73 replies to this topic

[paleo]

There's a huge difference between trying to avoid the latest fad and stick to whole foods, and trying to maximize saturated fat intake (especially animal saturated fats). Talk about a fad (and a poorly backed one, scientifically speaking).

Sure, if you consider over a million years of evolution eating a large amount of saturated fat a fad. As for science, gimme a break -- is this the same science that has been a proponent of a low fat diet for the last several decades? The same science that points to cholesterol and saturated fat being harmful yet at the same time pointing to polyunsaturated garbage vegetable and seed oils as healthy?

[jaydfox]

polyunsaturated garbage vegetable and seed oils

Well, if you're digging your veggies out of the garbage, of course they're not going to be good for you.

As for eating large amounts of saturated fat for over a million years, what's good for living a high-paced, action-packed, survival of the fittest, biggest, meanest, quickest, and most aggressive lifestyle, limited almost entirely by extrinsic mortality, isn't necessarily what's best for a long, stress-free, mildly active life, defined by intrinsic mortality.

For example, in rodent studies, eating lots and lots of calories, and having high growth and sex hormone levels, is great for growing big and fast, but it's a calorie restricted diet that leads to long lifespans. If you mean "healthy" as in big and fast, then high-cal is the way to go. If you mean "healthy" as in still alive and kickin' when everyone else has dropped dead of cancer or other age-related diseases, then low-cal is the way to go.

I never said a high saturated fat diet won't make you tough and active, and I even guessed correctly that you're a strength athlete. But what does that have to do with living longer and healthier at older ages?

[paleo]

Well, if you're digging your veggies out of the garbage, of course they're not going to be good for you.

As for eating large amounts of saturated fat for over a million years, what's good for living a high-paced, action-packed, survival of the fittest, biggest, meanest, quickest, and most aggressive lifestyle, limited almost entirely by extrinsic mortality, isn't necessarily what's best for a long, stress-free, mildly active life, defined by intrinsic mortality.

For example, in rodent studies, eating lots and lots of calories, and having high growth and sex hormone levels, is great for growing big and fast, but it's a calorie restricted diet that leads to long lifespans. If you mean "healthy" as in big and fast, then high-cal is the way to go. If you mean "healthy" as in still alive and kickin' when everyone else has dropped dead of cancer or other age-related diseases, then low-cal is the way to go.

I never said a high saturated fat diet won't make you tough and active, and I even guessed correctly that you're a strength athlete. But what does that have to do with living longer and healthier at older ages?

No, those oils are not going to be good for you because they are highly unstable and probably rancid before you even put them in your body.

As for comparisons between stress and activity levels back in the day and now -- many could argue that stress hasn't changed...maybe just in a different form, or maybe even less adrenaline now. Regardless, I have never stated to eat more calories then you expend.

As for calorie restriction, who knows. We're not rats but it would make sense in humans. Is it not possible to restrict calories on a high fat diet? Maybe it's the quality of the calorie and not quantity? Maybe calorie restriction means less carbs....who knows. I understand your point from an energy and strength point of view but I don't see how what I state can't extend to longevity as well. Ofcourse it can, but you seem to be always putting out ideas that you claim are mine, which aren't. I think the bottom line is that we are arguing what the optimal macronutrient profile should be for a healthy diet for a long life. I'm claiming that the diet needs to be about 2/3 to 3/4 from animal, and 1/4 to 1/3 plant, and you're probably stating the exact opposite. Am I right?

