Mon Jun 30, 2008 11:17am EDT
By Maggie Fox, Health and Science Editor
WASHINGTON (Reuters) - A drug developed using nanotechnology and a fungus that contaminated a lab experiment may be broadly effective against a range of cancers, U.S. researchers reported on Sunday.
The drug, called lodamin, was improved in one of the last experiments overseen by Dr. Judah Folkman, a cancer researcher who died in January. Folkman pioneered the idea of angiogenesis therapy -- starving tumors by preventing them from growing blood supplies.
Lodamin is an angiogenesis inhibitor that Folkman's team has been working to perfect for 20 years. Writing in the journal Nature Biotechnology, his colleagues say they developed a formulation that works as a pill, without side-effects.
They have licensed it to SynDevRx, Inc, a privately held Cambridge, Massachusetts biotechnology company that has recruited several prominent cancer experts to its board.
Tests in mice showed it worked against a range of tumors, including breast cancer, neuroblastoma, ovarian cancer, prostate cancer, brain tumors known as glioblastomas and uterine tumors.
It helped stop so-called primary tumors and also prevented their spread, Ofra Benny of Children's Hospital Boston and Harvard Medical School and colleagues reported.
"Using the oral route of administration, it first reaches the liver, making it especially efficient in preventing the development of liver metastasis in mice," they wrote in their report. "Liver metastasis is very common in many tumor types and is often associated with a poor prognosis and survival rate," they added.
'ALMOST CLEAN' LIVERS
"When I looked at the livers of the mice, the treated group was almost clean," Benny said in a statement. "In the control group you couldn't recognize the livers -- they were a mass of tumors."
The drug was known experimentally as TNP-470, and was originally isolated from a fungus called Aspergillus fumigatus fresenius.
Harvards's Donald Ingber discovered the fungus by accident while trying to grow endothelial cells -- the cells that line blood vessels. The mold affected the cells in a way known to prevent the growth of tiny blood vessels known as capillaries.
Ingber and Folkman developed TNP-470 with the help of Takeda Chemical Industries in Japan in 1990.
But the drug affected the brain, causing depression, dizziness and other side-effects. It also did not stay in the body long and required constant infusions. The lab dropped it.
Efforts to improve it did not work well. Then Benny and colleagues tried nanotechnology, attaching two "pom-pom"-shaped polymers to TNP-470, protecting it from stomach acid.
In mice, the altered drug, now named lodamin, went straight to tumor cells and helped suppress melanoma and lung cancer, with no apparent side effects, Benny said.
All untreated mice had fluid in the abdominal cavity, and enlarged livers covered with tumors. Mice treated with lodamin had normal-looking livers and spleens, the researchers said.
Twenty days after being injected with cancer cells, four out of seven untreated mice had died, while all treated mice were still alive, Benny's team reported.
"I had never expected such a strong effect on these aggressive tumor models," she said. The researchers believe lodamin may also be useful in other diseases marked by abnormal blood vessel growth, such as age-related macular degeneration.
(Editing by Todd Eastham)
Monday, June 30, 2008
Tuesday, June 10, 2008
Smoking causes middle-age mental decline
Lighting up affects mind as well as body, new study shows
updated 4:38 p.m. ET, Mon., June. 9, 2008
CHICAGO - Middle-aged adults who smoke tended to perform poorly on tests of memory and reasoning compared to nonsmokers, adding to the list of reasons not to smoke, French researchers said on Monday.
Analyzing previously collected data on about 5,000 British civil servants, the researchers found those who smoked were more likely than people who never smoked to be in the lowest-performing of five groups in tests of memory, reasoning, vocabulary and verbal fluency.
Smoking was associated with mental decline in middle age, as it is with dementia and a host of physical ills later in life, they found.
"Smoking in middle age is associated with memory deficit and decline in reasoning abilities," concluded Severine Sabia and colleagues from the National Institute of Health and Medical Research in Villejuif, France.
Compared to smokers, people who said they had quit cigarettes were more likely to adopt healthier behaviors, such as drinking less alcohol, being more physically active, and eating more fruits and vegetables, Sabia reported in the journal Archives of Internal Medicine.
The participants were aged 35 to 55 at the beginning of the study, which followed some subjects up to 17 years.
The study also demonstrated how difficult it can be to conduct long-term research on smokers: more than twice as many smokers as non-smokers refused to take the memory test again or were not able to be re-tested, in some cases because they died in the interim.
Copyright 2008 Reuters.
updated 4:38 p.m. ET, Mon., June. 9, 2008
CHICAGO - Middle-aged adults who smoke tended to perform poorly on tests of memory and reasoning compared to nonsmokers, adding to the list of reasons not to smoke, French researchers said on Monday.
Analyzing previously collected data on about 5,000 British civil servants, the researchers found those who smoked were more likely than people who never smoked to be in the lowest-performing of five groups in tests of memory, reasoning, vocabulary and verbal fluency.
Smoking was associated with mental decline in middle age, as it is with dementia and a host of physical ills later in life, they found.
"Smoking in middle age is associated with memory deficit and decline in reasoning abilities," concluded Severine Sabia and colleagues from the National Institute of Health and Medical Research in Villejuif, France.
Compared to smokers, people who said they had quit cigarettes were more likely to adopt healthier behaviors, such as drinking less alcohol, being more physically active, and eating more fruits and vegetables, Sabia reported in the journal Archives of Internal Medicine.
The participants were aged 35 to 55 at the beginning of the study, which followed some subjects up to 17 years.
The study also demonstrated how difficult it can be to conduct long-term research on smokers: more than twice as many smokers as non-smokers refused to take the memory test again or were not able to be re-tested, in some cases because they died in the interim.
Copyright 2008 Reuters.
Tuesday, June 3, 2008
Antibacterial wipes can spread superbugs: study
Tue Jun 3, 2008 1:11pm EDT
By Michael Kahn
LONDON (Reuters) - Disinfectant wipes routinely used in hospitals may actually spread drug-resistant bacteria rather than kill the dangerous infections, British researchers said on Tuesday.
While the wipes killed some bacteria, a study of two hospitals showed they did not get them all and could transfer the so-called superbugs to other surfaces, Gareth Williams, a microbiologist at Cardiff University, said.
The findings presented at the American Society of Microbiology's General Meeting in Boston focused on bacteria that included methicillin-resistant Staphylococcus aureus, or MRSA.
"What we have found is there is a high risk," Williams, who led the study, said by telephone. "We need to give guidance to the staff on how to use the wipes because we found there is a possibility of cross transfer."
MRSA infections can range from boils to more severe infections of the bloodstream, lungs and surgical sites. Most cases are associated with hospitals, nursing homes or other health care facilities.
The superbug can cause life-threatening and disfiguring infections and can often only be treated with expensive, intravenous antibiotics.
Experts have been saying for years that poor hospital practices spread dangerous bacteria, and yet many studies have shown that health care workers, including doctors and nurses, often fail to even wash their hands as directed.
The findings from a study of intensive care units at two Welsh hospitals suggest that even cleaning with antimicrobial wipes may not be enough depending on how staff use them.
The researchers found that many health care workers cleaned multiple surfaces near patients, such as bed rails, monitors and tables with a single wipe and risked sweeping the infections around rather than cleaning them up.
"We found that the most effective way to prevent the risk of MRSA spread in hospital wards is to ensure the wipe is used only once on one surface," Williams said.
