by Trevor Butterworth, Forbes, August 3, 2010 - "When did fun loving, freedom loving, hip, liberal people embrace The Ban as their now favorite implement, surpassing even the Joint and the Bong?" wrote "Scrubpine" some 330 comments into the 800 that greeted news of a new ordinance to ban the sale of pets in San Francisco. But while the rest of the country may laugh or sneer at the Singapore-like mentality of the city's politics, what Ban Francisco proscribes can turn into a federal prescription. What it frets about can eventually spook the nation. New York pet store owners are already worried that the match has been lit on their extinction. The center often fails to hold against a motivated extreme.
This is possibly why CTIA, the wireless association that represents such companies as Apple, AT&T, Motorola, and Verizon is suing the city over its recent "right to know" ordinance mandating retailers publish cellphone specific absorption rates (SAR) at the point of sale.
It's precisely the kind of slow fuse that can lead to a global panic--and just at the point where the mobile Web is set to utterly transform the way we compute. As the trade group statement put it, "displaying a phone's SAR value at the point-of-sale suggests to the consumer that there is a meaningful safety distinction between FCC-compliant devices with different SAR levels." According to CNET, just one phone on the U.S. market, the Motorola V195s comes in at the Federal Communications Commission limit SAR of 1.6 watts/kg.
What this means is that to anyone who isn't an engineer or a physicist, an SAR level will be interpreted as a radiation emission rate, and--wow--radiation is like really dangerous, so the higher the SAR level, the more likely you'll get cancer.
Think I'm underestimating the potential of the public to panic? Then it's time to remind ourselves of Maureen Dowd's slow dance in the New York Times with San Francisco Mayor Gavin Newsom, the dashing Einstein behind the ordinance. Newsom tells her he was alarmed by seeing "all these kids literally glued to their phones." He was alarmed by his pregnant wife using her cellphone. He thought about the soft skull of his baby daughter and how it was so much more at risk from radiation. "So I dusted off some studies and started doing research."
Because we live in a democratizing age of information, where it is increasingly elitist to claim expertise and utterly toxic to self-esteem to suggest that Googling a topic might not make you as knowledgeable as a physicist, Newsom's "research" carried the Board of Supervisors 10 to 1.
As Dowd wrote in the not-so-subtly titled "Are Cells the New Cigarettes?", CTIA's members "should be sending Mayor Newsom a bottle of good California wine for caring about whether kids' brains get fried." Doesn't this prove the CTIA's point? If no one actually knows what SAR levels mean, only the lowest possible SAR level is safe, because the underlying precautionary rhetoric involves drawing an inference about brain damage from a number. To wit, you're kid's brain is frying.
But As Geoffrey Kabat, an epidemiologist at Albert Einstein College of Medicine who is studying the numbers behind the cellphone panic points out, a key problem is with the way they're being interpreted:
"The frequency of the energy used in cellphone technology is so low--according to physicist Robert Park of the University of Maryland, approximately 1 million times lower than that which could damage DNA by ionization--that there is no known mechanism by which it could induce or promote cancer. But the epidemiologists who study cellphone use and the occurrence of brain tumors rarely make this point, thereby allowing journalists and others to confuse the radio frequency energy from cellphones with ionizing radiation, such as X-rays and gamma rays, which we know can cause cancer."
Kabat, who wrote Hyping Health Risks--a fascinating and detailed examination of how we fell for certain, illusory environmental hazards--is possibly the only epidemiologist in the world to have also published a book on Dostoyevsky (he got a Ph.D in Russian and comparative literature from Columbia before switching tracks). And the background in literary analysis and theory adds a crucial ability to explain why we, as a society, are prone to turning hypothetical risks into "social facts." The upshot is that most public alarms about health risks dispense with the tools required to make sense of the alarm--and we end up with "disembodied findings" and ideology.
As Dowd notes in a key moment of ideological self-revelation, "We don't yet really know the physical and psychological impact of being slaves to technology." But, apparently, we do know that we are "slaves." And the sublimated rage of a journalist whose profession is being eviscerated by the machine--a master of information who is now a servant--is possibly not a state of mind receptive to the kind of thought that produced the machine and legitimated its use.
