Re: ALA and Prostate Cancer

[Guest guest]

Hi Logan:

Well you may be concerned about what you would like to label

as 'propaganda'. I would prefer to stick to the facts.

I see the facts as follows: the study I referred to from the

Physicians Health Study (PHS) was **NOT** from 1994 as you state. It

was 2004. (PMID: 15213050). What is more it **WAS** posted here,

by me, very shortly after it was published. And this was AFTER I had

already warned here that there were several previous studies showing

a link between ALA and prostate cancer. It was these previous

studies that caused the PHS to take another look at their own data.

The 2004 PHS study was a **prospective** study of **47,866** men over

**fourteen** years, during which **2965 new cases** of prostate

cancer were reported. It was NOT some guy spending a few weeks

studying 25 patients.

Before the 2004 study was completed they had hoped/expected to find

that it was the animal food sources of ALA that were responsible for

the link. But they found the opposite. For advanced prostate

cancer, the aggressive type that kills people, the relative risk of

those consuming the most alpha-linolenic acid from **PLANT** sources

was 2.02 ......... **DOUBLE** the risk. So these results had the

effect of confirming, yet again, those from earlier, smaller studies.

As you are no doubt aware people in the far east have a low incidence

of prostate cancer and consume more soy products than we do in North

America. But there are indications it is most likely the soy PROTEIN

that confers the benefit. Not the fat.

In any event, as we all know, nutrition is far from being a

completely understood aspect of science. Who knows what may be

discovered in the future. We are each free agents, 'placing our

bets' on the information we find most persuasive. My best judgment

is that I may get too much alpha-linolenic acid already from the

other components of my diet. So to avoid overdosing I try to

minimize my intake of foods with the highest amounts of it (flax,

walnuts, soybean oil, canola oil ........).

In addition, the principal benefit of alpha-linolenic acid that I am

aware of is protection against CVD. But as we all know, for those on

a CRON diet (most of us here?) that risk, according to the risk

factor data in the WUSTL study, would seem to be pretty much

eliminated already. So it looks like even this benefit may be

irrelevant for us. If I was hypertensive with cholesterol of 300 and

triglycerides of 400 I very well might be tempted to run the risk of

getting prostate cancer later, in order to try to avoid dropping dead

in the street of CVD sooner. But I never have been. And for pretty

much anyone who has been on CRON for a year or more that is unlikely

to be an issue.

In addition, do not forget the link between ALA and lung cancer among

chinese women who do not smoke but cook with oils containing ALA.

Having said the above, there is nothing wrong with you coming to a

conclusion that is different from mine, even after we have each

reviewed the same evidence. (You usually do!!). Indeed you are

more than welcome. But I have looked and failed to find any

information relating of deficiency symptoms among people consuming

too little ALA. Nor have I been able to find the original source

from which it was concluded that ALA is an essential fat - rather

than the DHA and EPA that are derived from it.

So, it would be a great help to everyone here, if you know of some

serious sources outlining ALA deficiency symptoms and the levels of

intake at which they appear; or if you know who/where it was that

came to the conclusion that ALA is an essential nutrient, if you

could acquaint us with those sources.

I have chosen to get all the ALA I need from the foods I regularly

eat (I get plenty of DHA and EPA from fish) that contain modest

quantities of it, and avoid those containing the largest amounts.

But, given persuasive **evidence** that there is a better course, it

would likely only take 24 hours to shift my dietary habits.

Rodney.

>

> Rodney,

>

> I've become increasingly concerned about your propagandizing of

alpha-

> linolenic acid (ALA) equating to prostate cancer. ALA is an

> essential fatty acid and is not to be unnecessarily feared!

>

> First of all, the Physicians Health Study that you refer to making

> the allegation [PMID: 8158682] was published way back in 1994 which

> is seriously outdated.

>

> Second, the evidence is inconclusive on the allegation, as many

> studies do in fact conclude. I would further opine the allegation

> has no basis in actual proof, only hypothesizing due to lack of

> controlling for confounding variables or the researchers lack of

> comprehensive nutritional experience to make proper conclusions.

As

> an example counter-point, see PMID: 12429338.