By Michael Kahn
LONDON (Reuters) - Disinfectant wipes routinely used in hospitals may actually spread drug-resistant bacteria rather than kill the dangerous infections, British researchers said on Tuesday.
While the wipes killed some bacteria, a study of two hospitals showed they did not get them all and could transfer the so-called superbugs to other surfaces, Gareth Williams, a microbiologist at Cardiff University, said.
The findings presented at the American Society of Microbiology's General Meeting in Boston focused on bacteria that included methicillin-resistant Staphylococcus aureus, or MRSA.
"What we have found is there is a high risk," Williams, who led the study, said by telephone. "We need to give guidance to the staff on how to use the wipes because we found there is a possibility of cross transfer."
MRSA infections can range from boils to more severe infections of the bloodstream, lungs and surgical sites. Most cases are associated with hospitals, nursing homes or other health care facilities.
The superbug can cause life-threatening and disfiguring infections and can often only be treated with expensive, intravenous antibiotics.
Experts have been saying for years that poor hospital practices spread dangerous bacteria, and yet many studies have shown that health care workers, including doctors and nurses, often fail to even wash their hands as directed.
The findings from a study of intensive care units at two Welsh hospitals suggest that even cleaning with antimicrobial wipes may not be enough depending on how staff use them.
The researchers found that many health care workers cleaned multiple surfaces near patients, such as bed rails, monitors and tables with a single wipe and risked sweeping the infections around rather than cleaning them up.
"We found that the most effective way to prevent the risk of MRSA spread in hospital wards is to ensure the wipe is used only once on one surface," Williams said.
Celebrex Shows Promise in Lung Cancer Prevention
By Julie Steenhuysen
Reuters
CHICAGO
A high dose of the arthritis drug Celebrex showed early signs that it may help prevent lung cancer in heavy smokers, U.S. researchers said on Sunday.
The Pfizer Inc drug, also known as celecoxib, works by blocking the COX-2 enzyme that causes inflammation, which has been linked with cancer.
A six-month study of 212 current or heavy smokers found a reduction in a specific type of precancerous change in lung cells in people who took a high dose of Celebrex compared with those who took a placebo.
None of the study participants had any heart-related problems such as those with Merck & Co Inc's now withdrawn arthritis drug Vioxx, another COX-2 inhibitor.
"Celebrex was safe and we did not see any cardiovascular events," said Dr. Edward Kim of M.D. Anderson Cancer Center in Houston, who presented his findings at a meeting of the American Society of Clinical Oncology in Chicago.
He said the study suggests that a high dose of Celebrex might alter some of the cellular changes that lead up to lung cancer. But the finding is very early and would need to be confirmed in longer, larger studies.
"This is not a study where we go tell someone who is a heavy smoker to start taking Celebrex to prevent lung cancer," Kim said in an interview.
Lung cancer is the leading cause of cancer death in the United States, according to the American Cancer Society. In 2008, about 215,000 people will be diagnosed with lung cancer and about 114,000 people will die from it.
The study was started before news emerged in September 2004 that Vioxx doubled the risk of heart attack and stroke in certain patients.
Kim said the trial was put on hold in December 2004 at the request of Pfizer and the National Cancer Institute, which funded the trial, so the researchers could look for signs of heart attacks or strokes.
It was started up again in May 2005 after the researchers added safeguards, including consultations with cardiologists, to reduce heart risks.
EARLY SIGNS
Rather than a direct measure of cancer prevention, which could take many years, Kim said the researchers were looking for early changes in the body that might suggest the drug could reduce the chances of developing lung cancer.
Two large, long-running lung cancer prevention studies of beta-carotene and vitamin A supplements found they actually increased the risk of lung cancer.
"We have not had positive results with these studies. Now we would like to search for an intermediate endpoint or biomarker," Kim said at a media briefing.
"Perhaps that will lead us in the direction of who we need to target in the future," he said.
The researchers tested Celebrex in the study because studies in cells, mice and in people have shown the COX-2 enzyme is present at higher than normal levels in lung cancer and in precancerous lesions of the lung, Kim said. COX-2 is thought to play a role in the development of blood vessels that feed tumors.
Kim's study measured levels of the Ki-67 protein, a marker for cell growth. The researchers wanted to see if Celebrex had an impact on levels of this protein in tissue samples taken from the lungs of heavy smokers.
At the beginning of the study, the researchers took lung samples from six predetermined areas of the lung.
People in the study either got a 200 milligram or a 400 milligram dose of Celebrex twice a day, or a placebo.
After three months, they took more lung samples, and they took samples again at six months. Kim said the group that got the higher dose of Celebrex saw a reduction in levels of the Ki-67 protein.
Kim said it will be important to find better ways of identifying people who are at the highest risk for lung cancer for whom the benefits of taking a high-dose COX-2 inhibitor would outweigh any potential heart risks.
Reuters
CHICAGO
A high dose of the arthritis drug Celebrex showed early signs that it may help prevent lung cancer in heavy smokers, U.S. researchers said on Sunday.
The Pfizer Inc drug, also known as celecoxib, works by blocking the COX-2 enzyme that causes inflammation, which has been linked with cancer.
A six-month study of 212 current or heavy smokers found a reduction in a specific type of precancerous change in lung cells in people who took a high dose of Celebrex compared with those who took a placebo.
None of the study participants had any heart-related problems such as those with Merck & Co Inc's now withdrawn arthritis drug Vioxx, another COX-2 inhibitor.
"Celebrex was safe and we did not see any cardiovascular events," said Dr. Edward Kim of M.D. Anderson Cancer Center in Houston, who presented his findings at a meeting of the American Society of Clinical Oncology in Chicago.
He said the study suggests that a high dose of Celebrex might alter some of the cellular changes that lead up to lung cancer. But the finding is very early and would need to be confirmed in longer, larger studies.
"This is not a study where we go tell someone who is a heavy smoker to start taking Celebrex to prevent lung cancer," Kim said in an interview.
Lung cancer is the leading cause of cancer death in the United States, according to the American Cancer Society. In 2008, about 215,000 people will be diagnosed with lung cancer and about 114,000 people will die from it.
The study was started before news emerged in September 2004 that Vioxx doubled the risk of heart attack and stroke in certain patients.
Kim said the trial was put on hold in December 2004 at the request of Pfizer and the National Cancer Institute, which funded the trial, so the researchers could look for signs of heart attacks or strokes.
It was started up again in May 2005 after the researchers added safeguards, including consultations with cardiologists, to reduce heart risks.
EARLY SIGNS
Rather than a direct measure of cancer prevention, which could take many years, Kim said the researchers were looking for early changes in the body that might suggest the drug could reduce the chances of developing lung cancer.
Two large, long-running lung cancer prevention studies of beta-carotene and vitamin A supplements found they actually increased the risk of lung cancer.
"We have not had positive results with these studies. Now we would like to search for an intermediate endpoint or biomarker," Kim said at a media briefing.
"Perhaps that will lead us in the direction of who we need to target in the future," he said.
The researchers tested Celebrex in the study because studies in cells, mice and in people have shown the COX-2 enzyme is present at higher than normal levels in lung cancer and in precancerous lesions of the lung, Kim said. COX-2 is thought to play a role in the development of blood vessels that feed tumors.
Kim's study measured levels of the Ki-67 protein, a marker for cell growth. The researchers wanted to see if Celebrex had an impact on levels of this protein in tissue samples taken from the lungs of heavy smokers.
At the beginning of the study, the researchers took lung samples from six predetermined areas of the lung.