[opales]

I stumbled at the following interesting criticism of the hypothesis (well not the hypothsesis as such but consumption of ALA over EPA/DHA) in the Yahoo CRsupport group

http://health.groups...up/message/2294

[Athanasios]

Can I get a little cut and past action? [help]

[opales]

Interesting in depth Omega 3 LNA or EPA review

Hi All,

Interesting rebuttal on sci.life-extension to Michael's "LNA is best" theory.

http://groups.google.com/groups?hl=en&thre...50f%40pos\
ting.google.com&prev=/groups%3Foi%3Ddjq%
26as_ugroup%3Dsci.life-extension

Hi, Michael, and everyone. I have snipped most of the thread up to
this point because I think we are in substantial agreement on the
PC-ALA link. And I have kept, I think, the important points of
Michael's "ALA better" argument except for the Lyons study which I
probably should have left in. Apologies, if I have snipped too much.
They can always be added or referred. At least the post is a little
less intimidating by virtue of its length.

mikalra@... (Michael) wrote in message
news:<69779556.0110201834.48c91e9c@...>...
> All:
> The thrust of MY argument is that the PC connection, if true, should
> still not keep one away from ALA.


The risk for prostate cancer is 300% higher if taking a lot of ALA. In
the US this is equivalent to about 100,000 extra deaths/yr. About
400,000 men die of cardiovascular failure in the US yearly. And 30,000
die of PC and 200,000 incur the disease. So the above statement would
only make sense if ALA could prevent 25% or 100,000 of those deaths
over and above what Fish oil could prevent. While this is not totally
out of the question based on the evidence so far presented in this
thread I will introduce additional overwhelming evidence to the
contrary. I will infact show that fish oil is slightly better against
CHD and that there is far, far more evidence of its efficacy.
Furthermore the two studies below suggest the posiblity that ALA is
even more risky for readers of this group.


RESULTS: The relative risks (RRs) of prostate cancer for men in
successively higher quartiles of plasma alpha-linolenic acid level
were 3.0 (95% confidence interval [CI] = 1.2-7.3), 3.4 (95% CI =
1.6-7.5), and 2.1 (95% CI = 0.9-4.9), compared with those with levels
below the detection threshold (P trend = .03). For linoleic acid, RRs
in successively higher quartiles were 0.7 (95% CI = 0.4-1.5), 0.8 (95%
CI = 0.4-1.6), and 0.6 (95% CI = 0.3-1.3), with the lowest quartile as
referent (P trend = .24). The effect estimates were not notably
altered by adjustment for exercise, body mass, meat and dairy
consumption, or other fatty acid levels in the plasma. The RR for
eating red meat at least five times per week compared with less than
once a week was 2.5 (95% CI = 0.9-6.7) and was little changed by
adjustment for alpha-linolenic acid, although alpha-linolenic acid
levels were correlated with intake of red meat and butter. The
association of alpha-linolenic acid levels with prostate cancer was
greater among men with low linoleic acid and reduced meat intake.
PMID: 8158682

There was no clear association between the risk effect of total
omega-3 and total omega-6 fatty acids. There were no indications of a
relationship between fatty acids and more aggressive cancers. Our
results verify recent findings of a positive association between
alpha-linolenic acid and a negative association between the ratio of
linoleic to alpha-linolenic acid and the risk of prostate cancer.
PMID: 9178806

We have been paying far too mech attention to one study, the Lyons
before leaving it, I call your attention to the author's own logistic
analysis as to the relative efficacy of ALA and fish oil. ALA is only
slightly better with P=.11 vs .16 for fish oil. The huge confidence
interval of .05 to .84 indicates a good likely hood of a statistical
anamoly. Especially as the fish oil was more effective against non
fatal heart disease and complications. Below is the excerpt from the
full text.

With regard to any association between the plasma concentration of
major fatty acids and recurrence, only 18:3(-3) and 22:6(-3) tended to
be inversely associated with recurrence*** (P=0.11 and P=0.16,***
respectively, versus CO 1).

Then, the effect of traditional risk factors on recurrence was
analyzed with the multivariate Cox proportional-hazards model (Table
5T5T5). When the plasma fatty acid concentrations were entered into
the model, 18:3(-3) was the only fatty acid significantly associated
with CO 1 (risk ratio, 0.20; 95% CIs, 0.05 to 0.84 after adjustment
for age, sex, smoking, total cholesterol, blood pressure, leukocyte
count, and aspirin use). With regard to the effect of 18:3(-3) on CO 2
and CO 3, the associations were borderline nonsignificant (P=0.08 and
P=0.12).
Flull text at: http://circ.ahajourn...ull/99/6/779/T3
And at.
http://www.scielo.br/scielo.php?script=sci...1100006&l\
ng=en&nrm=iso

> With respect to RCTs & large scale prospective epidemiology with
> mortality endpoints, I picked the MOST favorable studies of which I'm
> aware for EPA/DHA fish rich in same. If you know of others more
> favorable, I'll be pleased to read 'em.