>

> Third, it is well-known that the prostate gland starts accumulating

> estrogen, starting at approximately the age of 50. In addition,

> approximately 75% of all breast cancers in women are estrogen-

> receptor positive. It is " normal " for the ratio of harmful-

specific

> estrogen to testosterone to gradually increase as men and women

age,

> contributing to all sorts of maladies and diseases. This hormonal

> imbalance can be prevented or minimized, but not by avoiding ALA.

>

> Fourth, if there is indeed any factual basis to the allegation, the

> primary confounding variables to control for are oxidization,

> mutagenicity and hydrolization. That would be an entirely

different

> aspect of ALA than a mere blanket demonization of the fat.

Unshelled

> walnuts and processed soy, canola, sunflower, safflower oils, et

al.

> are not in their naturally protective food matrix.

>

> Fifth, there is the possibility that ALA consumption cascades down

> into the Omega-6 pathway and into pro-inflammatory Arachidonic Acid

> (AA) production, leaving very little to be converted into anti-

> inflammatory GLA/EPA/DHA. Thus the problem would be with AA per

se,

> not ALA.

>

> Logan

>

> --- In , " Rodney " <perspect1111@y...

> > The latest report was from the Physicians Health Study. Prostate

> > cancer, as you know, is a VERY common cancer, nearly as common in

> > males (both for incidence and for deaths) as breast cancer is in

> > females.

[Guest guest]

I don't what propaganda you're talking about. We looked at the articles extensively and I couldn't conclude there WAS a reqt for ALA. It's not identified in my latest Lehninger Principles of Biochemistry. Surely the reqt is extremely small, not enough to worry a lack of because you can get enough in veggies.

Further, One PCa doctor says adult males don't MAKE EPA from ALA. Contrast that with Sear's book. On the chance that we don't manufacture it, Rodney's idea to use fish, IMO is a good idea.

So what's the problem? AFA PCa is concerned there is practically no info inre to supplements of any kind and we can get that info direct from practicing PCa doctors. We don't have to wonder about it. What they DOING in the PCa treatment facilities, is my best guess.

What does ALA do besides serve as precursor to EPA? Give me a ref for biochem equations please. Even Sears says the other uses are insignificant.

Regards.

----- Original Message -----

From: loganruns73

Sent: Sunday, December 19, 2004 4:13 AM

Subject: [ ] ALA and Prostate Cancer

Rodney,I've become increasingly concerned about your propagandizing of alpha-linolenic acid (ALA) equating to prostate cancer. ALA is an essential fatty acid and is not to be unnecessarily feared!First of all, the Physicians Health Study that you refer to making the allegation [PMID: 8158682] was published way back in 1994 which is seriously outdated.Second, the evidence is inconclusive on the allegation, as many studies do in fact conclude. I would further opine the allegation has no basis in actual proof, only hypothesizing due to lack of controlling for confounding variables or the researchers lack of comprehensive nutritional experience to make proper conclusions. As an example counter-point, see PMID: 12429338.Third, it is well-known that the prostate gland starts accumulating estrogen, starting at approximately the age of 50. In addition, approximately 75% of all breast cancers in women are estrogen-receptor positive. It is "normal" for the ratio of harmful-specific estrogen to testosterone to gradually increase as men and women age, contributing to all sorts of maladies and diseases. This hormonal imbalance can be prevented or minimized, but not by avoiding ALA.Fourth, if there is indeed any factual basis to the allegation, the primary confounding variables to control for are oxidization, mutagenicity and hydrolization. That would be an entirely different aspect of ALA than a mere blanket demonization of the fat. Unshelled walnuts and processed soy, canola, sunflower, safflower oils, et al. are not in their naturally protective food matrix.Fifth, there is the possibility that ALA consumption cascades down into the Omega-6 pathway and into pro-inflammatory Arachidonic Acid (AA) production, leaving very little to be converted into anti-inflammatory GLA/EPA/DHA. Thus the problem would be with AA per se, not ALA.Logan--- In , "Rodney" <perspect1111@y...> The latest report was from the Physicians Health Study. Prostate > cancer, as you know, is a VERY common cancer, nearly as common in > males (both for incidence and for deaths) as breast cancer is in > females.

[Guest guest]

This 2004 study makes a BIG difference than the one in 1994, but I

don't recall seeing it before. I find it compelling enough to back

up your " propagandizing " . I think you should reference it more often.

From what I remember reading, only about 10% of ALA is converted into

EPA/DHA -- assuming no enzyme defenciencies. So where is the rest

going??? If the 2004 study disavows AA as a factor, it seems to me

that merely oxidising ALA into calories could be harmful! Now that

is scary.

