Jennie Smith

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

The European Medicines Agency, following its February monthly meeting, said that, while there remained "concern" about a possible link between the Pandemrix influenza vaccine and reports of narcolepsy among young people in Finland and Sweden, the data were "insufficient to establish a causal relationship."

Moreover, EMA said in a press release Feb. 18, other non-Nordic countries have not reported similar increased narcolepsy rates following vaccination with Pandemrix. The agency pointed to Canada as one country where Pandemrix use was widespread during the 2009 H1N1 pandemic, but increased narcolepsy reports did not follow.

The agency therefore elected not to change its recommendations on Pandemrix unless it receives more compelling data to suggest a link. The study submitted to EMA by the Finnish government had compared the incidence of narcolepsy in people aged 4-19 years who were vaccinated with Pandemrix between Jan. 1, 2009 and Dec. 31, 2010, with unvaccinated people the same age. The Finnish study also reported a ninefold increase in reports of narcolepsy in the vaccinated population (an increase from 1 to 9 cases per 100,000 vaccinated).

"One possible explanation for the results is that Pandemrix may have interacted with an unknown local environmental and/or genetic factor in contributing to an increased risk," EMA said. An ongoing study epidemiologic study of narcolepsy and pandemic vaccines is currently being conducted by the European Centre for Disease Control and Prevention in nine E.U. countries, with final results expected in June.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

 (c) Smobserver Wikipedia/ Creative Commons  

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the Georges Pompidou European Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers' histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers', using a set of four images adapted from the Hamilton-Norwood scale of male pattern baldness. Case subjects' age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences.

Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

 (c) Smobserver Wikipedia/ Creative Commons  

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the Georges Pompidou European Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers' histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers', using a set of four images adapted from the Hamilton-Norwood scale of male pattern baldness. Case subjects' age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences.

Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

 (c) Smobserver Wikipedia/ Creative Commons  

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the Georges Pompidou European Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers' histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers', using a set of four images adapted from the Hamilton-Norwood scale of male pattern baldness. Case subjects' age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences.

Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Men with prostate cancer are twice as likely to have had male pattern baldness starting at age 20, according to results of a study that found no increased risk among men who began balding in their 30s or 40s.

The findings, published Feb. 16 in Annals of Oncology (doi:10.1093/annonc/mdq695), suggest that men with early baldness may benefit from routine prostate cancer screening or preventive measures that could include the systematic use of 5-alpha reductase inhibitors, the researchers wrote.

For their research, Dr. Michael Yassa, who was a radiation oncology fellow at the European Georges Pompidou Hospital in Paris at the time of the study, and his associates studied 388 men with a diagnosis of prostate cancer, recruited from radiation oncology clinics in three French institutions. The study also included 281 matched controls with no history of cancer or hormonal pathologies, but with family histories similar to those of the cases. The mean age of the subjects was 67.2, and the controls, 66.4.

All study participants were asked to report any personal history of prostate cancer and their fathers’ histories of the same, and to describe their balding pattern at ages 20, 30, and 40 along with their fathers’, using a set of four images adapted from the Hamilton–Norwood scale of male pattern baldness. Case subjects’ age at diagnosis, stage of disease at diagnosis, treatment, and other information were recorded.

The men with prostate cancer were twice as likely to have had male pattern baldness at age 20 (odds ratio [OR] 2.01). "This trend was lost at ages 30 or 40," the researchers wrote. No specific pattern of hair loss appeared to be a predictive factor for the development of prostate cancer.

Any balding present at age 20 was associated with an increased incidence of prostate cancer later in life. Cancer patients with early balding did not develop cancers younger – those with any pattern of balding by age 20 and 40 had a mean age of diagnosis of 64.4 and 64.5 years, respectively, compared with 64.3 years for patients with no balding by age 40. The researchers also found no associations between early balding and more aggressive types of tumors.

Dr. Yassa, now with the University of Montreal, and colleagues cited a number of earlier studies with conflicting evidence on the links between baldness and cancer. One Duke University study (Cancer Epidemiol. Biomarkers Prev. 2000;9:325-8) showed that men who developed vertex baldness by age 30 had nearly a twofold increase in risk of developing prostate cancer, but a more recent population-based study (Cancer Epidemiol. [doi:10.1016/j.canep.2010.02.003]) showed baldness at age 30 to be associated with 29% relative risk reduction for prostate cancer.