People in the study either got a 200 milligram or a 400 milligram dose of Celebrex twice a day, or a placebo.
After three months, they took more lung samples, and they took samples again at six months. Kim said the group that got the higher dose of Celebrex saw a reduction in levels of the Ki-67 protein.
Kim said it will be important to find better ways of identifying people who are at the highest risk for lung cancer for whom the benefits of taking a high-dose COX-2 inhibitor would outweigh any potential heart risks.
Celebrex Shows Promise in Lung Cancer Prevention
By Julie Steenhuysen
Reuters
CHICAGO
A high dose of the arthritis drug Celebrex showed early signs that it may help prevent lung cancer in heavy smokers, U.S. researchers said on Sunday.
The Pfizer Inc drug, also known as celecoxib, works by blocking the COX-2 enzyme that causes inflammation, which has been linked with cancer.
A six-month study of 212 current or heavy smokers found a reduction in a specific type of precancerous change in lung cells in people who took a high dose of Celebrex compared with those who took a placebo.
None of the study participants had any heart-related problems such as those with Merck & Co Inc's now withdrawn arthritis drug Vioxx, another COX-2 inhibitor.
"Celebrex was safe and we did not see any cardiovascular events," said Dr. Edward Kim of M.D. Anderson Cancer Center in Houston, who presented his findings at a meeting of the American Society of Clinical Oncology in Chicago.
He said the study suggests that a high dose of Celebrex might alter some of the cellular changes that lead up to lung cancer. But the finding is very early and would need to be confirmed in longer, larger studies.
"This is not a study where we go tell someone who is a heavy smoker to start taking Celebrex to prevent lung cancer," Kim said in an interview.
Lung cancer is the leading cause of cancer death in the United States, according to the American Cancer Society. In 2008, about 215,000 people will be diagnosed with lung cancer and about 114,000 people will die from it.
The study was started before news emerged in September 2004 that Vioxx doubled the risk of heart attack and stroke in certain patients.
Kim said the trial was put on hold in December 2004 at the request of Pfizer and the National Cancer Institute, which funded the trial, so the researchers could look for signs of heart attacks or strokes.
It was started up again in May 2005 after the researchers added safeguards, including consultations with cardiologists, to reduce heart risks.
EARLY SIGNS
Rather than a direct measure of cancer prevention, which could take many years, Kim said the researchers were looking for early changes in the body that might suggest the drug could reduce the chances of developing lung cancer.
Two large, long-running lung cancer prevention studies of beta-carotene and vitamin A supplements found they actually increased the risk of lung cancer.
"We have not had positive results with these studies. Now we would like to search for an intermediate endpoint or biomarker," Kim said at a media briefing.
"Perhaps that will lead us in the direction of who we need to target in the future," he said.
The researchers tested Celebrex in the study because studies in cells, mice and in people have shown the COX-2 enzyme is present at higher than normal levels in lung cancer and in precancerous lesions of the lung, Kim said. COX-2 is thought to play a role in the development of blood vessels that feed tumors.
Kim's study measured levels of the Ki-67 protein, a marker for cell growth. The researchers wanted to see if Celebrex had an impact on levels of this protein in tissue samples taken from the lungs of heavy smokers.
At the beginning of the study, the researchers took lung samples from six predetermined areas of the lung.
People in the study either got a 200 milligram or a 400 milligram dose of Celebrex twice a day, or a placebo.
After three months, they took more lung samples, and they took samples again at six months. Kim said the group that got the higher dose of Celebrex saw a reduction in levels of the Ki-67 protein.
Kim said it will be important to find better ways of identifying people who are at the highest risk for lung cancer for whom the benefits of taking a high-dose COX-2 inhibitor would outweigh any potential heart risks.
Reuters
CHICAGO
A high dose of the arthritis drug Celebrex showed early signs that it may help prevent lung cancer in heavy smokers, U.S. researchers said on Sunday.
The Pfizer Inc drug, also known as celecoxib, works by blocking the COX-2 enzyme that causes inflammation, which has been linked with cancer.
A six-month study of 212 current or heavy smokers found a reduction in a specific type of precancerous change in lung cells in people who took a high dose of Celebrex compared with those who took a placebo.
None of the study participants had any heart-related problems such as those with Merck & Co Inc's now withdrawn arthritis drug Vioxx, another COX-2 inhibitor.
"Celebrex was safe and we did not see any cardiovascular events," said Dr. Edward Kim of M.D. Anderson Cancer Center in Houston, who presented his findings at a meeting of the American Society of Clinical Oncology in Chicago.
He said the study suggests that a high dose of Celebrex might alter some of the cellular changes that lead up to lung cancer. But the finding is very early and would need to be confirmed in longer, larger studies.
"This is not a study where we go tell someone who is a heavy smoker to start taking Celebrex to prevent lung cancer," Kim said in an interview.
Lung cancer is the leading cause of cancer death in the United States, according to the American Cancer Society. In 2008, about 215,000 people will be diagnosed with lung cancer and about 114,000 people will die from it.
The study was started before news emerged in September 2004 that Vioxx doubled the risk of heart attack and stroke in certain patients.
Kim said the trial was put on hold in December 2004 at the request of Pfizer and the National Cancer Institute, which funded the trial, so the researchers could look for signs of heart attacks or strokes.
It was started up again in May 2005 after the researchers added safeguards, including consultations with cardiologists, to reduce heart risks.
EARLY SIGNS
Rather than a direct measure of cancer prevention, which could take many years, Kim said the researchers were looking for early changes in the body that might suggest the drug could reduce the chances of developing lung cancer.
Two large, long-running lung cancer prevention studies of beta-carotene and vitamin A supplements found they actually increased the risk of lung cancer.
"We have not had positive results with these studies. Now we would like to search for an intermediate endpoint or biomarker," Kim said at a media briefing.
"Perhaps that will lead us in the direction of who we need to target in the future," he said.
The researchers tested Celebrex in the study because studies in cells, mice and in people have shown the COX-2 enzyme is present at higher than normal levels in lung cancer and in precancerous lesions of the lung, Kim said. COX-2 is thought to play a role in the development of blood vessels that feed tumors.
Kim's study measured levels of the Ki-67 protein, a marker for cell growth. The researchers wanted to see if Celebrex had an impact on levels of this protein in tissue samples taken from the lungs of heavy smokers.
At the beginning of the study, the researchers took lung samples from six predetermined areas of the lung.
People in the study either got a 200 milligram or a 400 milligram dose of Celebrex twice a day, or a placebo.
After three months, they took more lung samples, and they took samples again at six months. Kim said the group that got the higher dose of Celebrex saw a reduction in levels of the Ki-67 protein.
Kim said it will be important to find better ways of identifying people who are at the highest risk for lung cancer for whom the benefits of taking a high-dose COX-2 inhibitor would outweigh any potential heart risks.
Genetic Link Tied to Smoking Addiction
Teams of Scientists Find Genetic Changes Linked to Cigarette Addiction, Lung Cancer
By SETH BORENSTEIN
The Associated Press
WASHINGTON
Scientists have pinpointed genetic variations that make people more likely to get hooked on cigarettes and more prone to develop lung cancer — a finding that could someday lead to screening tests and customized treatments for smokers trying to kick the habit.
The discovery by three separate teams of scientists makes the strongest case so far for the biological underpinnings of nicotine addiction and sheds more light on how genetics and lifestyle habits join forces to cause cancer.
