What does the latest "study" really tell us about eating fish?
- From: "montygram" <nazztrader@xxxxxxxxx>
- Date: 12 Oct 2005 15:21:09 -0700
I read a report of this study in Newsday newspaper, page A5, 10/11/2005
- that is the source of my information. Let's review it:
1. It is from the good people at Rush, who would not even answer a
basic question I put to them about a previous "study" of theirs
that concluded that "saturated fat," but not "animal fat" was
"associated" with Alzheimer's disease (AD) among a group of
people who did not consume any appreciable amount of coconut oil or
palm kernel oil. How is this possible? They would not answer when I
asked. After thinking it over, I realized what they had done, which
was to note that items like pork and beef were less healthy than
chicken and fish (in general). Why didn't they just say that, as
other researchers have? I don't know, but I doubt you will get an
answer if you ask them. I couldn't.
2. It appears that they are mining the same sources they did for the
other study. They give simple tests to old people and also ask them to
fill out questionnaires about what they ate. Many of them went on to
develop AD within a few years. Were their memories failing before
obvious signs of AD were present, and can we trust their memories at
that point? Unless there is a way to control for this, it cannot be
considered "science."
3. The conclusion was "eating fish at least once a week is good for
the brain, slowing age-related mental decline." Now I agree that
this makes sense, if the people ate fish low in fat as a substitute for
beef and pork (and fried chicken, as well as a few other nasty things
they would have eaten instead). But what about those great omega 3
PUFAs, you ask? On to the next item:
4. "The researchers looked for, but failed to find, a link between
omega-3 fatty acids and protection from brain decline." Just as I
have said here many times, it is not that fish is so good, but that
beef and pork (especially they way they are processed, prepared,
cooked, etc.) are so bad. I've eaten canned tuna which had a label
that said 0 grams of fat, so the fat is not the issue. Basically,
canned tuna with 0 grams of fat is a good source of protein, though a
bit serotogenic (so eating a lot would be unhealthy, though that was
not the case among these old folks) and the mercury levels could be a
concern to some. In other words, compared to a fried steak, high in
iron, oxidized cholesterol, arachidonic acid and other PUFAs, etc.,
something like canned tuna is much better. And that is what they
found. They just have not done enough objective research to understand
exactly what it going on here. Who has?
5. It turns out that more than 15 years ago, a study was done which
found that people who eat fried fish regularly are more likely to die
of heart attacks than those who rarely eat fish. As we now know,
it's only when cholesterol gets oxidized that it is a problem, so
this makes perfect sense. Source: American Health 8 (5): 104. "The
fish nobody knows." Barnett and Barone, 1989. See Bruce Fife's
book, "Saturated fat may save your life," page 55, for a discussion
of this study.
Here are some good sources. Note that in the first one listed, they
make the point about chicken and fish versus "red meat," and in the
second, they say "There were no associations of pancreatic cancer risk
with intake of poultry, fish, dairy products, eggs, total fat,
saturated fat, or cholesterol." Also noteworthy is that they appear to
be very interested in how people prepare the foods, which is something
the Rush people don't seem to be very concerned about. Thus, when
epidemiology is done correctly, it can be very useful in confirming
molecular-level evidence, which is truly scientific. Fish can be
reasonably healthy, but don't fry it and stay away from the kinds that
are high in omega 3s and pollutants.
Cancer Epidemiol Biomarkers Prev. 2004 Sep;13(9):1509-14.
Red meat, chicken, and fish consumption and risk of colorectal cancer.
English DR, MacInnis RJ, Hodge AM, Hopper JL, Haydon AM, Giles GG.
Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne,
Victoria, Australia. dallas.english@xxxxxxxxxxxxxxxx
BACKGROUND: Red meat and processed meat consumption have been
associated with increased risk of colorectal cancer in some, but not
all, relevant cohort studies. Evidence on the relationship between risk
of colorectal cancer and poultry and fish consumption is inconsistent.