The investigators in the current study speculated that androgens might be implicated in any link between early balding and cancer. "Finasteride blocks the conversion of testosterone to dihydrotestosterone, the active metabolite of testosterone, slowing the progression of androgenic alopecia and decreasing the incidence of prostate cancer," they wrote.

They also acknowledged that their own study was limited by its small size and a case-control design involving self-reporting, that could allow for recall and selective recall bias, and a lack of controlling for factors including African heritage and dietary differences. Neither Dr. Hassa nor his coauthors declared conflicts of interest.

Anorexia and bulimia can do measurable and likely irreversible damage to women’s eyes, researchers in Greece have found.

In a small study whose results were published online in the British Journal of Ophthalmology, Marilita M. Moschos, Ph.D., and her colleagues at the University of Athens reported finding "a significant anatomical and functional impairment, marked by a decrease in macular and retinal nerve fiber layer thickness as well as a decrease in electrical activity in the macula," among women with a history of anorexia or bulimia.

"The good thing is that the [anorexic and bulimic subjects] still had good vision," Dr. Moschos said in an interview. "But there is a crucial moment where if they lose more photoreceptors – for example, with untreated disease – "this will cause an irreversible vision loss."

For their research, Dr. Moschos and her colleagues evaluated macular and retinal nerve fiber layer thickness, as well as the electrical activity of the macula, in 13 female patients (mean age 28.6 years) with a diagnosis of anorexia nervosa (AN) – either of the calorie-restricting (n = 6) or binge-purge (n = 7) type, along with 20 healthy controls matched for age. Anorexic and bulimic patients had been diagnosed at least 8 years prior to the study and were in treatment at the time of the study, without current marked vitamin deficiencies [Br. J. Ophthalmol. 2010 [doi 10.1136/bjo.2009.177899]).

None of the anorexic or control patients had evidence of any visual failure; visual acuity for all remained normal. What the researchers found was subclinical damage to the structure of the anorexic women’s eyes. The anorexic women saw a mean foveal thickness of 140.04 mcm, compared with 150.85 in the control group. Retinal nerve fiber layers were also thinner – 116.42 mcm – in the superior area (vs. 123.15 in the control group) and 121.08 mcm in the inferior area (compared with 137.6 in the control group) around the optic nerve. With patients who self-induced vomiting, the damage was worse: in the left eye only, the calorie-restricting anorexics had a better foveal thickness (median 142 mcm) than did bulimics (median 134 mcm).

"Our results show that the retinal thickness of the macula is higher in restrictive-type anorectic patients than in binge-purge type patients, which means that the anatomical impairment of the fovea is greater in the AN binge-purge type, Dr. Moschos and colleagues wrote."

The possible reason for this, said Dr. Moschos in an interview, is that while calorie-restricting anorexics manage to obtain some vitamins, women who purge absorb fewer. "My opinion is that there is a correlation to vitamin deficiencies" over prolonged periods, she said.

Dr. Moschos and her colleagues noted that deficiencies of vitamin A in particular, a presumed culprit in one case study they cited of an anorexic with retinal lesions (J. Fr. Ophtalmol. 2007;30:15), were not seen among their subjects, whose own ocular changes, they speculated, were either caused by deficiencies of other nutrients or occurred in relation to dopamine, "an important neurotransmitter in the visual pathway."

The resxearchers mentioned several previous studies examining dopamine and physical changes to the retina. In people with Parkinson’s disease, "where there is a reduction in dopamine in the retina," they wrote, changes to retinal structure and function have been observed (Invest. Ophthalmol. Vis. Sci. 1990;31:2473-5).

And documented instances of impairment in visual discrimination learning among anorexics (Appetite 2003;40:85e9) "may be related to decreased appetitive function, possibly resulting from impaired dopaminergic neurotransmission, either as a result of food restriction or, more intriguingly, related to the underlying pathophysiology of AN itself," Dr. Moschos and her colleagues wrote.

The investigators acknowledged the limitations posed by the small size of their study, which is ongoing. Now, the group is extending the study to seek longer-term evidence of decline or even recovery in the young women’s maculae following treatment for their anorexia or bulimia. Currently, Dr. Moschos said, the wisdom that macular damage is irreversible stems from the fact that "what we know about maculae concerns much older people," than the anorexics in the study.

The study was funded by the University of Athens. Dr. Moschos and her colleagues reported no conflicts of interest.

Anorexia and bulimia can do measurable and likely irreversible damage to women’s eyes, researchers in Greece have found.

