Bad Science

[Guest guest]

I'd like to write a bit about bad science. I am going to use the

post below as an example. But I am not really talking about just that one

single study, for the problem is endemic within the research community.

 

Let me start with a quote from Gary Taub who wrote the article

" What If It's All Been a Big Fat Lie " URL to the interview follows the

quote.

" I just got off the phone with so-and-so, and he's [taken] credit for

getting Americans to eat less eggs and less fat. This guy's one of the worst

scientists I've ever talked to, and if he was involved in this, then there's

a story there. "

http://www.pbs.org/wgbh/pages/frontline/shows/diet/interviews/taubes.html

 

 

Now, lets look at the research below. When I studied science in

school, one is supposed to have a single variable. I see several here.

The controls ate more fruit & veggies & more fiber, as well as less beef.

The beef eaters also ate more fat. What is not stated, is even more

interesting. No mention of what kinds fats are eaten. Do the high fat

eaters eat a lot of butter & coconut oil? Or are they eating margarine,

potato chips, and French fries?

 

I see many things which might possibly account for the health

problems other than beef eating. And even it could be narrowed down to

beef -- are these people eating commercial beef which is raised on corn in

feedlots, and pumped up with growth hormones & antibiotics? Or are the

people eating beef from healthy cows allowed to graze, and not fed corn, and

nor given growth hormones & antibiotics?

 

It looks me to be really wretchedly planned research. Which makes

me wonder -- are these really bad scientists? Again, not just pointing a

finger at the research below, but the many many studies showing how bad it

is to eat various foods our ancestors thrived on. Or have these

scientists been bought off by people who want to prove how bad beef is for

one to eat?

 

 

Alobar

 

 

 

-

" JoAnn Guest " <angelprincessjo

;

<DietaryTipsForHBP >

Saturday, June 18, 2005 3:25 PM

N-Nitrosation: A Positive

Epidemiological Relationship between Red Meat Intake and Colorectal Cancer

 

 

N-Nitrosation: A Positive Epidemiological Relationship between Red Meat

intake and Colorectal Cancer

JoAnn Guest

Jun 18, 2005 13:22 PDT

================================================================================\

=========================================================Hughes

R, Pollock JR, Bingham S.

Dunn Human Nutrition Unit, Medical Research Council, Cambridge CB2 2XY,

UK.

 

 

 

 

Red meat increases colonic N-nitrosation, and this may explain the

positive epidemiological relationship between red meat intake and

colorectal cancer risk.

 

 

Vegetables, tea, and soy have been shown to block N-nitroso compound

(NOC) formation and are associated with protection against colorectal

cancer.

 

To determine whether these supplements affect fecal NOC

excretion during consumption of a high red meat (420 g/day) diet, 11

male volunteers were studied over a randomized series of 15-day dietary

periods. Seven of these subjects completed a further dietary period to test

the effects of soy (100 g/day).

 

Soy significantly suppressed fecal apparent total NOC (ATNC)

concentration (P == 0.02), but supplements of vegetables (400 g/day as

134 g broccoli, 134 g brussels sprouts, and 134 g petits pois) and tea

extract (3 g/day) did not affect mean levels of fecal ATNC, nitrogen and

ammonia excretion, and fecal water genotoxicity.

 

However, fecal weight was increased (P < 0.001) and associated with

reduced transit time (r == 0.594, P < 0.0001), so that contact between

ATNC, nitrite, and ammonia and the large bowel mucosa would have been

reduced. Longer transit times were associated with elevated fecal ATNC

concentrations (r == 0.42, P == 0.002). Fecal nitrite was significantly

suppressed during the tea supplement compared with the meat-only (P ==

0.0028) and meat + vegetables diets (P == 0.005 for microgram NO2/g).

 

Nutr Cancer 2002;42(1):70-7 PMID: 12235653 [PubMed - in process]

 

 

Effect of vegetables, tea, and soy on endogenous N-nitrosation, fecal

ammonia, and fecal water genotoxicity during a high red meat diet in

humans.

 

Oncol Rep, 12/02

 

--

 

 

Introduction Testicular cancer accounts for <2% of malignant neoplasms

in men but is the most common tumor in young adult men aged 15-44 years

in the United States.[1] The only well-established risk factor for

testicular cancer is cryptorchidism (nondescent of the testes into the

scrotum at birth) (reviewed in Reference 2).