"This is kind of a double whammy gene," said Christopher Amos, a professor of epidemiology at the M.D. Anderson Cancer Center in Houston and author of one of the studies. "It also makes you more likely to be dependent on smoking and less likely to quit smoking."
A smoker who inherits these genetic variations from both parents has an 80 percent greater chance of lung cancer than a smoker without the variants, the researchers reported. And that same smoker on average lights up two extra cigarettes a day and has a much harder time quitting than smokers who don't have these genetic differences.
The researchers disagreed on whether the variants directly increased the risk of lung cancer or did so indirectly, by causing more smoking.
The three studies, funded by governments in the U.S. and Europe, are being published Thursday in the journals Nature and Nature Genetics.
The scientists studied the genes of more than 35,000 white people of European descent in Europe, Canada and the United States. Blacks and Asians will be studied soon and may yield different results, scientists said.
They aren't quite sure if what they found is a set of variations in one gene or in three closely connected genes.
The gene variations, which govern nicotine receptors on cells, could eventually help explain some of the mysteries of chain smoking, nicotine addiction and lung cancer. These oddities include why there are 90-year-old smokers who don't get cancer and people who light up an occasional cigarette and don't get hooked.
"This is really telling us that the vulnerability to smoking and how much you smoke is clearly biologically based," said psychiatry professor Dr. Laura Bierut of Washington University in St. Louis, a genetics and smoking expert who did not take part in the studies. She praised the research as "very intriguing."
The smoking rate among U.S. adults has dropped from 42 percent in 1965 to less than 21 percent now.
The new studies are surprising in that they point to areas of the genetic code that are not associated with pleasure and the rewards of addiction.
That may help explain why some people can quit and others fail, said Dr. Nora Volkow, director of the National Institute of Drug Abuse in Bethesda, Md., which funded one of the studies.
"It opens our eyes," Volkow said Wednesday. "Not everyone takes drugs for the same reason. Not everyone smokes cigarettes for the same reasons."
One clue is in the location of the just-discovered variants, on the long arm of chromosome 15, Volkow said. It is in an area that, when damaged during tests on animals, makes them depressed and anxious. While some people smoke because it helps them focus or gives them a physiological reward, others do it to stave off depression.
That suggests that adding antidepressants to some smokers' treatment could help them kick the habit.
Bierut said a simple, inexpensive test could be developed to screen people for the variants. Kari Stefansson, lead author of the largest of the three studies, agreed. He is chief executive of deCode Genetics of Iceland, which already does prostate cancer genetic tests.
Such testing could carry risks all its own, bioethicist Arthur Caplan of the University of Pennsylvania warned. People who have been found to have a genetic predisposition to addiction and lung cancer could find it harder to get health or life insurance, or their employer might drop their coverage, he said.
"The good news is that getting these risk estimates will help focus anti-smoking campaigns, and some people will want to voluntarily get into anti-addiction programs early, where they will probably work better," Caplan said in an e-mail. But if such testing is done, it should be voluntary, and the results should be kept private, he said.
Smoking-related diseases worldwide kill about one in 10 adults, according to the World Health Organization.
Among the findings:
— Smokers who get the set of variants from only one parent see a risk of lung cancer that is about one-third higher than that of people without the variants. They also smoke about one more cigarette a day on average than other smokers. This group makes up about 45 percent of the population studied.
— Smokers who inherit the variants from both parents have nearly a 1-in-4 chance of developing lung cancer. Their cancer risk is 70 to 80 percent higher than that of smokers without the genetic variants. They smoke on average two extra cigarettes a day. This group accounts for about one in nine people of European descent.
— Smokers who don't have the variants are still more than 10 times more likely to get lung cancer than nonsmokers. Smokers without the variant have about a 14 percent risk of getting lung cancer. The risk of lung cancer for people who have never smoked is less than 1 percent, said another study author, Paul Brennan of the International Agency for Research on Cancer in Lyon, France.
Brennan and Amos, working on different teams, linked the genetic variation itself — when triggered by smoking — directly to lung cancer. Brennan said the nicotine receptors that the variants act on also can stimulate tumor growth.
But Stefansson said the increased lung cancer risk was indirect — the variants led to more smoking, which led to more cancer.
For Stefansson, the research hits home. His father, a smoker, died of lung cancer. And Stefansson, who doesn't smoke, frequently lectures his 23-year-old daughter "who smokes like a chimney." She acts as if she is immortal and smoking can't kill her, Stefansson said. But his own research shows that her genes are probably stacked against her.
———
By SETH BORENSTEIN
The Associated Press
WASHINGTON
Scientists have pinpointed genetic variations that make people more likely to get hooked on cigarettes and more prone to develop lung cancer — a finding that could someday lead to screening tests and customized treatments for smokers trying to kick the habit.
The discovery by three separate teams of scientists makes the strongest case so far for the biological underpinnings of nicotine addiction and sheds more light on how genetics and lifestyle habits join forces to cause cancer.
"This is kind of a double whammy gene," said Christopher Amos, a professor of epidemiology at the M.D. Anderson Cancer Center in Houston and author of one of the studies. "It also makes you more likely to be dependent on smoking and less likely to quit smoking."
A smoker who inherits these genetic variations from both parents has an 80 percent greater chance of lung cancer than a smoker without the variants, the researchers reported. And that same smoker on average lights up two extra cigarettes a day and has a much harder time quitting than smokers who don't have these genetic differences.
The researchers disagreed on whether the variants directly increased the risk of lung cancer or did so indirectly, by causing more smoking.
The three studies, funded by governments in the U.S. and Europe, are being published Thursday in the journals Nature and Nature Genetics.
The scientists studied the genes of more than 35,000 white people of European descent in Europe, Canada and the United States. Blacks and Asians will be studied soon and may yield different results, scientists said.
They aren't quite sure if what they found is a set of variations in one gene or in three closely connected genes.
The gene variations, which govern nicotine receptors on cells, could eventually help explain some of the mysteries of chain smoking, nicotine addiction and lung cancer. These oddities include why there are 90-year-old smokers who don't get cancer and people who light up an occasional cigarette and don't get hooked.
"This is really telling us that the vulnerability to smoking and how much you smoke is clearly biologically based," said psychiatry professor Dr. Laura Bierut of Washington University in St. Louis, a genetics and smoking expert who did not take part in the studies. She praised the research as "very intriguing."
The smoking rate among U.S. adults has dropped from 42 percent in 1965 to less than 21 percent now.
The new studies are surprising in that they point to areas of the genetic code that are not associated with pleasure and the rewards of addiction.
That may help explain why some people can quit and others fail, said Dr. Nora Volkow, director of the National Institute of Drug Abuse in Bethesda, Md., which funded one of the studies.
"It opens our eyes," Volkow said Wednesday. "Not everyone takes drugs for the same reason. Not everyone smokes cigarettes for the same reasons."
One clue is in the location of the just-discovered variants, on the long arm of chromosome 15, Volkow said. It is in an area that, when damaged during tests on animals, makes them depressed and anxious. While some people smoke because it helps them focus or gives them a physiological reward, others do it to stave off depression.
That suggests that adding antidepressants to some smokers' treatment could help them kick the habit.
Bierut said a simple, inexpensive test could be developed to screen people for the variants. Kari Stefansson, lead author of the largest of the three studies, agreed. He is chief executive of deCode Genetics of Iceland, which already does prostate cancer genetic tests.