As mobile devices are set to displace the desktop computing world, becoming life devices, it's no wonder CTIA is marshaling the lawyers. The numbers signal a culture war.
Trevor Butterworth is the editor of stats.org, an affiliate of George Mason University that looks at how numbers are used in public policy and the media. He writes a weekly column for Forbes.
July 9, 2009 — (BRONX, NY) — Elevated insulin levels in the blood appear to raise the risk of breast cancer in postmenopausal women, according to researchers at Albert Einstein College of Medicine of Yeshiva University. Their findings are published in the online version of the International Journal of Cancer.
Increased breast cancer risk for postmenopausal women has previously been linked to obesity and diabetes. Both conditions involve insulin resistance, which causes increases in circulating levels of insulin. Since insulin is known to promote cell division and enhance breast tumor growth in animal models, the Einstein scientists reasoned that relatively high insulin levels may contribute to breast cancer risk in women.
"Up to now, only a few studies have directly investigated whether insulin levels are associated with breast cancer risk, and those studies have yielded conflicting results," says Geoffrey Kabat, Ph.D., senior epidemiologist in the department of epidemiology and population health at Einstein and the lead author of the paper. "Those other studies were based on just a single baseline measurement of insulin, while our study involved analyzing repeated measurements of insulin taken over several years — which provides a more accurate picture of the possible association between insulin levels and breast cancer risk."
An earlier study linking insulin levels with breast cancer risk was carried out by Einstein researchers and was published in the January 7, 2009 issue of the Journal of the National Cancer Institute.
In the most recent study, Dr. Kabat and his colleagues analyzed data on 5,450 women enrolled in the Women's Health Initiative, a large multi-center study investigating the influence of a number of factors on women's health. Most of the women had participated in the clinical trial portion of the study and provided fasting blood samples at the start of the study (i.e., at baseline) and then at years one, three and six. The remaining women, who were enrolled in a separate "observational" component of the study, provided fasting blood samples at baseline and at year three of the study. Among all these women, 190 cases of breast cancer were identified over eight years of follow-up.
The analysis by Dr. Kabat and colleagues revealed a strong association between elevated insulin levels and increased risk for breast cancer.
After dividing the participants into three groups based on their insulin levels, the researchers found that women in the upper third for insulin level were more than twice as likely to develop breast cancer compared with women in bottom third for insulin level. The association between insulin level and breast cancer risk was even stronger for those women who had not received treatment in the clinical trial (i.e., the placebo participants) or were in the observational component: women in the upper third for insulin level had a more than three-fold increased risk for breast cancer compared with those in the bottom third.
Notably, the link between elevated insulin level and breast cancer was strongest among lean women and weakest among obese women (who, in general, have higher insulin levels compared with lean women). "This finding is potentially important because it indicates that, in postmenopausal women, insulin may be a risk factor for breast cancer that is independent of obesity," says Dr. Kabat. However, because the number of lean women was small, this finding is preliminary.
While these results require confirmation from other studies, Dr. Kabat notes that the current recommendations for reducing breast cancer risk in postmenopausal women — including maintaining a healthy weight and engaging in regular physical exercise — can help to reduce insulin levels.
The paper is entitled, "Repeated measures of serum glucose and insulin in relation to postmenopausal breast cancer". In addition to Dr. Kabat, other Einstein scientists involved in the study were Mimi Kim, Sc.D., Marc J. Gunter, Ph.D., Gloria Y.F. Ho, Ph.D., Howard D. Strickler, M.D., and Thomas E. Rohan, M.D., Ph.D., senior author of the study and chairman of the department of epidemiology & population health at Einstein.
June 30, 2009
PHILADELPHIA - Physiological changes associated with the metabolic syndrome may play a role in the risk of postmenopausal breast cancer, according to study results published in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.
The metabolic syndrome, or insulin resistance syndrome, consists of a constellation of factors including abdominal obesity, high blood glucose levels, impaired glucose tolerance, abnormal lipid levels and high blood pressure.
