [inhibitors of vascular endothelial growth factor (VEGF)] and the VEGF receptor (VEGFR) may be promising targets for breast cancer control (19,20). The loss of cell adhesion is related to cancer invasion and metastasis. MA is related to the expression of the cell-cell adhesion molecule E-cadherin in human cancer cell lines including breast cancer cells (21,22). E-cadherin-mediated signaling can influence invasive and metastatic behavior (23,24). VEGF and/or E-cadherin signaling may modulate breast cancer growth at the primary site, and invasion and metastasis in the MA-rich condition. In addition, leukotriene B4 (LTB4) enhances tumor growth in human cancer cells including breast cancer cells (25,26). Dietary supplementation with MA suppresses LTB4 in rats (27,28). Moreover, a nested case-control study revealed an inverse association between MA and breast cancer risk as well as overall cancer risk (29); in the present study, neither the n-6/n-3 ratio nor AA intake correlated with breast cancer risk. Collectively, MA may exert cancer preventive properties. However, MA shows different effects on different types of cancer cells (21,22). The present study was designed to explore the effect of MA on KPL-1 human breast cancer cell growth and metastasis. The mechanisms of action were investigated based on VEGF and E-cadherin signaling and the modulation of fatty acid composition.