X-Message-Number: 24575
Date: Tue, 31 Aug 2004 20:21:32 -0700 (PDT)
From: Doug Skrecky <>
Subject: life extension effect of beer??

[Maybe vitrification solutions could use a little of this stuff. 8/ ]

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Am J Clin Nutr. 1990 May;51(5):869-72.
Beer mitigates some effects of copper deficiency in rats.
  Because of an epidemiologic association of decreased risk of death from
ischemic heart disease with moderate use of alcoholic beverages, and
because numerous abnormalities found in people with ischemic heart
disease are also found in animals deficient in copper, rats were fed a
diet deficient in copper and were given either beer or water to drink.
Rats drinking beer lived nearly six times as long and had lower plasma
cholesterol, less cardiac enlargement, and higher liver copper. Apparent
absorption and biological half-life of oral radiocopper were increased by
beer. The effects were not attributable to alcohol, chromium, or copper in
beer. Beer intakes were similar to those of some people in the United
States. Results may explain seasonal cycles in plasma cholesterol and may
be germane to the epidemiology of ischemic heart disease because diets in
the United States seem to be low in copper.

Mutat Res. 2004 Apr 11;559(1-2):177-87.
Inhibitory effects of beer on heterocyclic amine-induced mutagenesis and
PhIP-induced aberrant crypt foci in rat colon.
  Anti-mutagenic and anti-carcinogenic effects of beer on heterocyclic
amine (HCA)-induced carcinogenesis were studied in vitro and in vivo.
Four commercial beers (two pilsner-type, black, and stout) showed
inhibitory effects against five HCAs, 2-amino-3,8-dimethylimidazo
[4,5-f]quinoxaline (MeIQx),
2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP),
3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2),
2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) and
2-amino-3-methylimidazo[4,5-f]-quinoline (IQ), in the Ames assay using
Salmonella typhimurium TA98 in the presence of rat S9 mix.
The inhibitory effects of dark-colored beers (stout and black beer) were
greater than those of pilsner-type beers. Dark-colored beers suppressed
CYP1A2 activity in a dose-dependent manner, suggesting that inhibition of
HCA activation is partly responsible for their strong anti-mutagenic
effects. Anti-mutagenic effects were also observed when the pooled human
S9 mix or activated IQ was used in the assay. The micronucleus test using
Chinese hamster lung CHL/IU cells showed that the addition of
freeze-dried samples of pilsner-type and stout beer to the culture medium
significantly reduced the number of cells with micronuclei induced with
PhIP or Trp-P-2. Single-cell gel electrophoresis assay (comet assay)
revealed that oral ingestion of pilsner-type and stout beers for 1 week
significantly inhibited DNA damage in the liver cells of male ICR mice
exposed to MeIQx (13 mg/kg, i.p.). A decrease in the formation of DNA
adducts was also observed using a 32P-postlabeling method. Male Fischer
344 rats orally received PhIP (75 mg/kg, five times a week for 2 weeks)
and aberrant crypt foci (ACF) formation in the colon was analyzed after 5
weeks. The number of ACF was significantly reduced in rats fed a diet
containing freeze-dried beer. These results suggest that beer inhibits
the genotoxic effects of HCAs and may reduce the risk of carcinogenesis
caused by food borne carcinogens.

J Agric Food Chem. 2003 Aug 27;51(18):5528-33.
Phenol antioxidant quantity and quality in foods: beers and the effect of
two types of beer on an animal model of atherosclerosis.
  The free phenols have been measured in 15 lagers, 6 porters and ales,
and 11 light and nonalcoholic beers. Phenols were measured
colorimetrically using an oxidation-reduction reaction with
Folin-Ciocalteu reagent and catechin as the standard. The order of phenol
concentration was ales > lagers > low calorie > nonalcoholic. The quality
of antioxidants of the major phenols in beers and the quality of beer
antioxidants were measured by (1) dose-response inhibition of lower
density lipoprotein oxidation and (2) concentration of phenols in the
beers at which 50% of the peroxide was destroyed in a luminescent assay
for antioxidant activity. The beers' lipoprotein antioxidant quality was
clearly superior to that of vitamin antioxidants and to that of the
phenol ingredients, suggesting synergism among the antioxidants in the
mixture. The average per capita consumption of beer in the United
States in 2000 was 225 mL/day, equivalent to 42 mg/day of catechin
equivalents. Beer provides more antioxidants per day than wine in the
U.S. diet. A dark beer and a lager beer were given at two concentrations
to cholesterol-fed hamsters, an animal model of atherosclerosis. At the
high dose ((1)/(2)-diluted beer) both lager and dark beer significantly
inhibited atherosclerosis compared to a control of 2% alcohol. At the
high dose, lager significantly decreased cholesterol and triglycerides,
and both beers acted as in vivo antioxidants by decreasing the
oxidizability of lower density lipoproteins. At the low dose
((1)/(10)-diluted beer) only th e lager beer significantly decreased
atherosclerosis compared to the 0.4% alcohol control. The polyphenols in
the beers appear to be responsible for the benefits of beer in this
model. Lager beer inhibited atherosclerosis at a human equivalent dose in
this hamster model of atherosclerosis.

Int J Cancer. 2004 Jan 20;108(3):404-11
Intake of beer inhibits azoxymethane-induced colonic carcinogenesis in
male Fischer 344 rats.
  Modulatory effects of beer consumption on azoxymethane (AOM)-induced rat
colonic carcinogenesis in male Fischer 344 rats were investigated. Single
cell gel electrophoresis assay indicated that DNA damage of colonocytes,
induced by a single AOM injection (15 mg/kg body weight), was
significantly reduced in rats fed beer or malt extract for 2 weeks.
Examination of aberrant crypt foci (ACF) formation in colonic mucosa,
induced by AOM (15 mg/kg body weight; twice weekly), revealed that
feeding of beer during the whole experimental period of 5 weeks
significantly reduced the number of ACF by 35%. In the post-initiation
protocol, a reduction in ACF formation by 26% was not significant. The
efficacy in inhibition of ACF formation varied with the brand of beer.
ACF formation was significantly reduced in rats treated with freeze-dried
beer (FD Beer), but not with ethanol, suggesting that nonvolatile
components of beer are responsible for the reduction. Significant
suppression of ACF formation was observed in groups treated with hot
water extract of malt, especially with extracts of colored malts,
although no reduction was observed by feeding with hops extract. A
long-term experiment of 42 weeks indicated that intake of beer decreased
tumor incidence by 22% and decreased the number of neoplastic lesions,
including adenocarcinomas and adenomas, by 44%. These results suggest
that components of beer have chemopreventive effects on colonic
carcinogenesis induced by AOM and that intake of beer may contribute to a
reduction in the risk of cancer susceptibility.

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