DOES GAINING WEIGHT GIVE WOMEN BREAST CANCER?

There are many articles just out which say that it does (e.g. here). They are all based on the study abstracted below. What the study in fact shows is that old ladies who say that they were once slim have more breast cancer. A rather different story, What? There is no objective data about fat in the article at all. Any interpretation is mere speculation. The fact that fat women overall get LESS breast cancer is glided over. If we were to take the findings below seriously, I think we would have to say to women: "Get fat while young to avoid breast cancer"! Excuse me while I laugh!

Adiposity, Adult Weight Change, and Postmenopausal Breast Cancer Risk

By Jiyoung Ahn et al.

Background: Obesity is a risk factor for postmenopausal breast cancer, but the role of the timing and amount of adult weight change in breast cancer risk is unclear.

Methods: We prospectively examined the relations of adiposity and adult weight change to breast cancer risk among 99 039 postmenopausal women in the National Institutes of Health-AARP Diet and Health Study. Anthropometry was assessed by self-report in 1996. Through 2000, 2111 incident breast cancer cases were ascertained.

Results: Current body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared), BMI at ages 50 and 35 years, and waist-hip ratio were associated with increased breast cancer risk, particularly in women not using menopausal hormone therapy (MHT). Weight gained between age 18 years and the current age, between ages 18 and 35 years, between ages 35 and 50 years, and between age 50 years and the current age was consistently associated with increased breast cancer risk in MHT nonusers (relative risk [RR], 2.15; 95% confidence interval [CI], 1.35-3.42 for a ~ 50-kg weight gain between age 18 years and the current age vs stable weight) but not in current MHT users. Risk associated with adult weight change was stronger in women with later vs earlier age at menarche (RR, 4.20; 95% CI, 2.05-8.64 for ~15 years vs RR, 1.51; 95% CI, 1.11-2.06 for 11-12 years; P = .007 for interaction). In MHT nonusers, the associations with current BMI and adult weight change were stronger for advanced disease than for nonadvanced disease (P = .009 [current BMI] and .21 [weight gain] for heterogeneity) and were stronger for hormone receptor-positive than hormone receptor-negative tumors (P < .001 for heterogeneity).

Conclusion: Weight gain throughout adulthood is associated with increased postmenopausal breast cancer risk in MHT nonusers.

Arch Intern Med. 2007;167:2091-2102




AN ASPIRIN THEORY BITES THE DUST

Cochrane review abstract below. It was another great theory but reality is pesky, as it often is

Low-dose aspirin for in vitro fertilisation

By VJ Poustie et al

Background: Low-dose aspirin is sometimes used to improve the outcome in women undergoing in vitro fertilisation, despite inconsistent evidence of efficacy and the potential risk of significant side affects. The most appropriate time to commence aspirin therapy and length of treatment required is also still to be determined.

Objectives: To determine the effectiveness of low-dose aspirin for improving the outcome of in vitro fertilisation and intracytoplasmic sperm injection treatment cycles.

Search strategy: We searched the Cochrane Menstrual Disorders and Subfertility Group Trials Register, Cochrane Central Register of Controlled Trials (April 2007), MEDLINE (1966 to March 2007) and EMBASE (1980 to March 2007) databases using the following research terms: "(aspirin OR acetylsalicylic acid) AND (in-vitro fertilisation OR intracytoplasmic sperm injection)" combined with the Cochrane Menstrual Disorders and Subfertility Group's search strategy for identifying randomised controlled trials for reports which appeared to describe randomised controlled trials of low-dose aspirin for women undergoing in vitro fertilisation.

Selection criteria: Prospective randomised controlled trials, published or unpublished, which addressed the objectives of the review. Quasi-randomised trials were excluded.

Data collection and analysis: Two authors independently selected studies to include in the review, extracted data and assessed trial quality.

Main results: The searches identified nine trials which were eligible for inclusion in the review, including a total of 1449 participants. No significant differences were found between the treatment and control groups for any of the outcomes assessed. Only two studies (involving 401 participants) investigated the effect of low-dose aspirin on live birth rate, and no significant difference was found between the treatment and control groups (RR 0.94, 95% CI 0.63 to 1.39). No significant difference was found in clinical pregnancy rate between treatment and control groups, based on results from 1240 participants in seven studies (RR 1.09, 95% CI 0.83 to 1.43). No data were reported on adverse events related to aspirin treatment in any of the included studies.

Authors' conclusions: Use of low-dose aspirin for women undergoing in vitro fertilisation cannot currently be recommended due to lack of adequate trial data. There is a need for randomised controlled trials investigating the use of low-dose aspirin for different patient groups undergoing in vitro fertilisation. We used control group data from the largest trial included in this review to determine that a sample size of 350 women in each group would be required in order to demonstrate a 10% improvement from the use of aspirin with 80% power at the 5% significance level. Until evidence from appropriately powered trials is available, this treatment can not be recommended.

Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD004832

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Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

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