Re: TO: Matti - can you defend the EFA claim as good as your Omega-3 claims?

Matti Narkia wrote:

Matti Narkia wrote:

Taka wrote:

But when we
are at it could you please post some modern studies in the defense of
your claim that the Omega-6 and Omega-3 fatty acids are essential for
humans? I would love to see such studies, not the old flawed Burr &
Burr stuff.

I don't believe this! It seems that you and monty have started to
promote EFA deficiency and mead acid without first doing your
homework, i.e. doing the Medline searches to find out what harmful
effects they possibly could cause! Here some results from such a
search, notice especially the studies suggesting that EFA deficiency
and mead acid (eicosatrienoic acid (20:3 n-9)) may promote cancer!

Piper CM, Carroll PB, Dunn FL.
Diet-induced essential fatty acid deficiency in ambulatory patient with type I diabetes mellitus.
Diabetes Care. 1986 May-Jun;9(3):291-3.
PMID: 3731994
<http://www.ncbi.nlm.nih.gov/pubmed/3731994>

"We report a case of symptomatic essential fatty acid deficiency
(EFAD) occurring in a free-living individual with type I diabetes
mellitus who was voluntarily following a high-carbohydrate,
fat-restricted diet. The patient was 43 yr old with type I diabetes
for 18 yr and no chronic complications. His self-imposed diet
excluded all red meats, fats, and oils. After several months of
this diet, the patient developed lethargy and a pruritic, diffuse,
scaly, and erythematous rash. Biochemical studies revealed a mildly
elevated SGOT and abnormally low levels of linoleic, linolenic, and
arachidonic fatty acids. Treatment with linoleic acid
supplementation in his diet improved the rash, normalized SGOT,
and corrected the fatty acid profile. We conclude that EFAD may
occur in a free-living individual after consuming a very-low-fat
diet."

Palmblad J, Wannemacher RW, Salem N Jr, Kuhns DB, Wright DG.
Essential fatty acid deficiency and neutrophil function: studies of lipid-free total parenteral nutrition in monkeys.
J Lab Clin Med. 1988 Jun;111(6):634-44.
PMID: 2836537
<http://www.ncbi.nlm.nih.gov/pubmed/2836537>

"These findings indicate that endogenous supplies of arachidonic
acid and other essential omega 6 fatty acids influence the
functional responsiveness of neutrophils. These studies also
indicate that altered neutrophil function is a feature of essential
fatty acid deficiency and that it may contribute to the increased
risk of infection and decreased inflammatory responses observed in
this condition."

Anderson GJ, Connor WE.
On the demonstration of omega-3 essential-fatty-acid deficiency in humans.
Am J Clin Nutr. 1989 Apr;49(4):585-7.
PMID: 2494878
<http://www.ajcn.org/cgi/reprint/49/4/585>

"Omega-3 fatty acid deficiency has been studied in experimental
animals for many years. All species of land animals studied to
date grow normally when fed a diet specifically deficient in w-3
fatty acids in contrast to growth failure in animals deficient in
w-6 fatty acids (1). Usually the diet deficient in w-3 fatty
acids lacks a-linolenic acid (1 8:3w-3), the precursor for
20:5w-3, 22:5w-3, and 22:6w-3, the latter metabolite being
present in particularly high proportions in the brain and retina.
Although mammals deficient in w-3 fatty acids do not develop
overt external abnormalities, nevertheless some signs of
the deficient state have been observed. These include decreased
visual acuity in rhesus monkeys (2), abnormal electroretinograms
in monkeys and in some rats (3, 4), reduced maze-running ability
in rats(5), and a reported rise in perinatal mortality in rats (6).
In contrast, fish grow poorly on such a diet and develop
cardiomyopathy and a shock syndrome (7).

On the other hand, skin lesions are the hallmark of w-6 fatty
acid deficiency in both humans and animals (8, 9). Skin lesions
have not been a conspicuous finding in the animals studies with
well-documented w-3 deficiency as this review will discuss.