 

An ecological study of per capita fat consumption and testicular cancer

rates[3] and a case-control study have been suggestive of increased

testicular cancer risk with a high-fat diet.[4]

 

Diets high in red meat and milk and low in fruits and green vegetables

have been associated with elevated risk of testicular cancer.[4-6]

 

Although testicular cancers can be divided clinically into slow-growing

seminomas, rapidly growing nonseminomas, and mixed germ cell tumors

(those with seminomatous and nonseminomatous elements), only one study

has analyzed diet in relation to histology.[4]

 

To evaluate the association of dietary factors with risk of testicular

cancer, we conducted a hospital-based case-control study at The

University of Texas M. D. Anderson Cancer Center.

 

Specifically, we examined whether testicular cancer risk increased with

a high dietary intake of fats, meat, and milk and low consumption of

fruits and vegetables. We also assessed whether the dietary factors

associated with risk varied by testicular cancer histopathology.

 

Methods We identified men with testicular cancer who registered at M. D.

Anderson Cancer Center (Houston, TX) between January 1990 and October

1996 through the M. D. Anderson Tumor Registry and the M. D. Anderson

Genitourinary Oncology Clinic. Potential cases were defined as men who

were alive during the data collection phase of the investigation, were

between the ages of 18 and 50 years at the time of diagnosis, and lived

in Texas, Louisiana, Arkansas, or Oklahoma.

 

The age restriction was chosen because testicular cancer occurs most

often between 18 and 50 years, and we restricted the region to the

south-central United States so that the cases and controls would be from

a defined geographic area. All men diagnosed with testicular cancer were

eligible for inclusion, regardless of their ethnicity, tumor stage, and

histology.

 

To identify controls, we asked each case to nominate healthy friends who

had never had cancer and were of the same ethnicity, age (±5 yr), and

state of residence as the case. We chose friend controls, because the

cases arose from an undefined population, which is a common concern with

hospital-based case-control studies. We assumed friends of cases, had

they developed testicular cancer, would have been more likely to have

come to M. D. Anderson Cancer Center than a population-based control

group. Cases and controls completed self-administered questionnaires

eliciting information on demographics; lifestyle habits; medical

history, including history of cryptorchidism, family history of cancer,

body size, and shape; and diet.

 

To assess diet, we used a modified and revised version of the National

Cancer Institute's (NCI's) Health Habits and History Questionnaire

(HHHQ), which contained 152 foods and beverages[7,8] and has been

validated in a range of populations.[9,10] The time period assessed by

the questionnaire was the year before cancer diagnosis for cases and the

previous year for controls.

 

From the information we calculated food consumption and nutrient intake

by using DietSys (version 4.0), the nutrient analysis program developed

for the NCI's HHHQ.[11] To adjust for total energy intake, all dietary

factors were analyzed per 1,000 kcal dietary intake according to the

nutrient density adjustment method described by Willett,[12] and we also

used total daily calories in multivariable modeling.

 

We contacted by mail 335 eligible men diagnosed with testicular cancer,

and 101 (30.1%) agreed to participate. We also approached 155 more men

in the outpatient Genitourinary Oncology Clinic, of whom 86 (55.5%)

agreed to participate. Of these 187 men, 25 were excluded because their

HHHQs were not completed and two were excluded because they reported

eating too many foods daily, leaving 160 cases for analysis.

 

We contacted 202 healthy potential controls by mail. Of these, 148 men

(73.3%) returned the questionnaires. Eleven controls were excluded

because they did not complete the HHHQ and one was excluded for

consuming too many food items per day, leaving 136 healthy controls for

analysis.

 

Because there were multiple cases who would be excluded in the analysis

of matched data because they did not have a friend control, we evaluated

the effect of dissolving the match on our crude and adjusted results. To

do so, we compared the unconditional and conditional logistic regression

point estimates for all cases and controls, regardless of matching.

Because the point estimates in both of these analyses were essentially

the same (data not shown), we presented the results with the matching

dissolved.

 

For descriptive analyses, we tested the differences in the means and

distributions of cases and controls by using Student's t-test and the X2

test.

 

Using unconditional logistic regression modeling, we adjusted for the

potential confounders of age, education, income, ethnicity, history of

cryptorchidism, and total daily caloric intake.

 

Age, years of education, and total daily calories were entered as

continuous variables, income as a scaled variable, and ethnicity and

history of cryptorchidism as categorical variables.

 

The quartile cut points used for dietary intake were based on the

consumption distribution among the controls. Multivariable trend tests

were calculated by entering the dietary component as a scaled variable

in the model. The model building strategy used stepwise backward

elimination, and the models were compared by using the likelihood ratio

test.[13] All significance tests were two-sided and the a was set at

0.05.