Such testing could carry risks all its own, bioethicist Arthur Caplan of the University of Pennsylvania warned. People who have been found to have a genetic predisposition to addiction and lung cancer could find it harder to get health or life insurance, or their employer might drop their coverage, he said.
"The good news is that getting these risk estimates will help focus anti-smoking campaigns, and some people will want to voluntarily get into anti-addiction programs early, where they will probably work better," Caplan said in an e-mail. But if such testing is done, it should be voluntary, and the results should be kept private, he said.
Smoking-related diseases worldwide kill about one in 10 adults, according to the World Health Organization.
Among the findings:
— Smokers who get the set of variants from only one parent see a risk of lung cancer that is about one-third higher than that of people without the variants. They also smoke about one more cigarette a day on average than other smokers. This group makes up about 45 percent of the population studied.
— Smokers who inherit the variants from both parents have nearly a 1-in-4 chance of developing lung cancer. Their cancer risk is 70 to 80 percent higher than that of smokers without the genetic variants. They smoke on average two extra cigarettes a day. This group accounts for about one in nine people of European descent.
— Smokers who don't have the variants are still more than 10 times more likely to get lung cancer than nonsmokers. Smokers without the variant have about a 14 percent risk of getting lung cancer. The risk of lung cancer for people who have never smoked is less than 1 percent, said another study author, Paul Brennan of the International Agency for Research on Cancer in Lyon, France.
Brennan and Amos, working on different teams, linked the genetic variation itself — when triggered by smoking — directly to lung cancer. Brennan said the nicotine receptors that the variants act on also can stimulate tumor growth.
But Stefansson said the increased lung cancer risk was indirect — the variants led to more smoking, which led to more cancer.
For Stefansson, the research hits home. His father, a smoker, died of lung cancer. And Stefansson, who doesn't smoke, frequently lectures his 23-year-old daughter "who smokes like a chimney." She acts as if she is immortal and smoking can't kill her, Stefansson said. But his own research shows that her genes are probably stacked against her.
———
Friday, May 30, 2008
Roche says Herceptin with chemo prolongs survival
REUTERS
Fri May 30, 2008 6:42am EDT
Reporting by Sam Cage and Paul Arnold; editing by Sue Thomas
ZURICH (Reuters) - Roche Holding AG's Herceptin, when added to chemotherapy Xeloda, prolonged survival without progression of breast cancer by three months compared to chemotherapy alone, the Swiss drugmaker said on Friday.
Roche also reported results from a mid-stage trial, which showed that patients whose disease had progressed during a Herceptin regimen benefited from a combination of Herceptin and pertuzumab, another Roche drug.
Roche stock rose 1.1 percent to 182.20 Swiss francs by 1013 GMT, versus a 0.6 percent rise in the European sector.
"Incremental positive news for Herceptin should also help sentiment towards Roche," Dresdner Kleinwort analysts said in a note.
The data are due to be presented at an American Society of Clinical Oncology (ASCO) meeting.
For the Roche statements, click here or here
Fri May 30, 2008 6:42am EDT
Reporting by Sam Cage and Paul Arnold; editing by Sue Thomas
ZURICH (Reuters) - Roche Holding AG's Herceptin, when added to chemotherapy Xeloda, prolonged survival without progression of breast cancer by three months compared to chemotherapy alone, the Swiss drugmaker said on Friday.
Roche also reported results from a mid-stage trial, which showed that patients whose disease had progressed during a Herceptin regimen benefited from a combination of Herceptin and pertuzumab, another Roche drug.
Roche stock rose 1.1 percent to 182.20 Swiss francs by 1013 GMT, versus a 0.6 percent rise in the European sector.
"Incremental positive news for Herceptin should also help sentiment towards Roche," Dresdner Kleinwort analysts said in a note.
The data are due to be presented at an American Society of Clinical Oncology (ASCO) meeting.
For the Roche statements, click here or here
Vitamin D for babies may prevent type 1 diabetes
REUTERS
Fri May 30, 2008 1:23pm EDT
By Anne Harding
NEW YORK (Reuters Health) - A new analysis of current research provides "the strongest evidence to date" that giving small children supplemental vitamin D will help prevent them from developing type 1 diabetes later on, according to the review's co-author.
"This is just another reason why current recommendations regarding vitamin D supplementation should be rigorously adhered to," Dr. Christos S. Zipitis told Reuters Health.
Vitamin D is produced in the skin with sun exposure. Deficiency in the nutrient can lead to a host of health problems, Zipitis said. Because breast milk typically contains little vitamin D, the American Academy of Pediatrics recommends vitamin D supplements for nursing infants and UK public health authorities say that all children should receive the supplements for at least the first two years of life.
There are a number of clues suggesting a link between low vitamin D levels and type 1 diabetes, Zipitis of Stockport National Health Service Foundation Trust and Dr. A. K. Akobeng of Booth Hall Children's Hospital in Manchester, UK, note in their report in the Archives of Disease in Childhood.
The investigators reviewed all published research on vitamin D supplementation and diabetes risk. Overall, they found, infants who were supplemented with Vitamin D were 29 percent less likely to develop type 1 diabetes than children who had not received supplements.
Proper clinical trials are required to determine the optimal dose and formulation of vitamin D, as well as when and for how long children should be given the supplements, Zipitis and Akobeng conclude.
In the meantime, Zipitis said, "I would advise parents to encourage their pediatricians to prescribe vitamin D supplements for their infants. However, parents can also obtain these over the counter and provided they are used as per manufacturer instructions they should be extremely safe to use."
Fri May 30, 2008 1:23pm EDT
By Anne Harding
NEW YORK (Reuters Health) - A new analysis of current research provides "the strongest evidence to date" that giving small children supplemental vitamin D will help prevent them from developing type 1 diabetes later on, according to the review's co-author.
"This is just another reason why current recommendations regarding vitamin D supplementation should be rigorously adhered to," Dr. Christos S. Zipitis told Reuters Health.
Vitamin D is produced in the skin with sun exposure. Deficiency in the nutrient can lead to a host of health problems, Zipitis said. Because breast milk typically contains little vitamin D, the American Academy of Pediatrics recommends vitamin D supplements for nursing infants and UK public health authorities say that all children should receive the supplements for at least the first two years of life.
There are a number of clues suggesting a link between low vitamin D levels and type 1 diabetes, Zipitis of Stockport National Health Service Foundation Trust and Dr. A. K. Akobeng of Booth Hall Children's Hospital in Manchester, UK, note in their report in the Archives of Disease in Childhood.
The investigators reviewed all published research on vitamin D supplementation and diabetes risk. Overall, they found, infants who were supplemented with Vitamin D were 29 percent less likely to develop type 1 diabetes than children who had not received supplements.
Proper clinical trials are required to determine the optimal dose and formulation of vitamin D, as well as when and for how long children should be given the supplements, Zipitis and Akobeng conclude.
In the meantime, Zipitis said, "I would advise parents to encourage their pediatricians to prescribe vitamin D supplements for their infants. However, parents can also obtain these over the counter and provided they are used as per manufacturer instructions they should be extremely safe to use."
Monday, May 12, 2008
Child safety seats should be centered in back seat
Child safety seats should be centered in back seat
REUTERS
Mon May 12, 2008 7:37am EDT
NEW YORK (Reuters Health) - Positioning child safety seats in the center of the back seat could cut infants' and toddlers' injury risks by nearly half, a new study suggests.
In a study of car crash data from 16 U.S. states, researchers found that children younger than 3 years old were 43 percent less likely to be injured when their seat was fastened in the center of the back seat rather than one of the side seats.