The first report of human w-3 fatty acid deficiency, by Holman
et al (10), appeared in 1982. A 7-y-old girl maintained on total
parenteral nutrition because of gunshot wounds developed
neurological and visual problems after switching from an
intravenous soybean oil preparation (adequate in both w-3 and
w-6 fatty acids) to one based on safflower oil (very low in w-3
fatty acids) and the same oil that had produced visual impairment
in monkeys (2). Of note was the absence of skin lesions. These
clinical symptoms disappeared within a few months after use of
the soybean oil preparation was resumed.

[...]

The most recently described cases of “ 18:3w-3 deficiency,”
reported by Bjerve et al ( 1 5, 16), occurred in anumber of
nursing-home patients in Norway, some semicomatose, who were
fed by gastric tube over several years. The diet of these patients
was based on a commercially available powder supplement containing
small amounts of corn oil (1.3 g/lOO g) and was mixed with
skim milk. The authors reported that the patients developed
low plasma levels of w-3 fatty acids and a scaly dermatitis.
These conditions improved after treatment with 1) a combination
of soybean oil and cod liver oil, 2) an unspecified oil mixture
furnishing more linoleic acid (18:2w-6) and 18:3w-3 than the
original diet, or 3) pure ethyl linolenate. The dermatitis was
specifically attributed to a lack of w-3 fatty acids in the diet.

However, before treatment the diet furnished only 0.5% of energy
as 18:2w-6 and the plasma 1 8:2aı-6 was low (9-1 5% of total plasma
fatty acids vs 35% in healthy control subjects [17]) and levels of
eicosatrienoic acid (20:3w-9) were substantially elevated. These
observations suggest that the patients were also deficient in w-6
fatty acids and that perhaps the skin lesions occurred from the w-6
deficiency.

[...]

Animals synthesize eicosatrienoic acid (20:3w-9) in response
to a general shortage of polyunsaturated fatty acids in the diet,
ie, when there is an insufficient cornbined intake of w-3 and w-6
fatty acids. Because dietary w-3 fatty acids can prevent the rise
in the concentration of 2O:3w-9 in plasma that is normally
associated with essential fatty acid deficiency (2 1), it is true
that 20:3w-9 alone is not a reliable indicator of w-6 fatty acid
status. However, this fatty acid is an early and reliable indicator
of total essential fatty acid deficiency, ie, a deficiency of both
w-6 and w-3 fatty acids (17). Experiments with animals and humans
have shown that dietary linoleic acid, but not linolenic acid, is
able to reverse both the elevated levels of plasma 2O:3w-9 and the
skin lesions associated with total essential fatty acid deficiency
(8, 9, 2 1). Such experiments buttress the well-accepted
recommendation that the requirement for linoleic acid represents a
minimum of 1-2% of calories."

In this context eicosatrienoic acid (20:3w-9) means mead acid.

Smith SS, Neuringer M, Ojeda SR.
Essential fatty acid deficiency delays the onset of puberty in the female rat.
Endocrinology. 1989 Sep;125(3):1650-9.
PMID: 2759037
<http://www.ncbi.nlm.nih.gov/pubmed/2759037>

"These results suggest that the delay in puberty resulting from EFA
deficiency is due to a reduced availability of arachidonic acid for
synthesis of bioactive metabolites. This results in delayed
development of both the hypothalamic and ovarian components of the
reproductive axis."

