When terms are new to people, eyes can start to glaze. But I think the gist will get through. Skip past the double-bond stuff if so inclined.
Alpha-linolenic acid is an omega-3 fatty acid. It has a backbone of 18 carbons, with double-bonds at positions 9, 12 & 15 (the last is 3 from the end, which makes it an omega-3).
The important omega-3 fatty acids are EPA (Eicosapentaenoic acid) & DHA (Docosahexaenoic acid). The body can synthesize EPA from ALA, by adding two more carbons up front plus two additional double-bonds. (It can also synthesize DHA from EPA, by again adding two more carbons up front plus a new double-bond.) But the fact is that not much ALA is converted to EPA - only a few percent, with not a lot of EPA as a result.
EPA/DHA is available from fish oil. In the past, vegans relied on ALA conversion, & some vegan sites insist that enough ALA is converted. This is not true & no longer needs to be argued, since there is now EPA from algae [1].
A major source of ALA is flaxseed oil. When I came across it over fifty years ago, it was as linseed oil - shellac & linseed oil makes a nice finish on woodwork projects.
Flaxseed oil is very unstable. Users know to buy cold-pressed refrigerated oil & keep it in the fridge. Even so, it has to be used-up quickly. I have never seen an account of what happens to unstable ALA once it enters the body. Budwig warned against using it without quark.
ALA should not be used for cooking. Apart from the inclination to oxidize quickly, it polymerizes at relatively low temperatures. Cooks Magazine found it ideal for "seasoning" a cast iron pan.
A major dietary source of ALA for some is canola oil. Rapeseed has a reputation as a crop no species would touch, because of the erucic acid content. Fatty acids are fascinating. Erucic acid can be synthesized from oleic acid (as in olive oil) by simply adding 4 carbons up front. Both are monounsaturated omega-9 fatty acids (double-bond 9 carbons from the end). But erucic acid is an antinutrient. Anyway, some clever Canadians were able to reduce the erucic acid from 20-54% to under 2%. The resulting oil: Can(Canadian)ola(oil). Chances are one's favorite restaurant uses it. It is sometimes touted as being healthy because of the omega-3 content. The USDA database says canola oil is 9.137% ALA.
Some men with PCa incorporate nuts into their diets. We use such meaningless terms: "nuts", "fats", "fruit", etc, & assign qualities to them as though an almond & a Brazil nut were interchangeable. The problem is that an English walnut is 9% ALA (9.080 - USDA). Almost 15% of walnut oil is ALA.
Studies - oldest first:
[2] (1993 - U.S.)
Giovannucci's original study that spotted the ALA-PCa association.
[3] (1994 - U.S.)
"In 1982, at the start of the Physicians' Health Study, 14916 U.S. male physicians provided plasma samples ..."
"We used a nested case-control design to compare the fatty acid compositions in plasma from 120 men who later developed prostate cancer with 120 matched controls who did not. "
"The relative risks (RRs) of prostate cancer for men in successively higher quartiles of plasma alpha-linolenic acid level were 3.0 ..., 3.4 ..., and 2.1 ..., compared with those with levels below the detection threshold"
"These results suggest that low plasma levels of alpha-linolenic acid might be associated with reduced risk of prostate cancer, independently of high meat intake."
[4] (2004 - Netherlands - meta-analysis)
"The objective of this meta-analysis was to estimate quantitatively the associations between intake of alpha-linolenic acid [ALA, the (n-3) fatty acid in vegetable oils], mortality from heart disease, and the occurrence of prostate cancer in observational studies. We identified 5 prospective cohort studies that reported intake of ALA and mortality from heart disease. We also reviewed data from 3 clinical trials on ALA intake and heart disease. In addition, we identified 9 cohort and case-control studies that reported on the association between ALA intake or blood levels and incidence or prevalence of prostate cancer."
"High ALA intake was associated with reduced risk of fatal heart disease in prospective cohort studies (combined relative risk 0.79 ..."
"However, epidemiologic studies also showed an increased risk of prostate cancer in men with a high intake or blood level of ALA (combined relative risk 1.70 ..."