Experts already recommend that parents position car seats in the center of the rear seat, and the current findings bolster that advice, according to Michael J. Kallan and colleagues at the University of Pennsylvania and Children's Hospital of Philadelphia.
Unfortunately, only 28 percent of children in their study were sitting in that position at the time of the car accident, the researchers report in the journal Pediatrics.
There are obstacles to placing a car seat in the center position, Kallan's team acknowledges.
It is physically harder to strap a child, especially a heavier child, into a center-positioned seat. A centered child seat can also make it difficult for other people to sit in the rear of the car.
But based on the current findings, the researchers write, this center position is the safest place for babies and toddlers to ride.
The results are based on data from 4,790 car crashes involving children ages 3 and younger that occurred between 1998 and 2006. At the time of the accident, 41 percent of the children were in a car seat positioned in the right-hand back seat, while 31 percent were in the left-hand seat.
The center position was the least popular, but the safest. The reason, in part, was that children in a centered seat were better protected during a side-impact crash, according to Kallan's team.
"Recommendations should continue to encourage families to install child-restraint systems in the center of the rear seat," the researchers conclude.
They note that there are several online resources for parents who need information on installing child safety seats. The Children's Hospital of Philadelphia maintains such a site, at www.chop.edu/carseat.
Parents can also go to a local child safety seat inspection station, where inspectors will give them advice on properly using the seats. The National Highway Traffic Safety Administration maintains a searchable database of inspection stations, here
SOURCE: Pediatrics, May 2008.
REUTERS
Mon May 12, 2008 7:37am EDT
NEW YORK (Reuters Health) - Positioning child safety seats in the center of the back seat could cut infants' and toddlers' injury risks by nearly half, a new study suggests.
In a study of car crash data from 16 U.S. states, researchers found that children younger than 3 years old were 43 percent less likely to be injured when their seat was fastened in the center of the back seat rather than one of the side seats.
Experts already recommend that parents position car seats in the center of the rear seat, and the current findings bolster that advice, according to Michael J. Kallan and colleagues at the University of Pennsylvania and Children's Hospital of Philadelphia.
Unfortunately, only 28 percent of children in their study were sitting in that position at the time of the car accident, the researchers report in the journal Pediatrics.
There are obstacles to placing a car seat in the center position, Kallan's team acknowledges.
It is physically harder to strap a child, especially a heavier child, into a center-positioned seat. A centered child seat can also make it difficult for other people to sit in the rear of the car.
But based on the current findings, the researchers write, this center position is the safest place for babies and toddlers to ride.
The results are based on data from 4,790 car crashes involving children ages 3 and younger that occurred between 1998 and 2006. At the time of the accident, 41 percent of the children were in a car seat positioned in the right-hand back seat, while 31 percent were in the left-hand seat.
The center position was the least popular, but the safest. The reason, in part, was that children in a centered seat were better protected during a side-impact crash, according to Kallan's team.
"Recommendations should continue to encourage families to install child-restraint systems in the center of the rear seat," the researchers conclude.
They note that there are several online resources for parents who need information on installing child safety seats. The Children's Hospital of Philadelphia maintains such a site, at www.chop.edu/carseat.
Parents can also go to a local child safety seat inspection station, where inspectors will give them advice on properly using the seats. The National Highway Traffic Safety Administration maintains a searchable database of inspection stations, here
SOURCE: Pediatrics, May 2008.
Prostate cancer deaths fall after screening program
Prostate cancer deaths fall after screening program
REUTERS
Mon May 12, 2008 7:38am EDT
NEW YORK (Reuters Health) - Prostate cancer deaths fell substantially in the decade after one Austrian state began free PSA screening tests for all men ages 45 to 75, according to a new study.
Researchers found that after the state of Tyrol began a program of free PSA screening and prostate cancer treatment in 1993, the expected death rate from prostate cancer dropped by 54 percent. That compared with a decline of 29 percent in the rest of Austria, where free screening was not available.
The findings, reported in the journal BJU International, suggest that routine PSA testing can save men's lives -- something that has long been an open question.
PSA tests measure the amount of a protein called prostate-specific antigen in a man's blood. Because prostate tumors cause PSA levels to rise, routine PSA testing can catch the cancer early.
But PSA screening is controversial because it is not clear that the benefits outweigh the risks. Prostate cancer is often very slow-growing, and PSA screening may lead to treatment of tumors that would never have become life-threatening; treatment can carry side effects, like incontinence and erectile dysfunction.
In addition, PSA concentrations can increase for a reason other than prostate cancer and confirmation of prostate cancer requires a biopsy of the prostate gland, which itself can have side effects, such as infection or bleeding.
However, in the current study, early detection through widespread PSA screening is likely the driving force behind the greater drop in death rates seen in Tyrol, according to the researchers.
Between 1993 and 2005, nearly 87 percent of men ages 45 to 75 in Tyrol had at least one PSA screening test, the study found. That was up from 11 percent before the free program began.
And while prostate cancer death rates declined throughout Austria during the same period, they fell faster in Tyrol.
"Before the program was introduced, prostate cancer death rates in the Tyrol were similar to the rest of the country," lead researcher Dr. Georg Bartsch, of the University of Innsbruck, said in a statement.
"But after the program was launched the death rate in the Tyrol started falling by an average of 7.3 percent a year, more than twice the 3.2 percent observed in the rest of Austria."
The researchers acknowledge, however, that routine PSA screening remains controversial, and questions such as which men stand to benefit most from screening are still unresolved.
In general, experts recommend that men speak with their doctors about the potential benefits and risks of PSA screening for them personally. The American Cancer Society recommends that doctors offer most men PSA testing and a digital rectal exam yearly, starting at age 50.
SOURCE: BJU International, April 2008.
REUTERS
Mon May 12, 2008 7:38am EDT
NEW YORK (Reuters Health) - Prostate cancer deaths fell substantially in the decade after one Austrian state began free PSA screening tests for all men ages 45 to 75, according to a new study.
Researchers found that after the state of Tyrol began a program of free PSA screening and prostate cancer treatment in 1993, the expected death rate from prostate cancer dropped by 54 percent. That compared with a decline of 29 percent in the rest of Austria, where free screening was not available.
The findings, reported in the journal BJU International, suggest that routine PSA testing can save men's lives -- something that has long been an open question.
PSA tests measure the amount of a protein called prostate-specific antigen in a man's blood. Because prostate tumors cause PSA levels to rise, routine PSA testing can catch the cancer early.
But PSA screening is controversial because it is not clear that the benefits outweigh the risks. Prostate cancer is often very slow-growing, and PSA screening may lead to treatment of tumors that would never have become life-threatening; treatment can carry side effects, like incontinence and erectile dysfunction.
In addition, PSA concentrations can increase for a reason other than prostate cancer and confirmation of prostate cancer requires a biopsy of the prostate gland, which itself can have side effects, such as infection or bleeding.
However, in the current study, early detection through widespread PSA screening is likely the driving force behind the greater drop in death rates seen in Tyrol, according to the researchers.
Between 1993 and 2005, nearly 87 percent of men ages 45 to 75 in Tyrol had at least one PSA screening test, the study found. That was up from 11 percent before the free program began.
And while prostate cancer death rates declined throughout Austria during the same period, they fell faster in Tyrol.
"Before the program was introduced, prostate cancer death rates in the Tyrol were similar to the rest of the country," lead researcher Dr. Georg Bartsch, of the University of Innsbruck, said in a statement.