Martín Peña G, Valero Zanuy MA, Llorente Abarca A, Acevedo Rodríguez MT.
[Essential fatty acid deficiency in enteral nutrition]
Nutr Hosp. 1990 Mar-Apr;5(2):123-5. Spanish.
PMID: 2127705
<http://www.ncbi.nlm.nih.gov/pubmed/2127705>

Related Articles, Links
Stĕpánková R, Funda DP, Smetana K Jr.
Essential fatty acid deficiency and bone fragility in rats.
Folia Biol (Praha). 1996;42(5):257-9.
PMID: 8997644
<http://www.ncbi.nlm.nih.gov/pubmed/8997644>

"This study demonstrates the effect of essential fatty acid
deficiency on the postnatal skeletal development in the rat.
Four groups (n = 10) of newborn Wistar rats were fed diets
containing high and low proportions of essential fatty acids
in the lipid fraction until day 16 after birth. Suckled
littermates were used as controls. X-ray and histological
studies showed the occurrence of multiple pathological fractures
of the long bones in 1-month-old rats fed a diet deprived of
essential fatty acids. No effect of high (51,000 IU/100 g diet)
and low (5,100 IU/100 g diet) concentrations of vitamin D2 was
observed in our experiment. Thus, these data suggest the
importance of essential fatty acids for bone pathology in
the rat."

Lloyd-Still JD, Bibus DM, Powers CA, Johnson SB, Holman RT.
Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis.
Acta Paediatr. 1996 Dec;85(12):1426-32.
PMID: 9001653
<http://www.ncbi.nlm.nih.gov/pubmed/9001653>

"CONCLUSIONS AND RELEVANCE: EFA deficiency may contribute to the
predisposition of CF infants to develop respiratory disease and to
the excess cytotoxic activity found in bronchoalveolar lavage fluid
at 2 months of age in the majority of screened infants."

Eynard AR.
Does chronic essential fatty acid deficiency constitute a pro-tumorigenic condition?
Med Hypotheses. 1997 Jan;48(1):55-62. Review.
PMID: 9049990
<http://www.ncbi.nlm.nih.gov/pubmed/9049990>

"Many experimental, clinical and epidemiological data indicate that
n-3 and n-6 essential fatty acids are therapeutic nutrients which
may delay the development as well as improve the course of cancer.
The present hypothesis correlates well with these data and it is
proposed that chronic essential fatty acid deficiency, when
coexisting with chronic hyperproliferative states (hyperplasias)
and de-differentiation (dysplasias) both acting synergistically,
may constitute a pro-tumorigenic situation. Evidence showing that,
indeed, these hyperproliferative states are consistently reported
in essential fatty acid deficiency in many species, including
humans, in malpighian layers of skin and the upper alimentary and
urinary tracts, among others, is discussed."

Eynard AR.
Is the risk of urinary tract tumorigenesis enhanced by a marginal chronic essential fatty acid deficiency (EFAD)?
Nutrition. 1998 Feb;14(2):211-6. Review.
PMID: 9530649
<http://www.ncbi.nlm.nih.gov/pubmed/9530649>

"A considerable amount of experimental, clinical and
epidemiological data indicate that dietary fats play a role
in urinary tract tumorigenesis. In rodents, chronic essential
fatty acid (EFA) deficiency seems to induce both urolithiasis
and transitional hyperplasias, followed by a tendency for
tumorigenesis of the urinary passages. High intake of saturated
fats or non-EFAs, conditions that may induce EFA deficiency
(EFAD) increase the risk of bladder cancer in case-control
studies. In other cell populations, EFAs are beneficial as
preventive and therapeutic nutrients for the treatment of cancer.
Thus, it is reasonable to assume that abnormal metabolism and/or
nutritional deprivation of EFA, by inducing a chronic or a
subclinical EFA deficiency, may enhance the risk of urothelial
tumorigenesis."

Eynard AR, Manzur T, Moyano A, Quiroga P, Muñoz S, Silva SM.
Dietary deficiency or enrichment of essential fatty acids modulates tumorigenesis in the whole body of cobalt-60-irradiated mice.
Prostaglandins Leukot Essent Fatty Acids. 1997 Mar;56(3):239-44.
PMID: 9089806
<http://www.ncbi.nlm.nih.gov/pubmed/9089806>

"It may be concluded that, when a tumor initiator injures the body
as a whole, EFAD, achieved either through a fat-free or an
oleic-supplemented diet, behaves as a general promoting condition
for tumorigenesis."

