Ray Peat in his own words/pufa/long w/references

[Guest guest]

I took some of our discussion and asked ray directly to clarify some

of this. Here is what he told me verbatim.

I don't think I could have said " reduces the need for efa, " because I

don't

know of any need; some people have probably paraphrased my argument.

I think the issue is just one of propaganda analysis, because

scientifically, no one ever refuted the refutation of essentiality

which

occurred when the " EFA deficiency syndrome " was cured with vitamin

B6. The

German demonstration that spontaneous cancer was eliminated on a fat

free

diet preceded the really awful, incompetent study that supposedly

demonstrated the essentiality of polyunsaturated fatty acids, and in

the 75

years since the German study a tremendous amount of information has

accumulated showing both the toxicity and the non-essentiality of the

polyunsaturated fatty acids. But there has been no financial support

for

publicizing the protective effect of not eating vegetable oils or fish

oils. To the contrary, vast amounts of money are being spent in the

promotion of the various polyunsaturated fats as foods.

The animals that don't eat them do have increased nutritional needs

for

vitamins and minerals, because their metabolic rate is so much

greater than

the PUFA-replete animals whose cardiolipin has degenerated. The recent

Stanford study that shows a much greater longevity for old people who

have

a very high oxygen consumption capacity is consistent with the

historical

animal studies. PUFA-deprived animals have a very high oxygen

consumption,

and are resistant to practically all causes of death and disease,

including

trauma and poisoning.

The editorial boards of many of the journals are packed with industry

flacks who are apparently willing to publish any junk that helps to

sell

soy oil, canola, waste fish oil, or algal oils. And researchers have

to get

grants to stay in business.

Lipids 1999 Apr;34(4):317-24

Docosahexaenoic acid ingestion inhibits natural killer cell activity

and

production of inflammatory mediators in young healthy men.

Kelley DS, PC, GJ, Schmidt PC, Ferretti A, kson KL,

Yu R,

Chandra RK, Mackey BE.

USDA, ARS, Western Human Nutrition Research Center, Presidio of San

Francisco,

California 94129, USA. Dkelley@...

The purpose of this study was to examine the effects of feeding

docosahexaenoic

acid (DHA) as triacylglycerol on the fatty acid composition,

eicosanoid

production, and select activities of human peripheral blood

mononuclear cells

(PBMNC). A 120-d study with 11 healthy men was conducted at the

Metabolic

Research Unit of Western Human Nutrition Reach Center. Four subjects

(control

group) were fed the stabilization diet throughout the study; the

remaining

seven

subjects were fed the basal diet for the first 30 d, followed by 6 g

DHA/d for

the next 90 d. DHA replaced an equivalent amount of linoleic acid;

the two

diets

were comparable in their total fat and all other nutrients. Both

diets were

supplemented with 20 mg D alpha-tocopherol acetate per day. PBMNC

fatty acid

composition and eicosanoid production were examined on day 30 and

113; immune

cell functions were tested on day 22, 30, 78, 85, 106, and 113. DHA

feeding

increased its concentration from 2.3 to 7.4 wt% in the PBMNC total

lipids, and

decreased arachidonic acid concentration from 19.8 to 10.7 wt%. It

also

lowered

prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) production, in

response to

lipopolysaccharide, by 60-75%. Natural killer cell activity and in

vitro

secretion of interleukin-1beta and tumor necrosis factor alpha were

significantly reduced by DHA feeding. These parameters remained

unchanged

in the

subjects fed the control diet. B-cell functions as reported here and

T-cell

functions that we reported previously were not altered by DHA

feeding. Our

results show that inhibitory effects of DHA on immune cell functions

varied

with

the cell type, and that the inhibitory effects are not mediated

through

increased production of PGE2 and LTB4.

J Bacteriol 1993 Sep;175(17):5324-8

Escherichia coli produces linoleic acid during late stationary phase.

Rabinowitch HD, Sklan D, Chace DH, s RD, Fridovich I.

Department of Biochemistry, Duke University Medical Center, Durham,

North

Carolina 27710.

Escherichia coli produces linoleic acid in the late stationary phase.

This was

the case whether the cultures were grown aerobically or anaerobically

on a

supplemented glucose-salts medium. The linoleic acid was detected by

thin-layer

chromatography and was measured as the methyl ester by gas

chromatography. The

linoleic acid methyl ester was identified by its mass spectrum. Lipids

extracted

from late-stationary-phase cells generated thiobarbituric acid-

reactive

carbonyl

products when incubated with a free radical initiator. In contrast,

extracts

from log-phase or early-stationary-phase cells failed to do so, in

accordance

with the presence of polyunsaturated fatty acid only in the

stationary-phase

cells.

Clin Sci (Lond) 1987 Mar;72(3):383-5

Effect of dietary linoleate content on the metabolic response of rats

to

Escherichia coli endotoxin.

Wan JM, Grimble RF.

Dietary fat influences many aspects of immune function. Escherichia

coli

endotoxin is a potent stimulator of interleukin 1 production from

macrophages.

The present study examines the effect of feeding with fat diets rich

(corn

oil)

and poor (coconut oil) in linoleate at high and low concentrations on

responses

to endotoxin. Spleen phosphatidylcholine linoleate contents were

higher in the

corn oil than in the coconut oil group and arachidonate

concentrations were

highest in the group fed a high concentration of corn oil. Coconut oil

completely abolished the responses to endotoxin. The inhibitory

effects of

coconut oil could largely be due to reduced prostaglandin and

leukotriene

synthesis.