Below I list 31 studies on n-3's and vascular diseases. Nine clinical
trials for fish oil, and 22 trials for fish or LNA. I list them in the
order of most efficacy for fish oil. ( They are numbered and the ones
povided by Michael carry an "M" with the number.) The very first is a
well designed study meant to answer the very question we have been
studying. After studying the below trials and others it is apparent to
me that:

1) Fish oil and/or the eating of fatty fish is one of the best therapys
available, better the the statin drugs and the B
vitamins,
and about as good as aerobic excersise.

2) It's affects should be additive to other regimens and as a preventative
measure it may be heads and shoulders over
the others.

3) Side effects are virtually non existent unlike LNA which has one very
dangerous one for men.

I have taken issue with the conclusions and headlines of a
few of the studies. In each case, the raw data in the full text does
not bear out the claims made in the abstracts or the hi numbers quoted
in the abstracts are only good for analysis against the lowest
quintile. The same can be said of many of the fish consumption
studies. My comments are interspersed among the studies, but always in
italics. Make up your own minds but even without my interpretations it
is obvious that fish oil is at least as good as LNA for heart health.

FISH OIL: Nine clinical trials. Eight positive. One no effect. Two
directly compare ALA and fish oil with fish oil the clear winner in
both. Taken as a whole the studies suggest somewhere between a 30 and
a 50% reduction in cardiac mortality. Somewhat less for ALA. These
studies were all done on heart patients. After the damage was done. As
a preventative measure n-3 fatty acids could be much more effective.
These are the abstracts.

[FunkOdyssey]

The plot thickens:

Hulbert AJ, Faulks SC, Buffenstein R.
Oxidation-resistant membrane phospholipids can explain longevity differences
among the longest-living rodents and similarly-sized mice.
J Gerontol A Biol Sci Med Sci. 2006 Oct;61(10):1009-18.
PMID: 17077193

Underlying causes of species differences in maximum life span (MLS) are
unknown, although differential vulnerability of membrane phospholipids to
peroxidation is implicated. Membrane composition and longevity correlate
with body size; membranes of longer-living, larger mammals have less
polyunsaturated fatty acid (PUFA). We determined membrane phospholipid
composition of naked mole-rats (MLS > 28.3 years) and similar-sized mice
(MLS = 3-4 years) by gas-liquid chromatography to assess if the
approximately 9x MLS difference could be explained. Mole-rat membrane
composition was unchanged with age. Both species had similar amounts of
membrane total unsaturated fatty acids; however, mice had 9 times more
docosahexaenoic acid (DHA). Because this n-3PUFA is most susceptible to
lipid peroxidation, mole-rat membranes are substantially more resistant to
oxidative stress than are mice membranes. Naked mole-rat peroxidation
indices, calculated from muscle and liver mitochondrial membranes, concur
with those predicted by MLS rather than by body size, suggesting that
membrane phospholipid composition is an important determinant of
longevity.Underlying causes of species differences in maximum life span
(MLS) are unknown, although differential vulnerability of membrane
phospholipids to peroxidation is implicated. Membrane composition and
longevity correlate with body size; membranes of longer-living, larger
mammals have less polyunsaturated fatty acid (PUFA). We determined membrane
phospholipid composition of naked mole-rats (MLS > 28.3 years) and
similar-sized mice (MLS = 3-4 years) by gas-liquid chromatography to assess
if the approximately 9x MLS difference could be explained. Mole-rat membrane
composition was unchanged with age. Both species had similar amounts of
membrane total unsaturated fatty acids; however, mice had 9 times more
docosahexaenoic acid (DHA). Because this n-3PUFA is most susceptible to
lipid peroxidation, mole-rat membranes are substantially more resistant to
oxidative stress than are mice membranes. Naked mole-rat peroxidation
indices, calculated from muscle and liver mitochondrial membranes, concur
with those predicted by MLS rather than by body size, suggesting that
membrane phospholipid composition is an important determinant of longevity.