Jeppesen PB, Høy CE, Mortensen PB.
Essential fatty acid deficiency in patients receiving home parenteral nutrition.
Am J Clin Nutr. 1998 Jul;68(1):126-33.
PMID: 9665106
<http://www.ncbi.nlm.nih.gov/pubmed/9665106>

Eynard AR, Jiang WG, Mansel RE.
Eicosatrienoic acid (20:3 n-9) inhibits the expression of E-cadherin and desmoglein in human squamous cell carcinoma in vitro.
Prostaglandins Leukot Essent Fatty Acids. 1998 Dec;59(6):371-7.
PMID: 10102382 [
<http://www.ncbi.nlm.nih.gov/pubmed/10102382>

"Eicosatrienoic acid (ETA 5,8,11, n-9) is abnormally increased by
essential fatty acid deficiency (EFAD), a condition associated with
alterations of cell proliferation and differentiation. In
comparison to certain EFAs, addition of ETA at a low concentration
resulted in a reduction in the expression of the cell-cell adhesion
molecule, E-cadherin, and to a lesser degree, of desmoglein, along
with increased invasion of Matrigel by human squamous cell
carcinoma (SCC) cells in vitro. At higher concentrations, ETA
stimulated the growth of SCC cells. As previously shown, n-6 EFAs
(mainly 18:3 n-6, GLA), up-regulated the expression of E-cadherin
and desmoglein. This is the first report showing that the abnormal
20:3 n-9 (Mead's acid) is a down regulator of antimetastatic
E-cadherin and desmoglein expression."

Jiang WG, Eynard AR, Mansel RE.
The pathology of essential fatty acid deficiency: is it cell adhesion mediated?
Med Hypotheses. 2000 Sep;55(3):257-62.
PMID: 10985920
<http://www.ncbi.nlm.nih.gov/pubmed/10985920>

"For almost 70 years, essential fatty acid deficiency has been
known to be associated with skin disorders, vessel abnormalities,
and increased tumorigenesis. However, the underlying molecular and
cellular mechanism is largely unknown. Recently, it has been
reported that essential fatty acids regulate cell adhesion by
modifying the expression of cell adhesion molecules. These findings
may provide molecular explanations for those phenomena seen in EFAD
and this paper aims to discuss these relationships and raise points
for further discussion."

Heyd VL, Eynard AR.
Effects of eicosatrienoic acid (20:3 n-9, Mead's acid) on some promalignant-related properties of three human cancer cell lines.
Prostaglandins Other Lipid Mediat. 2003 Jul;71(3-4):177-88.
PMID: 14518560
<http://www.ncbi.nlm.nih.gov/pubmed/14518560>

"The essential fatty acid deficiency (EFAD) is a metabolic
condition related to cancer development. We studied the effect
of eicosapentaenoic acid (EPA, 20:5 n-3) and eicosatrienoic acid
(ETA, 20:3 n-9), an essential fatty acid (EFA) and non-EFA
respectively, on tumour cells parameters linked to tumour
progression and metastases.

[...]

In conclusion, EFA (20:5 n-3) exhibited beneficial effects, whereas
unusual ETA showed an opposite effect on some tumour parameters.
The possible riskiness of EFA-deprivation, along with the
potential of EFA as natural nutrapeutic products for human tumour
prevention and treatment, makes EFA worthy of further
consideration."

Das UN.
Essential fatty acids: biochemistry, physiology and pathology.
Biotechnol J. 2006 Apr;1(4):420-39. Review.
PMID: 16892270 <http://www.ncbi.nlm.nih.gov/pubmed/16892270>

"Essential fatty acids (EFAs), linoleic acid (LA), and
alpha-linolenic acid (ALA) are essential for humans, and are
freely available in the diet. Hence, EFA deficiency is extremely
rare in humans."