METHODS: We conducted a prospective cohort study of 37,112 residents of
Melbourne, Australia recruited from 1990 to 1994. Diet was measured
with a food frequency questionnaire. We categorized the frequency of
fresh red meat, processed meat, chicken, and fish consumption into
approximate quartiles. Adenocarcinomas of the colon or rectum were
ascertained via the Victorian Cancer Registry. RESULTS: We identified
283 colon cancers and 169 rectal cancers in an average of 9 years of
follow-up. For rectal cancer, the hazard ratios [95% confidence
intervals (95% CI)] in the highest quartile of consumption of fresh red
meat and processed meat were 2.3 (1.2-4.2; P for trend = 0.07) and 2.0
(1.1-3.4; P for trend = 0.09), respectively. The corresponding hazard
ratios (95% CIs) for colon cancer were 1.1 (0.7-1.6; P for trend = 0.9)
and 1.3 (0.9-1.9; P for trend = 0.06). However, for neither type of
meat was the heterogeneity between subsites significant. Chicken
consumption was weakly negatively associated with colorectal cancer
(hazard ratio highest quartile, 0.7; 95% CI, 0.6-1.0; P for trend =
0.03), whereas hazard ratios for fish consumption were close to unity.
CONCLUSION: Consumption of fresh red meat and processed meat seemed to
be associated with an increased risk of rectal cancer. Consumption of
chicken and fish did not increase risk.
J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.
Meat and fat intake as risk factors for pancreatic cancer: the
multiethnic cohort study.
Nothlings U, Wilkens LR, Murphy SP, Hankin JH, Henderson BE, Kolonel
LN.
Cancer Research Center of Hawaii, Honolulu, HI, USA.
UNothlin@xxxxxxxxxxxxxxx
BACKGROUND: Meat intake has been associated with risk of exocrine
pancreatic cancer, but previous findings have been inconsistent. This
association has been attributed to both the fat and cholesterol content
of meats and to food preparation methods. We analyzed data from the
prospective Multiethnic Cohort Study to investigate associations
between intake of meat, other animal products, fat, and cholesterol and
pancreatic cancer risk. METHODS: During 7 years of follow-up, 482
incident pancreatic cancers occurred in 190,545 cohort members. Dietary
intake was assessed using a quantitative food frequency questionnaire.
Associations for foods and nutrients relative to total energy intake
were determined by Cox proportional hazards models stratified by gender
and time on study and adjusted for age, smoking status, history of
diabetes mellitus and familial pancreatic cancer, ethnicity, and energy
intake. Statistical tests were two-sided. RESULTS: The strongest
association was with processed meat; those in the fifth quintile of
daily intake (g/1000 kcal) had a 68% increased risk compared with those
in the lowest quintile (relative risk = 1.68, 95% confidence interval =
1.35 to 2.07; Ptrend < .01). The age-adjusted yearly incidence rates
per 100,000 persons for the respective quintiles were 41.3 and 20.2.
Intakes of pork and of total red meat were both associated with 50%
increases in risk, comparing the highest with the lowest quintiles
(both Ptrend < .01). There were no associations of pancreatic cancer
risk with intake of poultry, fish, dairy products, eggs, total fat,
saturated fat, or cholesterol. Intake of total and saturated fat from
meat was associated with statistically significant increases in
pancreatic cancer risk but that from dairy products was not.
CONCLUSION: Red and processed meat intakes were associated with an
increased risk of pancreatic cancer. Fat and saturated fat are not
likely to contribute to the underlying carcinogenic mechanism because
the findings for fat from meat and dairy products differed.
Carcinogenic substances related to meat preparation methods might be
responsible for the positive association.
J Nutr. 2004 Apr;134(4):776-84.
Meat consumption patterns and preparation, genetic variants of
metabolic enzymes, and their association with rectal cancer in men and
women.