.....
Fatty acid composition of naked mole-rat membranes from a variety of tissues
correlates better with their [maximum lifespan potential (MLSP)] than with
their body size. This finding suggests that the presence of relatively
peroxidation-resistant cellular membranes can explain the exceptional
longevity of naked mole-rats. Similarly, this may also be the explanation
for the relatively long MLSP of Homo sapiens. We have recently observed that
the extended longevity of wild-derived strains of mice relative to
laboratory mice is also associated with low PI in muscle and liver
phospholipids (26). Furthermore, in this respect, a senescence-prone
substrain of senescence-accelerated mice have brain mitochondrial membranes
with a significantly elevated PI compared to those from a
senescence-resistant substrain of these mice (27). This finding suggests
that the relationship between membrane composition and longevity holds true
for both intra- and interspecies comparisons. We cannot ascertain from these
results, however, whether this relationship is one of "cause and effect."
Only experimental manipulation of membrane fatty acid composition that
alters both PI and maximum longevity can prove a causal relationship. Such
an experiment is difficult in the naturally long-living naked mole-rat, but
it is of interest that the life-span-extending experimental treatment of
calorie restriction results in mitochondrial membrane fatty acid changes
that increase peroxidation-resistance in rats (28). Similarly, calorie
restriction can significantly reduce the PI of membrane phospholipids within
1 month in mice (29). It is not known whether dietary changes in PUFA
content alter membrane fatty acid composition with concomitant effects on
susceptibility to oxidative damage. However, our data collectively reveal
that composition of membrane bilayers may be an important determinant of
MLS.

[FunkOdyssey]

Does a direct relationship between dietary intake of DHA and membrane PI exist in humans? That is the important question to answer, and if there is indeed a link between the two, DHA supplementation seems like a very bad idea.

[Athanasios]

It is the continuous flow of studies like these that keep me taking 2 to 3 servings worth of fish via fish oil a week (currently i am getting .14g/d of DHA):

Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study.

    * Schaefer EJ,
    * Bongard V,
    * Beiser AS,
    * Lamon-Fava S,
    * Robins SJ,
    * Au R,
    * Tucker KL,
    * Kyle DJ,
    * Wilson PW,
    * Wolf PA.

Lipid Metabolism Laboratory, Jean Mayer US Department of Agriculture Human Nutrition REsearch Center on Aging, Tuffs University, Boston, MA 02111, USA. ernst.schaefer@tufts.edu

BACKGROUND: Docosahexaenoic acid (DHA) is an abundant fatty acid in the brain. In the diet, DHA is found mostly in fatty fish. The content of DHA has been shown to be decreased in the brain and plasma of patients with dementia. OBJECTIVE: To determine whether plasma phosphatidylcholine (PC) DHA content is associated with the risk of developing dementia. Design, Setting, and PARTICIPANTS: A prospective follow-up study in 899 men and women who were free of dementia at baseline, had a median age of 76.0 years, and were followed up for a mean of 9.1 years for the development of all-cause dementia and Alzheimer disease. MAIN OUTCOME MEASURES: Plasma PC fatty acid levels were measured at baseline. Cox proportional regression analysis was used to assess relative risks of all-cause dementia and Alzheimer disease according to baseline plasma levels. RESULTS: Ninety-nine new cases of dementia (including 71 of Alzheimer disease) occurred during the follow-up. After adjustment for age, sex, apolipoprotein E epsilon4 allele, plasma homocysteine concentration, and education level, subjects in the upper quartile of baseline plasma PC DHA levels, compared with subjects in the lower 3 quartiles, had a relative risk of 0.53 of developing all-cause dementia (95% confidence interval, 0.29-0.97; P=.04) and 0.61 of developing Alzheimer disease (95% confidence interval, 0.31-1.18; P=.14). Subjects in the upper quartile of plasma PC DHA levels had a mean DHA intake of 0.18 g/d and a mean fish intake of 3.0 servings per week (P<.001) in a subset of 488 participants. We found no other significant associations. CONCLUSION: The top quartile of plasma PC DHA level was associated with a significant 47% reduction in the risk of developing all-cause dementia in the Framingham Heart Study.