"But after the program was launched the death rate in the Tyrol started falling by an average of 7.3 percent a year, more than twice the 3.2 percent observed in the rest of Austria."
The researchers acknowledge, however, that routine PSA screening remains controversial, and questions such as which men stand to benefit most from screening are still unresolved.
In general, experts recommend that men speak with their doctors about the potential benefits and risks of PSA screening for them personally. The American Cancer Society recommends that doctors offer most men PSA testing and a digital rectal exam yearly, starting at age 50.
SOURCE: BJU International, April 2008.
Thursday, April 10, 2008
Painkillers help build muscle in older exercisers
Thu Apr 10, 2008 12:23pm EDT
Reuters.com
By Megan Rauscher
NEW YORK (Reuters Health) - In a study of healthy older adults lifting weights regularly, for 3 months, taking recommended daily doses of ibuprofen (like that in Advil) or acetaminophen (like that in Tylenol) led to substantially greater increases over inactive placebo in quadriceps muscle mass and strength.
Dr. Chad C. Carroll, a postdoctoral fellow working with Dr. Todd Trappe in the Human Performance Laboratory at Ball State University, Muncie, Indiana, reported the study results this week during the annual meeting of the American Physiological Society, part of the Experimental Biology 2008 scientific conference in San Diego.
Taking ibuprofen or acetaminophen regularly during resistance training seems to induce chances within the muscle that enhance the metabolic response to resistance exercise, which promotes additional muscle building and strength gains in the elderly, the researchers found.
During 12 weeks of supervised knee-extensor weight training, performed three times per week for 15 to 20 minutes, 36 men and women, between 60 and 78 years old, were randomly assigned to ibuprofen, acetaminophen, or placebo in doses mimicking what chronic users of these pain relievers were likely to be taking on a daily basis.
"We used 1200 milligrams a day for ibuprofen and 4000 milligrams per day of acetaminophen, which is the maximum over-the-counter daily dose," Dr. Trappe explained in an interview with Reuters Health.
As expected, resistance training alone (placebo group) increased quadriceps muscle mass and muscle strength. However, the increases were far greater in the ibuprofen and acetaminophen groups.
"The muscles of the ibuprofen and acetaminophen users got 40 to 60 percent bigger than the placebo group and their muscle strength also went up higher than the placebo group," Trappe said.
Specifically, muscle volume increased 11 percent in the ibuprofen group and 13 percent in the acetaminophen group, compared with 9 percent in the placebo group. Muscle strength increased 30 percent in the ibuprofen group and 28 percent in the acetaminophen group, compared with 23 percent in the placebo group.
These finding were somewhat surprising, Trappe said. In a prior study, his team measured muscle protein synthesis over a 24-hour period and found that ibuprofen and acetaminophen had a negative impact on muscle by blocking the COX enzyme.
Based on this acute study, "we figured that these drugs would actually get in the way of muscle building in the elderly -- the group that seems to benefit the most from doing resistance exercises," Trappe explained.
The researchers are now examining muscle biopsies taken from the study subjects before and after the 3-month period of resistance training to better understand the metabolic mechanism behind the apparent beneficial effects of ibuprofen and acetaminophen during weight training.
Reuters.com
By Megan Rauscher
NEW YORK (Reuters Health) - In a study of healthy older adults lifting weights regularly, for 3 months, taking recommended daily doses of ibuprofen (like that in Advil) or acetaminophen (like that in Tylenol) led to substantially greater increases over inactive placebo in quadriceps muscle mass and strength.
Dr. Chad C. Carroll, a postdoctoral fellow working with Dr. Todd Trappe in the Human Performance Laboratory at Ball State University, Muncie, Indiana, reported the study results this week during the annual meeting of the American Physiological Society, part of the Experimental Biology 2008 scientific conference in San Diego.
Taking ibuprofen or acetaminophen regularly during resistance training seems to induce chances within the muscle that enhance the metabolic response to resistance exercise, which promotes additional muscle building and strength gains in the elderly, the researchers found.
During 12 weeks of supervised knee-extensor weight training, performed three times per week for 15 to 20 minutes, 36 men and women, between 60 and 78 years old, were randomly assigned to ibuprofen, acetaminophen, or placebo in doses mimicking what chronic users of these pain relievers were likely to be taking on a daily basis.
"We used 1200 milligrams a day for ibuprofen and 4000 milligrams per day of acetaminophen, which is the maximum over-the-counter daily dose," Dr. Trappe explained in an interview with Reuters Health.
As expected, resistance training alone (placebo group) increased quadriceps muscle mass and muscle strength. However, the increases were far greater in the ibuprofen and acetaminophen groups.
"The muscles of the ibuprofen and acetaminophen users got 40 to 60 percent bigger than the placebo group and their muscle strength also went up higher than the placebo group," Trappe said.
Specifically, muscle volume increased 11 percent in the ibuprofen group and 13 percent in the acetaminophen group, compared with 9 percent in the placebo group. Muscle strength increased 30 percent in the ibuprofen group and 28 percent in the acetaminophen group, compared with 23 percent in the placebo group.
These finding were somewhat surprising, Trappe said. In a prior study, his team measured muscle protein synthesis over a 24-hour period and found that ibuprofen and acetaminophen had a negative impact on muscle by blocking the COX enzyme.
Based on this acute study, "we figured that these drugs would actually get in the way of muscle building in the elderly -- the group that seems to benefit the most from doing resistance exercises," Trappe explained.
The researchers are now examining muscle biopsies taken from the study subjects before and after the 3-month period of resistance training to better understand the metabolic mechanism behind the apparent beneficial effects of ibuprofen and acetaminophen during weight training.
Weight discrimination common, U.S. survey finds
Wed Apr 9, 2008 5:29pm EDT
09 Apr 2008
By Amy Norton
NEW YORK (Reuters Health) - Discrimination against the overweight may be about as prevalent as racial discrimination, the results of a survey of U.S. adults suggest.
Using data from a survey of nearly 2,300 Americans, researchers at Yale University, New Haven, Connecticut found that 5 percent of men and 10 percent of women said they had faced discrimination because of their weight -- ranging from job refusals to rude treatment in everyday life.
Among respondents who were severely obese -- having a body mass index
(BMI) of 35 or higher -- 40 percent reported instances of weight discrimination. A body mass index is the ratio between height and weight commonly used to classify individuals as over- or underweight.
Weight bias also rivaled the prevalence of other, long-recognized forms of discrimination, the researchers report in the International Journal of Obesity.
Among women, weight discrimination was the third most common form, behind sex and age discrimination. Among all adults, it came in fourth overall, after sex, age and racial discrimination.
The findings point to a need for "organized efforts" to combat weight bias, the researchers note in their report.
"In order to reduce weight bias, we need major shifts in societal attitudes," lead researcher Dr. Rebecca M. Puhl told Reuters Health.
This would include building awareness of weight discrimination and its consequences, Puhl noted, as well as improving media portrayals of obese individuals. Overweight people should also have legal protection against discrimination, she said.
The findings are based on a nationally representative sample of 2,290 Americans ages 25 to 74 who were surveyed between 1995 and 1996.
Respondents were asked whether they had ever been victims of discrimination based on race, religion, sex or various other reasons, including weight.
Of the men and women who reported weight discrimination, 60 percent said they had experienced work-related discrimination, such as not being hired, being passed over for promotion, or being wrongly fired.
