RE: evolution and diet (was: FITNESS: Diet and Exercise)

From: gts (gts_2000@yahoo.com)
Date: Tue Apr 15 2003 - 20:18:02 MDT

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    Brian Atkins wrote:

    > So IMO the whole HCA thing is likely overblown

    Possibly, and possibly not. The jury is still out on HCA's. I'll agree
    completely that the evidence from nutrition science is so far inconclusive.

    Again I want to emphasize that paleodiet theory rests on evolution science,
    not nutrition science. We know with a high degree of confidence approaching
    certainty that fire-cooking was not an important part of the diet of early
    hominids. The only real question is whether it arose far enough in the past
    that we can say safely that we are genetically adapted to HCA's.
    Conservative paleodieters prefer not to take their chances, so they prepare
    their meats in ways that minimize the risks.

    My own view is that HCA's are carcinogenic but that they might be rendered
    safe or safer in diets rich in antioxidants. This would not mean however
    that I think we are actually adapted to them. Like AGE's, they have no food
    value and may present a risk to health.

    It's a bit like my argument about tomatoes: non-paleolithic tomatoes are
    very rich in glutamate, which in excess can cause nervous system damage. Is
    it safe nevertheless to eat a lot of tomatoes? Do the known benefits of
    tomatoes (e.g., lycopene) outweigh the risks of eating a non-paleolithic
    food known to be rich in a known excitotoxin? I think the only honest answer
    is "Probably, but then perhaps not." No one really knows. We do however know
    with complete certainty that our prehistoric ancestors did not eat tomatoes,
    which places tomatoes in the "dubious" category alongside HCA's from
    fire-cooking.

    Below is some evidence that suggests we are not adapted to HCA's. I offer it
    not as conclusive proof, but rather to show that it should be a matter of
    concern.

    -gts

    ABSTRACT:
    Dietary intake of heterocyclic amines, meat-derived mutagenic activity, and
    risk of colorectal adenomas.
    Cancer Epidemiol Biomarkers Prev 2001 May;10(5):559-62 (ISSN: 1055-9965)
    Sinha R; Kulldorff M; Chow WH; Denobile J; Rothman N
    Division of Cancer Epidemiology and Genetics, National Cancer Institute,
    NIH, Rockville, Maryland 20892, USA.
    Meats cooked well-done by high temperature techniques produce mutagenic
    compounds such as heterocyclic amines (HCAs), but the amounts of these
    compounds vary by cooking techniques, temperature, time, and type of meat.
    We investigated the role of HCAs in the etiology of colorectal adenomas and
    the extent to which they may explain the previously observed risk for red
    meat and meat-cooking methods. In a case-control study of colorectal
    adenomas, cases (n = 146) were diagnosed with colorectal adenomas at
    sigmoidoscopy or colonoscopy, and controls (n = 228) were found not to have
    colorectal adenomas at sigmoidoscopy. Using a meat-derived HCA and mutagen
    database and responses from a meat-cooking questionnaire module, we
    estimated intake of 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline
    (DiMeIQx), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx),
    2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and mutagenic
    activity. We calculated odds ratios and 95% confidence intervals using
    logistic regression adjusting for several established risk factors for
    colorectal adenomas or cancer. The odds ratios (95% confidence interval; P
    for trend test) fifth versus first quintiles are: 2.2 (1.2-4.1; P = 0.02)
    for DiMeIQx; 2.1 (1.0-4.3; P = 0.002) for MeIQx; 2.5(1.1-5.5; P = 0.02) for
    PhIP; and 3.1 (1.4-6.8; P = 0.001) for mutagenic activity. When the three
    HCAs were adjusted for the other two, only the trend for MeIQx (P = 0.04)
    remained statistically significant. When we tried to disentangle the
    relative contribution of the three HCAs from the meat variables, we found
    that MeIQx remained significantly associated with risk even when adjusted
    for red meat but not vice versa. When MeIQx and well-done meat were analyzed
    in the same model, the risks were attenuated for both. Mutagenic activity
    from meat remained significantly associated with increased risk even when
    adjusted for intake of red meat or well-done red meat, whereas the red meat
    and well-done red meat associations were no longer significant when adjusted
    for total mutagenic activity. In conclusion, we found an elevated risk of
    colorectal adenomas associated with high intake of certain HCAS: Further,
    mutagenic activity from cooked meat consumption, a measure that integrates
    all of the classes of mutagens, was strongly associated with risk and
    explained the excess risk with intake of well-done red meat.



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