Didn't we already have the ALA vs EPA/DHA is an EFA debate in here?

I don't really remember the particulars, but I thought it was settled

that ALA constitutes an EFA vs EPA/DHA.

I'm throwing my flax seed out, all 20 lbs of it. :-)

Logan

--- In , " Rodney " <perspect1111@y...> >

I see the facts as follows: the study I referred to from the

> Physicians Health Study (PHS) was **NOT** from 1994 as you state.

It

> was 2004. (PMID: 15213050). What is more it **WAS** posted here,

> by me, very shortly after it was published. And this was AFTER I

had

> already warned here that there were several previous studies

showing

> a link between ALA and prostate cancer. It was these previous

> studies that caused the PHS to take another look at their own data.

[Guest guest]

Hi Logan:

If yer could find a way to squeeze the ALA and starch out of yer flax

seeds I'd bet you'd have something pretty healthy left.

Rodney.

>

> I'm throwing my flax seed out, all 20 lbs of it. :-)

>

> Logan

[Guest guest]

Before you throw your flax seed out, read the paper carefully. I

don't have access to the full paper, but the abstract below has some

clues that may be significant.

1) " We prospectively evaluated the association between intakes ... "

Was the consumption of fatty acids determined in 2000 after 14 years

of follow up, or in 1986 when the 47,866 men were selected? If in

2000, the intake would have relied on memory which might not be

accurate. You need to look at the full paper for the methodology.

2) " ALA intake was unrelated to the risk of total prostate cancer. "

So, ALA does not increase your risk of getting prostate cancer. THIS

IS AN IMPORTANT CONCLUSION.

3) " the multivariate relative risks (RRs) of advanced prostate cancer

from comparisons of extreme quintiles of ALA from nonanimal sources

and ALA from meat and dairy sources were 2.02 (95% CI: 1.35, 3.03) and

1.53 (0.88, 2.66), respectively. "

It is interesting that vegetable ALA (nonanimal sources) has an RR of

2.02 while animal sources have only a 1.53 RR. Animal fats have only

about 1% ALA, whereas vegetable oils can be much higher in ALA (flax

53%, canola 10%, soybean 7%, walnut 5%). Of these vegetable oils

which are the most commonly used commercially? Canola and soybean.

These oils are also frequently hydrogenated and they may contain

trans-ALA and other trans-fatty acids. The study does not seem to

differentiate or even mention vegetable hydrogenated oils or

trans-fatty acids. Is it possible that vegetable oils have a higher

RR because of hydrogenation? Is it possible that it is the

trans-fatty acids that are responsible for increasing the RR of

advanced prostrate cancer? Since the RR for animal sources

was 1.53, a relationship between ALA and advanced PC cannot be

excluded.

4) " EPA and DHA intakes may reduce the risk of total and advanced

prostate cancer. "

These are animal fats from fish.

IMO, this paper shows that vegetable fats are worse than animal fats

for advanced prostrate cancer. I don't think that ALA from plants is

metabolized differently from ALA from animal sources. However,

knowing that vegetable fats are frequently hydrogenated whereas the

animal fats are not, it is more reasonable for me to believe that it

is the hydrogenation of the vegetable fats that makes the difference

between the RR of 2.02 and 1.53. Another factor, may be that it is

easier to ingest larger quantities of ALA from vegetable sources than

from animal sources, but I cannot accept this as the

reason because the popular vegetable ois are so much higher in

ALA, and I would have expected a much higher difference in RR if ALA

were really the culprit. With the vegetable oils you are consuming 7%

to 10% ALA compared with 1% ALA for animal fat, and the difference is

only 0.49 increase in RR? Not very convincing.

Tony

>>>

Am J Clin Nutr. 2004 Jul;80(1):204-16.

Dietary intake of n-3 and n-6 fatty acids and the risk of prostate

cancer.

Leitzmann MF, Stampfer MJ, Michaud DS, Augustsson K, Colditz GC,

Willett WC, Giovannucci EL.

Nutritional Epidemiology Branch, Division of Cancer Epidemiology and

Genetics, National Cancer Institute, National Institutes of Health,

Department of Health and Human Services, Bethesda, MD 20892, USA.

leitzmann@...

