Wednesday, January 23, 2008

Black breast cancer is different

Leftists have a religious belief that all races are the same except for hair, lips and skin. Why there are no differences other than the visible ones is never explained. And they only admit the visible differences because they cannot be denied. We repeatedly find that the truth is very different, however -- including a quite stark difference noted below:

Black British women in Hackney, East London, are diagnosed with breast cancer 21 years younger than white British women, according to a Cancer Research UK study published online in the British Journal of Cancer. In the first UK study to look at the patterns of breast cancer in black British women, the researchers studied 102 black women and 191 white women diagnosed with breast cancer at Homerton University Hospital in Hackney, East London, between 1994 and 2005. They found the black patients were diagnosed with breast cancer at an average age of 46 while the white patients were diagnosed at an average age of 67.

Researchers based at the Institute of Cancer and Cancer Research UK clinical centre at Barts and the London School of Medicine and Dentistry also found that survival was poorer among black women with smaller tumours. In addition, their initial findings suggest that tumours in the younger black patients were more likely to be aggressive, and a higher proportion of tumours were basal-like - meaning they were less likely to respond to newer types of targeted breast cancer treatments like Herceptin. If these results are confirmed in larger studies, the findings could have implications for diagnosis, screening and treatment of black British breast cancer patients in the future.

Study author Dr Rebecca Bowen, said: "Twenty five per cent of all breast cancer cases diagnosed in London during the period studied were in women aged 45 or younger - but this figure rose to 45 per cent among the black population in Hackney. We think the differences in the way tumours of black and white women behave can be put down to the biological differences between the two ethnic groups. We're now trying to find out why the tumours are so different so that we can develop new treatments to target the aggressive forms of breast cancer seen in young black women."

Until recently, UK cancer registries have not collected ethnicity data routinely, but incidence of breast cancer among black British women is thought to be lower than the white population. American research has suggested that African-American women get breast cancer at a younger age and at a more advanced stage - but this is the first UK study to draw these conclusions.

Dr Bowen added: "We've just received funding for the next stage of our research which will allow us to determine the type of cancers these women are getting at this young age. It's important that we use the information learnt from this study to raise awareness of breast cancer risk factors and the importance of early detection among the black population."

Dr Lesley Walker, Cancer Research UK's director of cancer information, said: "This is very interesting research. The fact that black women are being diagnosed with breast cancer at a much younger age than white women is clearly worrying. If these results are confirmed in follow-up studies, it might be appropriate to alter screening services offered to black women to better reflect the age at which they are diagnosed with breast cancer - but at the moment it's too early to suggest any changes to the screening programme because the study was so small. "These findings highlight the need for all women to be breast aware, report any changes to the doctor promptly and attend screening appointments when invited, as early detection is important for successful treatment."



Early onset of breast cancer in a group of British black women

By RL Bowen et al.

Since there are no published data on breast cancer in British black women, we sought to determine whether, like African-American women, they present at a younger age with biologically distinct disease patterns. The method involved a retrospective review of breast cancer to compare age distributions and clinicopathological features between black women and white women in the UK, while controlling for socioeconomic status. All women presented with invasive breast cancer, between 1994 and 2005, to a single East London hospital.

Black patients presented significantly younger (median age of 46 years), than white patients (median age of 67 years (P=0.001)). No significant differences between black and white population structures were identified. Black women had a higher frequency of grade 3 tumours, lymph node-positive disease, negative oestrogen receptor and progesterone receptor status and basal-like (triple negative status) tumours. There were no differences in stage at presentation; however, for tumours of ~2 cm, black patients had poorer survival than white patients (HR=2.90, 95% CI 0.98-8.60, P=0.05).

Black women presented, on average, 21 years younger than white women. Tumours in younger women were considerably more aggressive in the black population, more likely to be basal-like, and among women with smaller tumours, black women were more than twice as likely to die of their disease. There were no disparities in socioeconomic status or treatment received. Our findings could have major implications for the biology of breast cancer and the detection and treatment of the disease in black women.

British Journal of Cancer 8 January 2008

Study Suggests Nano-sized Ultrafine Particles May Be Most Damaging Component of Air Pollution for Heart Disease

Among genetically modified and badly maltreated mice, anyway. The journal abstract is here

A new study indicates that ultrafine particles-particles of less than 0.18 micrometers-from vehicle emissions may be the most damaging components of air pollution in triggering plaque buildup in the arteries, which can lead to heart attack and stroke. The findings appear in an open access article in the 17 January online edition of the journal Circulation Research.