Affecting roughly 47 million Americans, the metabolic syndrome is also associated with poor diet and lack of physical activity. It can also increase the risk for diabetes and heart disease.
The metabolic syndrome is characterized by elevated insulin levels, and in recent years scientists have proposed that insulin may contribute directly or indirectly to the development of breast cancer. Researchers suspect that the metabolic syndrome could influence the risk for breast cancer by affecting interrelated hormones, such as insulin, estrogen, cytokines and growth factors.
"This study suggests that having the metabolic syndrome itself or some of its components may increase a woman's risk of postmenopausal breast cancer. However, much more work is needed to understand the role of these metabolic factors and their interplay with better established breast cancer risk factors, such as reproductive and hormonal factors," said researcher Geoffrey C. Kabat, Ph.D., senior epidemiologist in the department of epidemiology and population health at Albert Einstein College of Medicine, New York.
Studies to date have evaluated individual components of the metabolic syndrome and breast cancer, with inconsistent results, according to Kabat. For the first time, Kabat and colleagues assessed whether women who met the criteria of having the metabolic syndrome were at greater risk for postmenopausal breast cancer.
In this longitudinal study, the researchers used existing data from the Women's Health Initiative - a large, national study designed to assess major causes of chronic disease in women. Participants included postmenopausal women aged 50 to 79 years at enrollment who had repeated measurements of components of metabolic syndrome over an eight-year period. These included blood levels of glucose, HDL-cholesterol and triglycerides, as well as waist girth and blood pressure.
Results showed a modest positive association of having the metabolic syndrome as a whole, according to Kabat. Of the 4,888 women with baseline measurements who did not have diabetes, 165 incident cases of breast cancer were diagnosed during the follow-up period. Presence of the metabolic syndrome at baseline was not associated with breast cancer risk.
However, in analyses that made use of the repeated measurements, "women who had the metabolic syndrome during the three to five years prior to breast cancer diagnosis had roughly a doubling of risk," he said.
Findings also showed significant associations with elevated blood glucose levels, triglycerides and diastolic blood pressure. For diastolic blood pressure, the result was stronger, with more than a two-fold increased risk (relative risk = 2.4). Generally, for both triglycerides and glucose the relative risk was about 1.7 for all breast cancer.
"We know a great deal about breast cancer, but we can't identify who is likely to get it. The effect of different variables associated with increased glucose and insulin levels needs to be evaluated further in larger studies," Kabat said. "We need to deepen our understanding of these different interrelated behaviors and physiological factors to see how they affect breast cancer."
Tim Byers, M.D., M.P.H., associate dean of the Colorado School of Public Health and interim director of the University of Colorado Cancer Center, believes these findings are important because the results show possible mechanisms that might explain the observation that increased weight is a risk factor for postmenopausal breast cancer.
"We have assumed that the relationship between weight and breast cancer risk is due to increased circulating estrogens among postmenopausal women who are overweight or obese," he said. "An alternative explanation is explored here: that some other aspect of the metabolic syndrome might be involved, such as growth-stimulating effects of insulin, or insulin-like growth factors."
Based on the results of this study, Byers stated that researchers now need to look more closely at dynamic changes in insulin over time, in factors tied to inflammation, and in the specific ways in which estrogen metabolism is tied to features of the metabolic syndrome.
"Though estrogens are produced in adipose tissues, just how these are metabolized in various subgroups of women needs better study," he said. "In addition, the hyper-inflammatory state of obesity and the metabolic syndrome need to be better described relative to cancer risk."
May 28, 2009 — (BRONX, NY) — Eating red or white meat, including meat cooked at high temperatures, does not increase the risk of breast cancer in postmenopausal women, according to a large study conducted by researchers at Albert Einstein College of Medicine of Yeshiva University. The study was published this month in the International Journal of Cancer.
A number of previous studies have found that eating red meat or meat cooked at high temperatures increases the risk of breast cancer. (High temperatures — caused by grilling, barbecuing or pan-frying — produce high amounts of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) in meat; HCAs and PAHs are mutagens (chemicals capable of causing mutations in DNA) that can cause breast tumors in laboratory animals.)