Murtaugh MA, Ma KN, Sweeney C, Caan BJ, Slattery ML.
Department of Family and Preventive Medicine, University of Utah, Salt
Lake City, UT 84101, USA. mmurtaugh@xxxxxxxxxxxx
Meat consumption, particularly of red and processed meat, is one of the
most thoroughly studied dietary factors in relation to colon cancer.
However, it is not clear whether meat, red meat, heterocyclic amines
(HCA), or polycyclic aromatic hydrocarbons (PAH) are associated with
the risk for rectal cancer. Rectal cancer cases (n = 952) and controls
(n = 1205) from Utah and Northern California were recruited from a
population-based case-control study between September 1997 and February
2002. Detailed in-person interviews regarding lifestyle, medical
history, and diet were conducted. DNA was extracted from peripheral
lymphocytes obtained from whole-blood samples, and glutathione
S-transferase (GST)M1 enzyme and N-acetyl transferase (NAT)2 enzyme
genotypes were assessed. Although energy and cholesterol intakes were
higher among cases than controls, adjustment for confounders accounted
for the differences. Increased consumption of well-done red meat [odds
ratio (OR) 1.33 95% CI 0.98, 1.79] was associated with an (P = 0.04)
increase in risk for rectal cancer among men. The mutagen index,
calculated on the bases of reported amount, doneness, and method of
cooking meat, was also positively but not significantly (P = 0.24)
associated with risk of rectal cancer for men (OR 1.37 95% CI 0.98,
1.92). NAT2-imputed phenotype and GSTM1 did not consistently modify
rectal cancer risk associated with meat intake. These data suggest that
mutagens such as HCA that form when meat is cooked may be culpable
substances in rectal cancer risk, not red meat itself.
Environ Mol Mutagen. 2004;44(1):44-55.
Meat-related mutagens/carcinogens in the etiology of colorectal cancer.
Cross AJ, Sinha R.
Nutritional Epidemiology Branch, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health,
Department of Health and Human Services, Rockville, Maryland 20852,
USA. crossa@xxxxxxxxxxxx
Diets containing substantial amounts of red or preserved meats may
increase the risk of various cancers, including colorectal cancer. This
association may be due to a combination of factors such as the content
of fat, protein, iron, and/or meat preparation (e.g., cooking or
preserving methods). Red meat may be associated with colorectal cancer
by contributing to N-nitroso compound (NOC) exposure. Humans can be
exposed to NOCs by exogenous routes (from processed meats in
particular) and by endogenous routes. Endogenous exposure to NOCs is
dose-dependently related to the amount of red meat in the diet.
Laboratory results have shown that meats cooked at high temperatures
contain other potential mutagens in the form of heterocyclic amines
(HCAs) and polycyclic aromatic hydrocarbons (PAHs). To investigate the
role of these compounds, we have created separate databases for HCAs
and PAHs, which we have used in conjunction with a validated
meat-cooking food frequency questionnaire. The role of meat type,
cooking methods, doneness levels, and meat-cooking mutagens has been
examined in both case-control studies and prospective cohort studies,
with mixed results. Here, we review the current epidemiologic knowledge
of meat-related mutagens, and evaluate the types of studies that may be
required in the future to clarify the association between meat
consumption and colorectal cancer.
JAMA. 2005 Jan 12;293(2):172-82.
Meat consumption and risk of colorectal cancer.
Chao A, Thun MJ, Connell CJ, McCullough ML, Jacobs EJ, Flanders WD,
Rodriguez C, Sinha R, Calle EE.
Epidemiology and Surveillance Research, American Cancer Society,
Atlanta, Ga 30329-4251, USA.