A team from University of California, Los Angeles (UCLA); the University of Southern California; the University of California, Irvine; and Michigan State University contributed to the research, which was led by Dr. Andre Nel, UCLA's chief of nanomedicine. The study was primarily funded by the National Institute of Environmental Health Sciences and the US Environmental Protection Agency (EPA).

The EPA currently regulates fine particles at 2.5 micrometers, but doesn't monitor particles in the nano- or ultrafine range. These particles are too small to capture in a filter, so new technology must be developed to track their contribution to adverse health effects.

The UCLA research team previously reported that diesel exhaust particles interact with artery-clogging fats in low-density lipoprotein (LDL) cholesterol to activate genes that cause the blood-vessel inflammation that can lead to heart disease. In the current study, researchers exposed mice with high cholesterol to one of two sizes of air pollutant particles from downtown Los Angeles freeway emissions and compared them with mice that received filtered air that contained very few particles. The study, conducted over a five-week period [Five whole weeks!] , required a complex exposure design that was developed by teams led by Dr. Michael Kleinman, professor of community and environmental medicine at UC Irvine, and Dr. Constantinos Sioutas, professor of civil and environmental engineering at USC. Researchers found that mice exposed to ultrafine particles exhibited 55% greater atherosclerotic-plaque development than animals breathing filtered air and 25% greater plaque development than mice exposed to fine-sized particles.

Pollutant particles are coated in chemicals sensitive to free radicals, which cause the cell and tissue oxidation. Oxidation leads to the inflammation that causes clogged arteries. Samples from polluted air revealed that ultrafine particles have a larger concentration of these chemicals and a larger surface area where these chemicals thrive, compared with larger particles, Sioutas noted.

Scientists also identified a key mechanism behind how these air pollutants are able to affect the atherosclerotic process. Using a test developed by Dr. Mohamad Navab, study co-author and a UCLA professor of medicine, researchers found that exposure to air pollutant particles significantly decreased the anti-inflammatory protective properties of HDL cholesterol.

To explore if air particle exposure caused oxidative stress throughout the body-which is an early process triggering the inflammation that causes clogged arteries-researchers checked for an increase in genes that would have been activated to combat this inflammatory progression. They found greater levels of gene activation in mice exposed to ultrafine particles, compared to the other groups. The next step will be to develop a biomarker that could enable physicians to assess the degree of cardiovascular damage caused by air pollutants or measure the level of risk encountered by an exposed person.

Previous studies assessing the cardiovascular impact of air pollution have taken place over longer periods of exposure time, such as five to six months. The current study demonstrated that ill effects can occur more quickly, in just five weeks.

The research team included investigators from the fields of nanomedicine, cardiology and genetics. Additional co-authors included Berenice Barajas, Xuping Wang, Brian J. Bennett and Ke Wei Gong of the David Geffen School of Medicine at UCLA, and Jack Harkema from the department of pathobiology and diagnostic investigation at Michigan State University.



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].

9). And how odd it is that we never hear of the huge American study which showed that women who eat lots of veggies have an INCREASED risk of stomach cancer? So the official recommendation to eat five lots of veggies every day might just be creating lots of cancer for the future! It's as plausible (i.e. not very) as all the other dietary "wisdom" we read about fat etc.

10). And will "this generation of Western children be the first in history to lead shorter lives than their parents did"? This is another anti-fat scare that emanates from a much-cited editorial in a prominent medical journal that said so. Yet this editorial offered no statistical basis for its opinion -- an opinion that flies directly in the face of the available evidence.

Even statistical correlations far stronger than anything found in medical research may disappear if more data is used. A remarkable example from Sociology:
"The modern literature on hate crimes began with a remarkable 1933 book by Arthur Raper titled The Tragedy of Lynching. Raper assembled data on the number of lynchings each year in the South and on the price of an acre's yield of cotton. He calculated the correlation coefficient between the two series at -0.532. In other words, when the economy was doing well, the number of lynchings was lower.... In 2001, Donald Green, Laurence McFalls, and Jennifer Smith published a paper that demolished the alleged connection between economic conditions and lynchings in Raper's data. Raper had the misfortune of stopping his analysis in 1929. After the Great Depression hit, the price of cotton plummeted and economic conditions deteriorated, yet lynchings continued to fall. The correlation disappeared altogether when more years of data were added."
So we must be sure to base our conclusions on ALL the data. But in medical research, data selectivity and the "overlooking" of discordant research findings is epidemic.

"What we should be doing is monitoring children from birth so we can detect any deviations from the norm at an early stage and action can be taken". Who said that? Joe Stalin? Adolf Hitler? Orwell's "Big Brother"? The Spanish Inquisition? Generalissimo Francisco Franco Bahamonde? None of those. It was Dr Colin Waine, chairman of Britain's National Obesity Forum. What a fine fellow!


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