Lukovac S, Los EL, Stellaard F, Rings EH, Verkade HJ.
Essential fatty acid deficiency in mice impairs lactose digestion.
Am J Physiol Gastrointest Liver Physiol. 2008 Jul 24. [Epub ahead of print]
PMID: 18653724
<http://ajpgi.physiology.org/cgi/content/abstract/ajpgi.90206.2008v1>

"EFA deficiency in mice inhibits the capacity to digest lactose,
but does not affect small intestinal histology. These data
underscore the observation that EFA deficiency functionally impairs
the small intestine, which in part may be mediated by low LA levels
in the enterocytes. "

More studies about omega-3 deficiency:

Neuringer M, Connor WE, Van Petten C, Barstad L.
Dietary omega-3 fatty acid deficiency and visual loss in infant
rhesus monkeys.
J Clin Invest. 1984 Jan;73(1):272-6.
PMID: 6317716
<http://www.jci.org/articles/view/111202>

Neuringer M, Connor WE, Lin DS, Barstad L, Luck S.
Biochemical and functional effects of prenatal and postnatal omega 3
fatty acid deficiency on retina and brain in rhesus monkeys.
Proc Natl Acad Sci U S A. 1986 Jun;83(11):4021-5.
PMID: 3459166
<http://www.pnas.org/content/83/11/4021>
<http://www.pnas.org/content/83/11/4021.full.pdf+html> (full text PDF)

Coti Bertrand P, O'Kusky JR, Innis SM.
Maternal dietary (n-3) fatty acid deficiency alters neurogenesis in the
embryonic rat brain.
J Nutr. 2006 Jun;136(6):1570-5.
PMID: 16702323
<http://jn.nutrition.org/cgi/content/full/136/6/1570>

Guesnet P, Pascal G, Durand G.
Dietary alpha-linolenic acid deficiency in the rat. I. Effects on
reproduction and postnatal growth.
Reprod Nutr Dev. 1986;26(4):969-85.
PMID: 2877477
<http://www.ncbi.nlm.nih.gov/pubmed/2877477>


"However, this deficiency did cause abnormally high rates of
perinatal mortality from birth to postpartum day 3, namely on the
average, for successive gestations: 18.5% in deficient pups vs 5.2%
in the controls, and for successive generations: 16.6% in deficient
pups vs 5.3% in the controls. Rat n-3 PUFA requirement during
reproduction has been discussed; it appears to be more than 100
mg/100 g of feed. But this need should also be estimated in
relation to n-6 PUFA supply; for female rats during reproduction,
the ratio n-6: n-3 should be less than 10."

Holman RT, Johnson SB, Hatch TF.
A case of human linolenic acid deficiency involving neurological
abnormalities.
Am J Clin Nutr. 1982 Mar;35(3):617-23.
PMID: 6801965
<http://www.ncbi.nlm.nih.gov/pubmed/6801965>
<http://www.ajcn.org/cgi/reprint/35/3/617> (full text PDF)

"A 6-yr-old girl who lost 300 cm of intestine was maintained by
total parenteral nutrition. After 5 months on a preparation rich
in linoleic acid but low in linolenic acid she experienced episodes
of numbness, paresthesia, weakness, inability to walk, pain in the
legs, and blurring of vision. Diagnostic analysis of fatty acids
of serum lipids revealed marginal linoleate deficiency and
significant deficiency of linolenate. When the regimen was
changed to emulsion containing linolenic acid neurological
symptoms disappeared. Analysis indicated that linoleate deficiency
had worsened but linolenate deficiency had been corrected. The
requirement for linolenic acid is estimated to be about 0.54% of
calories."