CONTEXT: Consumption of red and processed meat has been associated with
colorectal cancer in many but not all epidemiological studies; few
studies have examined risk in relation to long-term meat intake or the
association of meat with rectal cancer. OBJECTIVE: To examine the
relationship between recent and long-term meat consumption and the risk
of incident colon and rectal cancer. DESIGN, SETTING, AND PARTICIPANTS:
A cohort of 148 610 adults aged 50 to 74 years (median, 63 years),
residing in 21 states with population-based cancer registries, who
provided information on meat consumption in 1982 and again in 1992/1993
when enrolled in the Cancer Prevention Study II (CPS II) Nutrition
Cohort. Follow-up from time of enrollment in 1992/1993 through August
31, 2001, identified 1667 incident colorectal cancers. Participants
contributed person-years at risk until death or a diagnosis of colon or
rectal cancer. MAIN OUTCOME MEASURE: Incidence rate ratio (RR) of colon
and rectal cancer. RESULTS: High intake of red and processed meat
reported in 1992/1993 was associated with higher risk of colon cancer
after adjusting for age and energy intake but not after further
adjustment for body mass index, cigarette smoking, and other
covariates. When long-term consumption was considered, persons in the
highest tertile of consumption in both 1982 and 1992/1993 had higher
risk of distal colon cancer associated with processed meat (RR, 1.50;
95% confidence interval [CI], 1.04-2.17), and ratio of red meat to
poultry and fish (RR, 1.53; 95% CI, 1.08-2.18) relative to those
persons in the lowest tertile at both time points. Long-term
consumption of poultry and fish was inversely associated with risk of
both proximal and distal colon cancer. High consumption of red meat
reported in 1992/1993 was associated with higher risk of rectal cancer
(RR, 1.71; 95% CI, 1.15-2.52; P = .007 for trend), as was high
consumption reported in both 1982 and 1992/1993 (RR, 1.43; 95% CI,
1.00-2.05). CONCLUSIONS: Our results demonstrate the potential value of
examining long-term meat consumption in assessing cancer risk and
strengthen the evidence that prolonged high consumption of red and
processed meat may increase the risk of cancer in the distal portion of
the large intestine.
Int J Cancer. 2005 Sep 10;116(4):592-8.
Dietary patterns and risk of prostate cancer in Ontario, Canada.
Walker M, Aronson KJ, King W, Wilson JW, Fan W, Heaton JP, MacNeily A,
Nickel JC, Morales A.
Division of Cancer Care and Epidemiology, Department of Community
Health and Epidemiology, Cancer Research Institute, Queen's University,
Kingston, Onatrio, Canada.
Dietary patterns reflect combinations of dietary exposures, and here we
examine these in relation to prostate cancer risk. In a case-control
study, 80 incident primary prostate cancer cases and 334 urology clinic
controls were enrolled from 1997 through 1999 in Kingston, Ontario,
Canada. Food-frequency questionnaires were completed prior to diagnosis
and assessed intake in the 1-year period 2-3 years prior to enrollment.
Among controls, dietary intake was used in principal components
analyses to identify patterns that were then evaluated with all
subjects in relation to prostate cancer risk using unconditional
logistic regression, controlling for age. Four dietary patterns were
identified: Healthy Living, Traditional Western, Processed and
Beverages. Increased prostate cancer risk is apparent in relation to
the Processed pattern, composed of processed meats, red meats, organ
meats, refined grains, white bread, onions and tomatoes, vegetable oil
and juice, soft drinks and bottled water. The OR for the highest
tertile compared to baseline is 2.75 (95% CI 1.40-5.39), with a
dose-response pattern (trend test p < 0.0035). Our results suggest that
a dietary pattern including refined grain products, processed meats and
red and organ meats contributes to increased prostate cancer risk.
Since dietary information was collected before subjects knew their
diagnosis, recall bias was avoided. (c) 2005 Wiley-Liss, Inc.
Nutr Hosp. 2005 Jul-Aug;20(4):235-41.
Colorectal cancer: lifestyle and dietary factors.
Correa Lima MP, Gomes-da-Silva MH.