But a link between meat in the diet and breast cancer in women hasn't been established. "Previous epidemiologic studies in humans looking at the amount of meat in the diet and estimated intakes of HCAs and PAHs in relation to breast cancer risk have yielded inconsistent results," says lead author Geoffrey C. Kabat, Ph.D., M.S., senior epidemiologist in the department of epidemiology and population health at Einstein.
To clarify this issue, Dr. Kabat and his colleagues analyzed data on 120,755 postmenopausal women who participated in the NIH-AARP Diet and Health Study, a collaboration between the National Institutes of Health and American Association of Retired Persons. When the women enrolled in the study (between 1995 and 1996), they gave detailed information on what types of food they ate and how often they ate certain foods. In addition, they provided information on meat-preparation methods.
Over the next eight years, approximately three percent, or 3,818, of the women developed breast cancer. The researchers found no evidence that the amount of meat consumed, meat-cooking methods used, or meat-mutagen intake was associated with an increased risk for breast cancer. Reported meat intake included steak, hamburger, chicken, pork, processed meat and meat cooked at high temperatures.
The study also found that consumption of meat or meat cooked at high temperatures, through grilling and oven-broiling, did not increase breast cancer rates in subgroups including obese women, those who did not have children, who were consumers of alcohol, who were smokers, who used menopausal hormone therapy, who had low levels of physical activity, or had a low intake of fruits or vegetables.
Neither the current study nor earlier studies assessed the diets of younger women. "So we haven't ruled out the possibility that eating meat and exposure to meat mutagens at a younger age — particularly during adolescence when the breasts are developing — may increase one's risk of breast cancer," says Dr. Kabat.
The study, "Meat intake and meat preparation in relation to risk of postmenopausal breast cancer in the NIH-AARP diet and health study," appeared in the May 15, 2009 issue of the International Journal of Cancer. Study co-authors include Amanda J. Cross, Yikyung Park, Arthur Schatzkin, and Rashmi Sinha of the National Cancer Institute; Albert R. Hollenbeck, of AARP; and Thomas E. Rohan, Chairman, Department of Epidemiology & Population Health at Einstein.
Reuters –8/19/2008 Smokers who carry more weight around their waistlines may be at greater risk of lung cancer, according to a new study.
The finding, along with the fact that lung cancer risk is actually higher among leaner smokers, provides “intriguing” evidence that how a smoker stores fat could play a role in his or her likelihood of developing lung cancer, Dr. Geoffrey C. Kabat of the Albert Einstein College of Medicine in the Bronx, New York, told Reuters Health.
Several studies have found that a lower body mass index (BMI) means a higher lung cancer risk among smokers. “Reflex explanations” for the link include the fact that smokers are skinnier than non-smokers, Kabat noted in an interview, as well as the tendency for people to gain weight after they quit smoking.
Another proposed mechanism for the relationship is that people lose weight when they develop lung cancer.
But careful analysis of the data doesn’t bear out these explanations, Kabat said. To better understand the relationship, he and his colleagues looked at data from the Women’s Health Initiative.
Over the course of 8 years, 1,365 of the study’s 161,809 participants developed lung cancer. When the researchers looked at BMI after adjusting for weight circumference, they found that both smokers and ex-smokers with lower BMIs had a greater lung cancer risk.
But when they looked at waist circumference independent of BMI, they found that a larger waistline conferred a greater likelihood of lung cancer for smokers and ex-smokers. There was no relationship between BMI or waist circumference and lung cancer risk among never-smokers.
The findings, reported in the American Journal of Epidemiology, must be confirmed by other investigators, and don’t offer any clues on the mechanism behind the relationship, Kabat noted.
However, he speculated, “it may have to do with the storage, the mobilization, and the metabolization of carcinogens. These carcinogens … tend to be stored in fat tissue. That may play a role in the development of lung cancer. It may be that it’s linked to smoking but that it plays a role on top of smoking.”
He added: “We’re not ready to give people advice, because overall the advice would not be changed. We’re not advocating that people lose weight so that they have a lower risk of lung cancer. Smoking is so far and away the dominant risk factor.”