[5] (2004 - U.S. - Giovannucci again)
"A cohort of 47,866 US men aged 40-75 y with no cancer history in 1986 was followed for 14 y."
"During follow-up, 2,965 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 ... and 1.53 ..., respectively."
"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."
[6] ( 2006 - Denmark)
"Men with BPH had similar levels of ALA in leukocytes {white blood cells} and in prostate tissue, but men with prostate cancer had more ALA in prostate tissue than in leukocytes."
"The PSA level was significantly positively correlated with ALA level in prostate tissue"
"This study ... does not support the hypothesis that intake of marine n-3 PUFAs might protect against prostate cancer, but lends support to the deleterious role of ALA in the development of prostate cancer."
The issue is how lipids get into the lipid rafts of prostatic cells - particularly PCa cells. We have indications (because of competition between ALA & LA (linoleic acid)), that the omega-6 linoleic acid may prevent excessive uptake of ALA. {At the same time, We know that the marine omega-3s EPA & DHA can compete with arachidonic acid [AA] for a place in the lipid rafts. AA is the pro-inflammatory metabolite of LA. It's all a bit more complicated than the Abstract seems to imply.}
Anyway, ALA in PCa cells is NOT a good thing. Did the ALA get there because of preferrential uptake? Or because of a lack of opposing linoleic acid?
[7] (2006 - U.S.)
"A cohort of 29,592 male participants (age 55-74 years) in the screening arm of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial was followed for an average of 5.1 years."
A negative study, but not designed to look at progression.
[8] (2008 - UK/Europe)
"There were significant positive associations between myristic, alpha-linolenic, and eicosapentaenoic acids and risk of high-grade prostate cancer."
I have no idea why EPA would be in that list.
[9] (2008 - Jamaica)
"men with high linolenic acid proportions were at increased likelihood of PCa (tertile 3 vs. tertile 1: OR, 2.06 ..."
"High blood linolenic acid was directly related to prostate cancer."
[10] (2009 - U.S.) Part of the Wendy Demark-Wahnefried flaxseed study.
"This study provides evidence that prostatic ALA, independent of the amount of ALA consumed, is positively associated with biomarkers of aggressive prostate cancer and that genetic variation may modify this relationship."
Fine, but let's not forget the possible protective role of linoleic acid too.
[11] (2013 - U.S.) A huge study.
"Among 288,268 men with average follow-up of nine years, 23,281 prostate cancer cases (18,934 nonadvanced and 2,930 advanced including 725 fatal cases) were identified."
"α-Linolenic acid (ALA) intake was related to increased risk of advanced prostate cancer (HRQ5 vs. Q1, 1.17 ..." Seems like a smallish risk factor.
"Eicosapentanoic acid (EPA) intake was related to decreased risk of fatal prostate cancer (HRQ5 vs. Q1, 0.82" Thank goodness for that.
"ALA, and EPA intakes were related to the risk of advanced or fatal prostate cancer but not to nonadvanced prostate cancer."
...
Alpha-linolenic acid [ALA] & linoleic acid [LA] are described as essential fatty acids, because the body can't make them. Stearic acid (tallow) can be made into oleic acid (think olive oil) by placing a double-bond in the 9th position. We lack the enzymes 12-dehydrogenase & 15-dehydrogenase which could get double bonds in the 12th & 15th positions to make ALA. Thus, we have control of how much ALA is in our bodies - via dietary control.
It appears that it might be unwise to limit intake of linoleic acid [LA] too much, since it seems to oppose ALA.
Bit of trivia: If we did produce 12-dehydrogenase, we could turn oleic acid into LA. & if we had 15-dehydrogenase, we could turn LA into ALA. They are that close.
-Patrick
[1] nordicnaturals.com/en/Produ...
[2] ncbi.nlm.nih.gov/pubmed/810...
[3] ncbi.nlm.nih.gov/pubmed/815...
[4] jn.nutrition.org/content/13...
[5] ajcn.nutrition.org/content/...
[6] ncbi.nlm.nih.gov/pubmed/164...
[7] ncbi.nlm.nih.gov/pubmed/167...
[8] ncbi.nlm.nih.gov/pubmed/189...
[9] ncbi.nlm.nih.gov/pubmed/219...