Bjerve KS, Mostad IL, Thoresen L.
Alpha-linolenic acid deficiency in patients on long-term gastric-tube
feeding: estimation of linolenic acid and long-chain unsaturated n-3
fatty acid requirement in man.
Am J Clin Nutr. 1987 Jan;45(1):66-77.
PMID: 2879436
<http://www.ncbi.nlm.nih.gov/pubmed/2879436>
<http://www.ajcn.org/cgi/reprint/45/1/66> (free full text PDF)

Bjerve KS, Thoresen L, Mostad IL, Alme K.
Alpha-linolenic acid deficiency in man: effect of essential fatty acids
on fatty acid composition.
Adv Prostaglandin Thromboxane Leukot Res. 1987;17B:862-5.
PMID: 2890285
<http://www.ncbi.nlm.nih.gov/pubmed/2890285>

Bjerve KS, Fischer S, Alme K.
Alpha-linolenic acid deficiency in man: effect of ethyl linolenate on
plasma and erythrocyte fatty acid composition and biosynthesis of
prostanoids.
Am J Clin Nutr. 1987 Oct;46(4):570-6.
PMID: 3310599 [
<http://www.ncbi.nlm.nih.gov/pubmed/3310599>
<http://www.ajcn.org/cgi/reprint/46/4/570> (free full text PDF)

Bjerve KS.
n-3 fatty acid deficiency in man.
J Intern Med Suppl. 1989;731:171-5.
PMID: 2565114
<http://www.ncbi.nlm.nih.gov/pubmed/2565114>

Bjerve KS, Fischer S, Wammer F, Egeland T.
alpha-Linolenic acid and long-chain omega-3 fatty acid supplementation
in three patients with omega-3 fatty acid deficiency: effect on
lymphocyte function, plasma and red cell lipids, and prostanoid
formation.
Am J Clin Nutr. 1989 Feb;49(2):290-300.
PMID: 2563625
<http://www.ncbi.nlm.nih.gov/pubmed/2563625>
<http://www.ajcn.org/cgi/reprint/49/2/290> (free full text PDF)

>
Studies about omega-6 deficiency and cancer:

Dippenaar N, Booyens J, Fabbri D, Katzeff IE.
The reversibility of cancer: evidence that malignancy in melanoma cells
is gamma-linolenic acid deficiency-dependent.
S Afr Med J. 1982 Oct 2;62(15):505-9.
PMID: 7123414
<http://www.ncbi.nlm.nih.gov/pubmed/7123414>

"Certain metabolic abnormalities are common to all malignant cells,
and Horrobin proposed that the underlying cause is the inability of
cancer cells to produce prostaglandin E1 (PGE1). This appears to be
due to the lack of the enzyme delta-6-desaturase which converts the
essential fatty acid, linoleic acid, to gamma-linolenic acid (GLA),
from which PGE1 is then synthesized. Our studies strongly support
this contention. Addition to GLA to cancer cells, thus bypassing
the block in the metabolic pathway, results in very marked,
statistically highly significant inhibition of growth, while having
no effect at all on normal cells. Our finding of the regression
of cancer through such proposed normalization offers preliminary
hope for a new effective and harmless approach to the treatment of
cancer."

Dippenaar N, Booyens J, Fabbri D, Engelbrecht P, Katzeff IE.
The reversibility of cancer: evidence that malignancy in human hepatoma
cells is gamma-linolenic acid deficiency-dependent.
S Afr Med J. 1982 Oct 30;62(19):683-5.
PMID: 6291176
<http://www.ncbi.nlm.nih.gov/pubmed/6291176>

"A further critical test of Horrobin's hypothesis that malignancy
in cells may be dependent on gamma-linolenic acid (GLA) deficiency,
has revealed that GLA supplementation produces a highly significant
reduction in the growth rate (up to 87%) of a cultured human
hepatoma cell line, compared with the growth rate of untreated
hepatoma cells. This supports our previous suggestion that this
hypothesis requires urgent further investigation at all levels
including trials in human cancer patients."

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition
.

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