Many also cited day-to-day types of discrimination, like being treated with less respect or courtesy than others, or being "perceived as inferior." And compared with victims of other forms of discrimination, those subjected to weight bias were more likely to say they had been called names or overtly insulted.
Women were particularly likely to perceive weight bias, with twice as many women as men reporting such discrimination.
This may not be surprising, according to Puhl, given the "stringent and unrealistic ideals of thinness that are placed on women in North America."
Indeed, the study found that women seemed to be vulnerable to weight discrimination even if they were moderately overweight, whereas only severely obese men reported discrimination at a rate comparable with their female counterparts.
"This means we need to be especially aware of the negative experiences and effects of weight bias among females," Puhl said.
SOURCE: International Journal of Obesity, online March 4, 2008.
09 Apr 2008
By Amy Norton
NEW YORK (Reuters Health) - Discrimination against the overweight may be about as prevalent as racial discrimination, the results of a survey of U.S. adults suggest.
Using data from a survey of nearly 2,300 Americans, researchers at Yale University, New Haven, Connecticut found that 5 percent of men and 10 percent of women said they had faced discrimination because of their weight -- ranging from job refusals to rude treatment in everyday life.
Among respondents who were severely obese -- having a body mass index
(BMI) of 35 or higher -- 40 percent reported instances of weight discrimination. A body mass index is the ratio between height and weight commonly used to classify individuals as over- or underweight.
Weight bias also rivaled the prevalence of other, long-recognized forms of discrimination, the researchers report in the International Journal of Obesity.
Among women, weight discrimination was the third most common form, behind sex and age discrimination. Among all adults, it came in fourth overall, after sex, age and racial discrimination.
The findings point to a need for "organized efforts" to combat weight bias, the researchers note in their report.
"In order to reduce weight bias, we need major shifts in societal attitudes," lead researcher Dr. Rebecca M. Puhl told Reuters Health.
This would include building awareness of weight discrimination and its consequences, Puhl noted, as well as improving media portrayals of obese individuals. Overweight people should also have legal protection against discrimination, she said.
The findings are based on a nationally representative sample of 2,290 Americans ages 25 to 74 who were surveyed between 1995 and 1996.
Respondents were asked whether they had ever been victims of discrimination based on race, religion, sex or various other reasons, including weight.
Of the men and women who reported weight discrimination, 60 percent said they had experienced work-related discrimination, such as not being hired, being passed over for promotion, or being wrongly fired.
Many also cited day-to-day types of discrimination, like being treated with less respect or courtesy than others, or being "perceived as inferior." And compared with victims of other forms of discrimination, those subjected to weight bias were more likely to say they had been called names or overtly insulted.
Women were particularly likely to perceive weight bias, with twice as many women as men reporting such discrimination.
This may not be surprising, according to Puhl, given the "stringent and unrealistic ideals of thinness that are placed on women in North America."
Indeed, the study found that women seemed to be vulnerable to weight discrimination even if they were moderately overweight, whereas only severely obese men reported discrimination at a rate comparable with their female counterparts.
"This means we need to be especially aware of the negative experiences and effects of weight bias among females," Puhl said.
SOURCE: International Journal of Obesity, online March 4, 2008.
Tuesday, January 8, 2008
Healthy life 'can give you another 14 years'
By Nic Fleming, Medical Correspondent
Last Updated: 1:53am GMT 08/01/2008
http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2008/01/08/nhealth108.xml
A healthy lifestyle can increase a person's lifespan by as much as 14 years, scientists have claimed.
Researchers have calculated people can extend the length of their lives by up to 17 per cent by not smoking, drinking only moderately, eating healthily and keeping physically active.
advertisement
Many studies have highlighted the health risks associated with cigarettes, excessive alcohol consumption, poor diet and lack of exercise. However, few have looked at the combined effects of all four on longevity.
Prof Kay-Tee Khaw, a gerontologist at Cambridge University who led the new study, said: "There were substantial differences in mortality associated with the four health behaviours combined.
"The results strongly suggest that these four achievable lifestyle changes could have a marked improvement on the health of middle-aged and older people, which is particularly important given the ageing population in the UK and other European countries."
Prof Khaw and colleagues, whose study is published in the journal PLoS Medicine, surveyed 20,244 men and women living in Norfolk in the mid-1990s. The participants, none of whom had known cancer or heart disease, were aged between 45 and 79.
They were given a point for each of four healthy behaviours - not smoking, exercising, alcohol intake of less than 15 units per week (less than five large glasses of wine or five pints of medium-strength lager) and having vitamin C levels equivalent to eating five servings of fruit and vegetables a day.
When in 2006 - an average of 11 years later - the researchers re-contacted those who took part, they found 1,987 had died since they were first interviewed.
Those who scored zero points, by having smoked, drank, failed to exercise and failed to eat enough fruit and vegetables, were four times more likely to have died than those who scored four points.
On this basis, the healthiest group in the study were calculated to have a lifespan that was, on average, 14 years longer than those with the least healthy lifestyle.
Those with one point - for displaying only one healthy behaviour - were 2.5 times as likely to have died than the healthiest group.
Smokers were 77 per cent more likely to have died during the study period, and low alcohol intake was associated with a 26 per cent increased chance of survival.
Being physically active and having levels of vitamin C equivalent to eating five servings of fruit and vegetables increased chances of still being alive by the end of study by 24 per cent and 44 per cent, respectively.
Last Updated: 1:53am GMT 08/01/2008
http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2008/01/08/nhealth108.xml
A healthy lifestyle can increase a person's lifespan by as much as 14 years, scientists have claimed.
Researchers have calculated people can extend the length of their lives by up to 17 per cent by not smoking, drinking only moderately, eating healthily and keeping physically active.
advertisement
Many studies have highlighted the health risks associated with cigarettes, excessive alcohol consumption, poor diet and lack of exercise. However, few have looked at the combined effects of all four on longevity.
Prof Kay-Tee Khaw, a gerontologist at Cambridge University who led the new study, said: "There were substantial differences in mortality associated with the four health behaviours combined.
"The results strongly suggest that these four achievable lifestyle changes could have a marked improvement on the health of middle-aged and older people, which is particularly important given the ageing population in the UK and other European countries."
Prof Khaw and colleagues, whose study is published in the journal PLoS Medicine, surveyed 20,244 men and women living in Norfolk in the mid-1990s. The participants, none of whom had known cancer or heart disease, were aged between 45 and 79.
They were given a point for each of four healthy behaviours - not smoking, exercising, alcohol intake of less than 15 units per week (less than five large glasses of wine or five pints of medium-strength lager) and having vitamin C levels equivalent to eating five servings of fruit and vegetables a day.
When in 2006 - an average of 11 years later - the researchers re-contacted those who took part, they found 1,987 had died since they were first interviewed.
Those who scored zero points, by having smoked, drank, failed to exercise and failed to eat enough fruit and vegetables, were four times more likely to have died than those who scored four points.
On this basis, the healthiest group in the study were calculated to have a lifespan that was, on average, 14 years longer than those with the least healthy lifestyle.
Those with one point - for displaying only one healthy behaviour - were 2.5 times as likely to have died than the healthiest group.
Smokers were 77 per cent more likely to have died during the study period, and low alcohol intake was associated with a 26 per cent increased chance of survival.
Being physically active and having levels of vitamin C equivalent to eating five servings of fruit and vegetables increased chances of still being alive by the end of study by 24 per cent and 44 per cent, respectively.
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