Department of Food and Nutrition, Mato Grosso Federal University,
Cuiaba, Brasil. marihele@xxxxxxxxxxx
INTRODUCTION: Colorectal cancer is the most common tumor in the
developed countries, and the number of new cases annualy is
aproximately equal for men and women. Several environmental factors can
interact in all steps of carcinogenesis. Lately the balance between
genetic predisposition and these factors, including nutritional
components and lifestyle behaviors, determines individual
susceptibility to develop colorectal cancer. The aim of this study is
to revise the references about lifestyle include diet, physical
exercise, tobacco smoking and use of alcohol, and the risk of
colorectal cancer in databases published during 1994-2004. DIETARY
FACTORS: According to the reports high intake of red meat, and
particularly of processed meat and positive energetic balance (high
intake of total fat and carbohydrate) was associated with a moderate
but significant increase in colorectal cancer risk. Convincing
preventive factors include increase consumption of a wide variety of
fruit and vegetable, particularly, dark-green leafy, cruciferous, a
deep-yellow on tones, and fibre. LIFESTYLE: Physical activity as a
means for the primary prevention of colorectal cancer. There is a
probable synergic effect among physical inactivity, high energy intake
and obesity and incidence of colorectal cancer. A growing body of
evidence supports that avoidance overweight and the use of tobacco and
alcohol is recommended to prevent colorectal cancer. CONCLUSION:
Current data suggest that lifestyle modification including proper diet
such as the ones rich in vegetable and poor in red meat and fat,
regular physical activity and maintaining an appropriate body weight
and avoiding the use of tobacco and alcohol may lead to reduce
colorectal cancer risk.
Cancer Res. 2005 Sep 1;65(17):8034-41.
Meat, meat cooking methods and preservation, and risk for colorectal
adenoma.
Sinha R, Peters U, Cross AJ, Kulldorff M, Weissfeld JL, Pinsky PF,
Rothman N, Hayes RB.
Nutritional Epidemiology Branch, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA.
sinhar@xxxxxxx
Cooking meat at high temperatures produces heterocyclic amines (HCAs)
and polycyclic aromatic hydrocarbons (PAHs). Processed meats contain
N-nitroso compounds. Meat intake may increase cancer risk as HCAs,
PAHs, and N-nitroso compounds are carcinogenic in animal models. We
investigated meat, processed meat, HCAs, and the PAH benzo(a)pyrene and
the risk of colorectal adenoma in 3,696 left-sided (descending and
sigmoid colon and rectum) adenoma cases and 34,817 endoscopy-negative
controls. Dietary intake was assessed using a 137-item food frequency
questionnaire, with additional questions on meats and meat cooking
practices. The questionnaire was linked to a previously developed
database to determine exposure to HCAs and PAHs. Intake of red meat,
with known doneness/cooking methods, was associated with an increased
risk of adenoma in the descending and sigmoid colon [odds ratio (OR),
1.26; 95% confidence interval (95% CI), 1.05-1.50 comparing extreme
quintiles of intake] but not rectal adenoma. Well-done red meat was
associated with increased risk of colorectal adenoma (OR, 1.21; 95% CI,
1.06-1.37). Increased risks for adenoma of the descending colon and
sigmoid colon were observed for the two HCAs:
2-amino-3,8-dimethylimidazo[4,5]quinoxaline and
2-amino-1-methyl-6-phenylimidazo[4,5]pyridine (OR, 1.18; 95% CI,
1.01-1.38 and OR, 1.17, 95% CI, 1.01-1.35, respectively) as well as
benzo(a)pyrene (OR, 1.18; 95% CI, 1.02-1.35). Greater intake of bacon
and sausage was associated with increased colorectal adenoma risk (OR,
1.14; 95% CI, 1.00-1.30); however, total intake of processed meat was
not (OR, 1.04; 95% CI, 0.90-1.19). Our study of screening-detected
colorectal adenomas shows that red meat and meat cooked at high
temperatures are associated with an increased risk of colorectal
adenoma.
.
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