This post is prompted by a new Canadian study [1].
Much as with early coffee studies, researchers often seem to have made up their minds about alcohol & PCa risk ahead of the study. The following is from the new paper:
- "Findings add to the accumulating evidence that high alcohol consumption increases the risk of high-grade PCa"
- "No association was found for wine consumption."
Which seems to rule out alcohol itself. Unless the polyphenols in wine, such as the flavonoids, negate its harmful effects. Oh, and:
"High cumulative consumption of spirits was associated with a lower risk of low-grade PCa" {risk factor =0.75} Which leaves beer:
"The {risk factor} for high-grade PCa associated with high beer intake was 1.37 ..; it was 1.49 ... among current drinkers and 1.68 ... after adjusting for screening recency."
It is often stated in glycemic index (GI) tables that the GI of red wine is zero. In any case, it is too low to be measured. It is commonly assumed that the GI of beer is high - how else to explain 'beer belly'. In fact, the GI of beer is quite low. But if one has a beer gut, it's likely that the total glycemic load has been frequently sufficient to raise triglycerides and add to visceral fat deposits. Visceral fat is associated with advanced PCa.
[2] Red Wine.
"The levels of resveratrol found in food varies considerably. Red wine contains between 0.2 and 5.8 mg/l, depending on the grape variety. White wine has much less because red wine is fermented with the skins, allowing the wine to extract the resveratrol, whereas white wine is fermented after the skin has been removed." [Wiki]
Vineyards often have a rosebush growing at the end of each row of vines. These are akin to the canary in the mineshaft, warning, in this case, of fungal attack. In practice, the roses are mostly for show, since the vines are usually sprayed on a schedule to prevent fungal problems. This limits the resveratrol content of the grapes, since resveratrol is produced as a response to grape stress, such as fungal attack.
[2A] Red Wine - null findings.
[2Aa] (1999 - The Netherlands)
[2Ab] (2006 - U.S. - VITAL study)
[2Ac] (2010 - U.S.)
[2B] Red Wine - increased risk.
[2Ba] ... see [2Cb]
"Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, ... null or slight increased risks were observed for men who consumed >4 glasses/week"
[2C] Red Wine - decreased risk.
[2Ca] (2005 - U.S.)
"Each additional glass of red wine consumed per week showed a statistically significant 6% decrease in relative risk"
[2Cb] (2005 - U.S.)
"Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed <or=4 glasses of red wine/week"
[3] White wine.
[3A] White wine - null findings.
[3Aa] ... see [2Ca]
[3Ab] ... see [2Ac]
[3B] White wine - increased risk.
[3Ba] ... see [2Aa]
[3Bb] ... see [2Ab]
[4] Beer.
Beer in America is an increasingly complex subject. Here in Asheville, we have the highest concentration of breweries in the U.S. The beers on offer tend to be high in flavor, with a higher specific gravity & calorie content than beers of the past. At the same time, there is great interest in hops, & a good selection of hoppy IPAs (India pale ales) IPAs are now remarkably popular.
Hops were traditionally added to beer to extend life, but they have taken on an importance way beyond their antibacterial properties. For a beer drinker, the hops used might deliver a significant dose of flavonoids - especially from IPAs.
Xanthohumol (a prenylflavonoid) has been studied with respect to PCa cells. (There are over 300 PubMed hits for <Xanthohumol>.
[4ha] (2007 - U.S.) "... decreased cell viability in a dose dependent manner ..."
[4hb] (2006 - Belgium) "... proved to be the most active {hop} compound in inhibiting the growth of the cell lines" "PC-3 and DU145."
[4hc] (2008 - Belgium) "... hop-derived prenylflavanones ... induce a caspase-independent form of cell death, suggested to be autophagy."
[4hd] (2010 - U.S.) "Promotion of apoptosis in cancer cells could potentially lead to the regression and improved prognosis of hormone-refractory prostate cancer. Xanthohumol (XN), a prenylated chalcone-derived from hops, has shown strong antitumorigenic activity towards diverse types of cancer cells. In the present study, the growth-inhibitory and apoptosis-inducing activity of XN was tested in hormone-sensitive and hormone-refractory human prostate cancer cells lines. Cell growth/viability assay (MTS) demonstrated that prostate cancer cells are highly sensitive to XN at a concentration range of 20-40 μM. The primary mode of tumor cell destruction was apoptosis ..."
[4he] (2016 - Poland) "TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is an endogenous ligand, which plays role in immune surveillance and anti-tumor immunity. It has ability to selectively kill tumor cells showing no toxicity to normal cells." ... "The findings suggest that xanthohumol is a compound of potential use in chemoprevention of prostate cancer due to its sensitization of cancer cells to TRAIL-mediated apoptosis."
[4A] Beer - null findings.
[4Aa] ... see [2Aa]
[4Ab] ... see [2Ca]
[4Ac] ... see [2Ab]
[4Ad] ... see [2Ac]
[4Ae] (1984 - U.S.)
[4Af] ... see [5Ba]
[5] Liquor
[5A] Liquor - null findings.
[5Aa] ... see [2Ac]
[5Ab] ... see [2Ca]
[5Ac] ... see [2Ab]
[5B] Liquor - increasd risk.
[5Ba] (2001 - U.S.)
"moderate liquor consumption was associated with a significant 61-67% increased risk of prostate cancer")
...
The case against alcohol as having a role in PCa incidence is extraordinarily weak IMO.
It would be useful to have studies that focus on PCa progression.
Meanwhile, my doctors warn me to cut down, but I'm disinclined.
PCa is a stressful condition. There are meds for stress, of course, but drinks with friends, wine with a meal, a glass or two of Scotch in the evening can lighten the day. It is said that alcohol increases cortisol levels (the 'stress hormone'), but it also raises serotonin, at least in the short term.
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/276...
[2Aa] ncbi.nlm.nih.gov/pubmed/106...
[2Ab] ncbi.nlm.nih.gov/pubmed/171...
[2Ac] ncbi.nlm.nih.gov/pubmed/195...
[2Ca] ncbi.nlm.nih.gov/pubmed/153...
[2Cb] ncbi.nlm.nih.gov/pubmed/172...
[4ha] ncbi.nlm.nih.gov/pubmed/165...
[4hb] ncbi.nlm.nih.gov/pubmed/166...
[4hc] ncbi.nlm.nih.gov/pubmed/177...
[4hd] ncbi.nlm.nih.gov/pubmed/209...
[4he] ncbi.nlm.nih.gov/pubmed/273...
[4Ae] ncbi.nlm.nih.gov/pubmed/669...
[5Ba] ncbi.nlm.nih.gov/pubmed/115...