BACKGROUND: Laboratory studies have shown that n-3 fatty acids inhibit

and n-6 fatty acids stimulate prostate tumor growth, but whether the

dietary intake of these fatty acids affects prostate cancer risk in

humans remains unclear. OBJECTIVE: We prospectively evaluated the

association between intakes of alpha-linolenic (ALA; 18:3n-3),

eicosapentaenoic (EPA; 20:5n-3), docosahexaenoic (DHA; 22:6n-3),

linoleic (LA; 18:2n-6), and arachidonic (AA; 20:4n-6) acids and

prostate cancer risk. DESIGN: A cohort of 47 866 US men aged 40-75 y

with no cancer history in 1986 was followed for 14 y. RESULTS: During

follow-up, 2965 new cases of total prostate cancer were ascertained,

448 of which were advanced prostate cancer. ALA intake was unrelated

to the risk of total prostate cancer. In contrast, the multivariate

relative risks (RRs) of advanced prostate cancer from comparisons of

extreme quintiles of ALA from nonanimal sources and ALA from meat and

dairy sources were 2.02 (95% CI: 1.35, 3.03) and 1.53 (0.88, 2.66),

respectively. EPA and DHA intakes were related to lower prostate

cancer risk. The multivariate RRs of total and advanced prostate

cancer from comparisons of extreme quintiles of the combination of EPA

and DHA were 0.89 (0.77, 1.04) and 0.74 (0.49, 1.08), respectively. LA

and AA intakes were unrelated to the risk of prostate cancer. The

multivariate RR of advanced prostate cancer from a comparison of

extreme quintiles of the ratio of LA to ALA was 0.62 (0.45, 0.86).

CONCLUSIONS: Increased dietary intakes of ALA may increase the risk of

advanced prostate cancer. In contrast, EPA and DHA intakes may reduce

the risk of total and advanced prostate cancer.

PMID: 15213050

[Guest guest]

But the question remains, why use ALA when EPA is readily available in capsules or fish?

About 1/6 males get PCa. Perhaps those are the ones that don't convert ALA to EPA.

Previously, we noted the U.S. consumption of soybean oil is a lot higher than other countries. Soybean oil is a major source of ALA.

I can't take the exactness of the numbers to convince me of something I don't need to do anyway. Books offer no exact conversion factors to EPA, so I can't even guess how much I need. Nor do they state the exact EPA I need to avoid CVD and PCa. Nor do they state the conversion to eicosanoids and how much of that I need. There was an article Alan posted that stated if we eat FishEPA, the concentration in arterial linings increases. I guess "softens" the plaques to lower ischemic stroke risk.

But in Japanese, the risk of hemo stroke increases and exceeds the risk of Ischemic stroke after about 80yo. All we have is that eating fish is rec'd about 3 times per week.

We get enough ALA without trying, if we use the 1.1 to 2 grams as an RDA. Those are mostly derived from what people are doing - not what they require.

Lastly, many of the EPA papers talk about tests run with FishEPA and then make a statement that assumes the EPA we get from ALA has the same value. They didn't run the test comparing ALA intake with FishEPA intake. I recall one that did that compare and FishEPA was significantly better.

But even all that doesn't mean ALA causes PCa or feeds the carcinoma. Studies of PCa are far behind CVD, lung cancer, stroke studies. So a logical safe conclusion was don't eat ALA. UNLESS we could find something that ALA precurses that is so important that we need that particular substrate. I'm still waiting for that. Somewhere in Sear's "Antiaging Zone", he states these other uses are not significant.

Regards.