 

Results In Table 1 we present selected demographic characteristics for

cases and controls grouped by histopathological type. There were 82 men

diagnosed with nonseminoma tumors, 46 men diagnosed with pure seminomas,

and 32 men diagnosed with mixed germ cell tumors. The ethnic

distribution of men with nonseminoma, seminoma, and mixed germ cell

tumors was generally similar to that of controls.

 

The controls tended to be older, had more education, and had higher

incomes than the cases, although not all these factors were

statistically significant across all histological groups. Although we

tried to match on age, the cases tended to identify friend controls that

were older than themselves. For this reason, in our analyses we

consistently controlled for age as a confounder.

 

History of cryptorchidism was significantly more common in all

histological groups than in the controls. As shown in Table 2, there

were many differences in dietary intake between controls and cases (all

histopathological types combined).

 

The cases had significantly higher daily total energy, total fat,

saturated fat, and meat intake than controls (p == 0.0001, 0.0002,

0.0001, and 0.006, respectively). Although lower in cases than controls,

milk consumption (including whole, 2%, and skim) was not significantly

different. Dietary fiber intake was significantly lower in cases than

controls (p == 0.006), as was fruit consumption (p == 0.05). Consumption

of vegetables and dark green and deep yellow fruits and vegetables was

lower in cases than controls, but the difference was of borderline

statistical significance (p == 0.09 and 0.08, respectively).

 

Dietary intake further varied by the cases' histology. Men diagnosed

with nonseminoma testicular cancer consumed significantly more fats and

meats and significantly less dietary fiber and vegetables than controls.

 

 

The men with seminomas had significantly higher intakes of fats and meat

than controls but fiber, fruits, and vegetable intake similar to

controls. Men diagnosed with mixed germ cell tumors consumed more fats

and less fruit than controls.

 

Multivariable logistic regression analyses of individual dietary

components (comparing lowest with highest quartiles of consumption)

adjusting for age, education, income, ethnicity, cryptorchidism, and

total daily calories.

 

Increasing total fat, saturated fat, meat, and cholesterol consumption

were associated with increasing risk of nonseminoma testicular cancer,

with odds ratios (ORs) of 6.3, 2.3, 5.3, and 4.6 for the highest

quartiles, respectively. An inverse relation was observed for calcium

and dietary fiber intake and nonseminoma cancer risk and no consistent

trend was observed for milk, fruit, vegetable, or dark green and deep

yellow fruit and vegetable consumption.

 

Risk for seminoma testicular cancer increased with increasing intake of

meat and total cholesterol (the ORs for the highest vs. the lowest

quartiles were 3.6 and 3.1, respectively). Increased total and saturated

fat intakes were marginally associated with increased seminoma risk (the

ORs for the highest vs. the lowest quartiles were 1.9 and 2.1,

respectively). Higher total fat consumption was nearly significantly

related to increased mixed germ cell tumor risk (the OR for the highest

vs. the lowest quartile was 4.2).

 

When multivariable regression analysis with backward elimination was

used to assess the independent effects of multiple dietary components,

only saturated fat remained in the model for nonseminoma testicular

cancer (Table 3). In multivariable regression analyses for seminoma and

mixed germ cell tumor risk, the only dietary variables that remained in

each of the models were cholesterol and total fat, respectively (Table

3).

 

Discussion There are few published studies of the relation between diet

and testicular cancer. The results of our case-control analysis provide

evidence that dietary habits, particularly high total fat and saturated

fat intake, may increase risk of testicular cancer.

 

We also found an association with increased meat intake and increased

seminoma risk.

 

This agrees with an investigation in Uruguayan men in which higher red

meat consumption and total fat intake were associated with increased

risk of seminomas.[4]

 

In that study, no associations were observed for nonseminoma tumors, but

the results were based on a limited number of cases (30 seminoma and 28

nonseminoma cancers).[4]

 

We found an inverse association between dietary fiber and testicular

cancer risk that has not been previously reported. Our findings are

weakly supportive of previous studies in which higher intakes of fruits

and vegetables were associated with decreased risk of testicular cancer.

 

 

Gallagher and co-workers[6] conducted a large Canadian population-based

study and reported that green vegetable consumption had a protective

relative risk of 0.5 (95% confidence interval == 0.3-0.9) in the highest

compared with the lowest quartile.

 

In a case-control study in England, Davies and colleagues[5] collected

data on fresh fruit and vegetable consumption in adolescence. Although

cases tended to have eaten fewer oranges, apples, and vegetable and

fruit salads than the population controls, the difference was not

statistically significant.[5] The weak associations found in our study

with fruit and vegetables were not consistent across testicular cancer

histologies in the multivariable analysis, despite reports that these

foods reduce the risk of many cancers (reviewed in Reference 14).