PMID: 17101822

[scottl]

Cnorwood19,

I posted several abstracts/questions along the same lines (don't remember if it was in this thread or another) as well as PMing MR who is probably too busy or tired of answering questions on this topic. I agree completely and think one should take the certain benefit over the potential harm (we're still talking animal studies and lots of animal studies don't pan out in people as Adam's recent post in the methodology section points out). Even if both the benefit and harm are both correct (far from certain) I think one can make a case for taking the fish oil with the benefits and doing what one can to minimize the harm.

[scottl]

I don't have access to the original, but someone just posted this elsewhere:

Aging Cell. 2006 Dec 5; [Epub ahead of print] Links
N-3 polyunsaturated fatty acids impair lifespan but have no role for metabolism.

* Valencak TG,
* Ruf T.

Research Institute of Wildlife Ecology, University of Veterinary Medicine, Savoyenstrasse 1, A-1160 Vienna, Austria.

Although generally considered as beneficial components of dietary fats, polyunsaturated fatty acids (PUFA) have been suspected to compromise maximum lifespan (MLSP) in mammals. Specifically, high amounts of phospholipid PUFAs are thought to impair lifespan due to an increase in the susceptibility of membranes to lipid peroxidation and its damaging effect on cellular molecules. Also, there is evidence from in vitro studies suggesting that highly unsaturated PUFAs elevate basal metabolic rate (BMR). Previous comparative studies in this context were based on small sample sizes, however, and, except for one study, failed to address possible confounding influences of body weight and taxonomic relations between species. Therefore, we determined phospholipid membrane composition in skeletal muscle from 42 mammalian species to test for a relation with published data on MLSP, and with literature data on BMR (30 species). Using statistical models that adjust for the effects of body weight and phylogeny, we found that among mammals, MLSP indeed decreases as the ratio of n-3 to n-6 PUFAs increases. In contrast to previous studies, we found, however, no relation between MLSP and either membrane unsaturation (i.e. PUFA content or number of double bonds) or to the very long-chain, highly unsaturated docosahexaenoic acid (DHA) . Similarly, our data set gave no evidence for any notable relation between muscle phospholipid fatty acid composition and BMR, or MLSP and BMR in mammals. These results contradict the 'membrane pacemaker theory of aging', that is, the concept of a direct link between high amounts of membrane PUFAs, elevated BMR, and thus, impaired longevity.

[Athanasios]

Thanks for the abstract, scottl, it is good info. It would seem awfully odd to get decreased AD and dementia with an impaired lifespan,IMO, via the theory that MR points to. Although, all the studies I have seen are not conclusive enough, for me, to be sure without further research, but I feel safe with the level of intake I am getting. I will be watching for further development though.

[boily]

I've been taking 1.8g of EPA and 1.2g of DHA for over a year.(Got this dosing amount from Mercola.com) After reading the AOR article I have just changed to 1.6g of EPA and 0.3g of DHA. I'm also thinking of adding in some krill oil. Good idea, anyone taking it? I already take 5mg of astaxanthin a day, so maybe I don't need krill?

Any opinions on this change? I've been sorting through the info and arrived at this. Have I got it right?

Will be interesting to see if I notice any mood changes......

[FunkOdyssey]

I personally think that is a reasonable adjustment. I'm taking between 150mg DHA and 1g EPA and 225mg DHA, 1.5g EPA depending on whether I remember that third capsule or not.