----- Original Message -----

From: citpeks

Sent: Monday, December 20, 2004 6:47 PM

Subject: [ ] Re: ALA and Prostate Cancer

Before you throw your flax seed out, read the paper carefully. Idon't have access to the full paper, but the abstract below has someclues that may be significant.1) "We prospectively evaluated the association between intakes ..."Was the consumption of fatty acids determined in 2000 after 14 yearsof follow up, or in 1986 when the 47,866 men were selected? If in2000, the intake would have relied on memory which might not beaccurate. You need to look at the full paper for the methodology.2) "ALA intake was unrelated to the risk of total prostate cancer."So, ALA does not increase your risk of getting prostate cancer. THISIS AN IMPORTANT CONCLUSION.3) "the multivariate relative risks (RRs) of advanced prostate cancerfrom comparisons of extreme quintiles of ALA from nonanimal sourcesand ALA from meat and dairy sources were 2.02 (95% CI: 1.35, 3.03) and1.53 (0.88, 2.66), respectively."It is interesting that vegetable ALA (nonanimal sources) has an RR of2.02 while animal sources have only a 1.53 RR. Animal fats have onlyabout 1% ALA, whereas vegetable oils can be much higher in ALA (flax53%, canola 10%, soybean 7%, walnut 5%). Of these vegetable oilswhich are the most commonly used commercially? Canola and soybean. These oils are also frequently hydrogenated and they may containtrans-ALA and other trans-fatty acids. The study does not seem todifferentiate or even mention vegetable hydrogenated oils ortrans-fatty acids. Is it possible that vegetable oils have a higherRR because of hydrogenation? Is it possible that it is thetrans-fatty acids that are responsible for increasing the RR ofadvanced prostrate cancer? Since the RR for animal sourceswas 1.53, a relationship between ALA and advanced PC cannot beexcluded. 4) "EPA and DHA intakes may reduce the risk of total and advancedprostate cancer."These are animal fats from fish.IMO, this paper shows that vegetable fats are worse than animal fatsfor advanced prostrate cancer. I don't think that ALA from plants ismetabolized differently from ALA from animal sources. However,knowing that vegetable fats are frequently hydrogenated whereas theanimal fats are not, it is more reasonable for me to believe that itis the hydrogenation of the vegetable fats that makes the differencebetween the RR of 2.02 and 1.53. Another factor, may be that it iseasier to ingest larger quantities of ALA from vegetable sources thanfrom animal sources, but I cannot accept this as thereason because the popular vegetable ois are so much higher inALA, and I would have expected a much higher difference in RR if ALAwere really the culprit. With the vegetable oils you are consuming 7%to 10% ALA compared with 1% ALA for animal fat, and the difference isonly 0.49 increase in RR? Not very convincing.Tony>>>Am J Clin Nutr. 2004 Jul;80(1):204-16.Dietary intake of n-3 and n-6 fatty acids and the risk of prostatecancer.Leitzmann MF, Stampfer MJ, Michaud DS, Augustsson K, Colditz GC,Willett WC, Giovannucci EL.Nutritional Epidemiology Branch, Division of Cancer Epidemiology andGenetics, National Cancer Institute, National Institutes of Health,Department of Health and Human Services, Bethesda, MD 20892, USA.leitzmann@...BACKGROUND: Laboratory studies have shown that n-3 fatty acids inhibitand n-6 fatty acids stimulate prostate tumor growth, but whether thedietary intake of these fatty acids affects prostate cancer risk inhumans remains unclear. OBJECTIVE: We prospectively evaluated theassociation between intakes of alpha-linolenic (ALA; 18:3n-3),eicosapentaenoic (EPA; 20:5n-3), docosahexaenoic (DHA; 22:6n-3),linoleic (LA; 18:2n-6), and arachidonic (AA; 20:4n-6) acids andprostate cancer risk. DESIGN: A cohort of 47 866 US men aged 40-75 ywith no cancer history in 1986 was followed for 14 y. RESULTS: Duringfollow-up, 2965 new cases of total prostate cancer were ascertained,448 of which were advanced prostate cancer. ALA intake was unrelatedto the risk of total prostate cancer. In contrast, the multivariaterelative risks (RRs) of advanced prostate cancer from comparisons ofextreme quintiles of ALA from nonanimal sources and ALA from meat anddairy sources were 2.02 (95% CI: 1.35, 3.03) and 1.53 (0.88, 2.66),respectively. EPA and DHA intakes were related to lower prostatecancer risk. The multivariate RRs of total and advanced prostatecancer from comparisons of extreme quintiles of the combination of EPAand DHA were 0.89 (0.77, 1.04) and 0.74 (0.49, 1.08), respectively. LAand AA intakes were unrelated to the risk of prostate cancer. Themultivariate RR of advanced prostate cancer from a comparison ofextreme quintiles of the ratio of LA to ALA was 0.62 (0.45, 0.86).CONCLUSIONS: Increased dietary intakes of ALA may increase the risk ofadvanced prostate cancer. In contrast, EPA and DHA intakes may reducethe risk of total and advanced prostate cancer.PMID: 15213050