 

We did not find an association between milk intake and testicular cancer

risk, which is in contrast to the results of Davies and colleagues,[5]

who found that for every increased quarter pint of milk consumed per day

during adolescence the relative risk was 1.39 (95% confidence interval ==

1.19-21.9). However, the results of the British study should be viewed

somewhat cautiously, inasmuch as it was unclear whether consumption of

milk itself or some component in the milk (such as saturated fat or

calcium) increased risk. In our study, we found dietary calcium intake

to have a significant inverse dose-response gradient with risk of

nonseminoma testicular cancer.

 

To our knowledge, no other previous study has reported an association

with calcium intake and testicular cancer.

 

 

The association with dietary fat should be interpreted cautiously,

because spurious associations with cancer in case-control studies have

been reported (reviewed in Reference 12). We observed a higher reported

total daily caloric intake in the cases than in the controls. To

possibly explain this, we examined weight, body mass index, and crude

estimators of physical activity (in adolescence, age 20, and adulthood)

and found them to be similar between cases and controls (data not

shown).

 

There has been considerable controversy over whether increased total

caloric intake itself increases cancer risk or whether a dietary

component (such as saturated fat) is the factor that increases risk. For

example, Slattery and co-workers[19] reported that colon cancer risk was

not associated with dietary fat, protein, or carbohydrate intake after

adjustment for total energy intake.

 

Certainly, the finding that caloric restriction in mice reduces the

incidence of sporadic and induced tumors supports the hypothesis that

higher caloric intake increases cancer risk.[20] However, to conclude

that higher saturated fat intake is associated with increased risk of

testicular tumors or to speculate on possible biologic mechanisms would

be premature.

 

Although we report many interesting associations, there are several

limitations in our study. Because cases reported diet for the year

previous to diagnosis and controls reported diet for the previous year,

we were concerned that the discrepancy in reporting years could affect

our results. We therefore introduced a term for year of diagnosis into

the model to evaluate the impact on the point estimates, but that had

little effect.

 

We also split the case group by stratifying on the year of the case's

diagnosis (i.e., 1990-93 and 1994-96) and compared these results with

those of our analysis for all cases and controls combined; again there

were no differences in the point estimates. Of greater concern is the

potential for bias in dietary recall inherent in case-control studies,

although Willett[12] suggests that diet can be adequately recalled for

up to 10 years with acceptable levels of misclassification.

 

In comparisons of prospectively and retrospectively collected diet data,

Wilkens and co-workers[21] reported that fat intakes were overreported

by colon cancer cases compared with controls but not by prostate or

breast cancer cases. However, a prospectively designed study for a rare

tumor (such as testicular cancer) would be inefficient. It is therefore

impossible to determine the extent and direction of recall bias among

the testicular cancer patients and controls, although this remains a

possible explanation for our observations.

 

We used friends of cases as controls, because we thought

population-based controls would not reflect the population from which

the cases arose, despite the problem that friends might be too " similar "

to cases. We do not believe " over-matching " occurred, because our

controls were significantly older and better educated than our cases.

However, this implies that the associations found between diet and

testicular cancer may be spurious because of the inclusion of more

highly educated controls.

 

For example, the more educated controls may be more conscious of fat

intake and methods to reduce dietary fat consumption. Also,

participation in this study was less than ideal, particularly for cases.

The effect of the low response on the associations found with diet is

difficult to predict but remains a concern in this investigation.

 

There were several limitations to our study, but it did reveal specific

dietary components that were associated with testicular cancer risk.

Because high total and saturated fat and meat intakes were found to be

consistently and significantly associated with risk of testicular

cancer, more dietary studies addressing this issue are needed.

 

Cholesterol intake, although likely correlated with meat consumption,

should also be examined. Future research should include an evaluation of

dietary calcium and fiber, inasmuch as we found higher intakes reduced

risk. Clarification of the role of genetic and early life exposures in

the etiology of testicular cancer and the identification of other risk

factors (including diet) could provide further insights into this cancer

that occurs at a relatively young age.

 

Acknowledgments and Notes

 

The authors thank all the men who participated in the study, Dr. Maureen

Goode (Dept. of Scientific Publications, The University of Texas M. D.

Anderson Cancer Center) for editing the manuscript, and Dr. Philip

Beckett (Texas Children's Hospital, Baylor College of Medicine) for

helpful comments. This work was supported by The University of Texas M.

D. Anderson Cancer Center Education Program in Cancer Prevention, which

is supported by National Cancer Institute Grant R25-CA-57730.

 

 

 

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