In a small study whose results were published online in the British Journal of Ophthalmology, Marilita M. Moschos, Ph.D., and her colleagues at the University of Athens reported finding "a significant anatomical and functional impairment, marked by a decrease in macular and retinal nerve fiber layer thickness as well as a decrease in electrical activity in the macula," among women with a history of anorexia or bulimia.

"The good thing is that the [anorexic and bulimic subjects] still had good vision," Dr. Moschos said in an interview. "But there is a crucial moment where if they lose more photoreceptors – for example, with untreated disease – "this will cause an irreversible vision loss."

For their research, Dr. Moschos and her colleagues evaluated macular and retinal nerve fiber layer thickness, as well as the electrical activity of the macula, in 13 female patients (mean age 28.6 years) with a diagnosis of anorexia nervosa (AN) – either of the calorie-restricting (n = 6) or binge-purge (n = 7) type, along with 20 healthy controls matched for age. Anorexic and bulimic patients had been diagnosed at least 8 years prior to the study and were in treatment at the time of the study, without current marked vitamin deficiencies [Br. J. Ophthalmol. 2010 [doi 10.1136/bjo.2009.177899]).

None of the anorexic or control patients had evidence of any visual failure; visual acuity for all remained normal. What the researchers found was subclinical damage to the structure of the anorexic women’s eyes. The anorexic women saw a mean foveal thickness of 140.04 mcm, compared with 150.85 in the control group. Retinal nerve fiber layers were also thinner – 116.42 mcm – in the superior area (vs. 123.15 in the control group) and 121.08 mcm in the inferior area (compared with 137.6 in the control group) around the optic nerve. With patients who self-induced vomiting, the damage was worse: in the left eye only, the calorie-restricting anorexics had a better foveal thickness (median 142 mcm) than did bulimics (median 134 mcm).

"Our results show that the retinal thickness of the macula is higher in restrictive-type anorectic patients than in binge-purge type patients, which means that the anatomical impairment of the fovea is greater in the AN binge-purge type, Dr. Moschos and colleagues wrote."

The possible reason for this, said Dr. Moschos in an interview, is that while calorie-restricting anorexics manage to obtain some vitamins, women who purge absorb fewer. "My opinion is that there is a correlation to vitamin deficiencies" over prolonged periods, she said.

Dr. Moschos and her colleagues noted that deficiencies of vitamin A in particular, a presumed culprit in one case study they cited of an anorexic with retinal lesions (J. Fr. Ophtalmol. 2007;30:15), were not seen among their subjects, whose own ocular changes, they speculated, were either caused by deficiencies of other nutrients or occurred in relation to dopamine, "an important neurotransmitter in the visual pathway."

The resxearchers mentioned several previous studies examining dopamine and physical changes to the retina. In people with Parkinson’s disease, "where there is a reduction in dopamine in the retina," they wrote, changes to retinal structure and function have been observed (Invest. Ophthalmol. Vis. Sci. 1990;31:2473-5).

And documented instances of impairment in visual discrimination learning among anorexics (Appetite 2003;40:85e9) "may be related to decreased appetitive function, possibly resulting from impaired dopaminergic neurotransmission, either as a result of food restriction or, more intriguingly, related to the underlying pathophysiology of AN itself," Dr. Moschos and her colleagues wrote.

The investigators acknowledged the limitations posed by the small size of their study, which is ongoing. Now, the group is extending the study to seek longer-term evidence of decline or even recovery in the young women’s maculae following treatment for their anorexia or bulimia. Currently, Dr. Moschos said, the wisdom that macular damage is irreversible stems from the fact that "what we know about maculae concerns much older people," than the anorexics in the study.

The study was funded by the University of Athens. Dr. Moschos and her colleagues reported no conflicts of interest.

Anorexia and bulimia can do measurable and likely irreversible damage to women’s eyes, researchers in Greece have found.

In a small study whose results were published online in the British Journal of Ophthalmology, Marilita M. Moschos, Ph.D., and her colleagues at the University of Athens reported finding "a significant anatomical and functional impairment, marked by a decrease in macular and retinal nerve fiber layer thickness as well as a decrease in electrical activity in the macula," among women with a history of anorexia or bulimia.

"The good thing is that the [anorexic and bulimic subjects] still had good vision," Dr. Moschos said in an interview. "But there is a crucial moment where if they lose more photoreceptors – for example, with untreated disease – "this will cause an irreversible vision loss."

For their research, Dr. Moschos and her colleagues evaluated macular and retinal nerve fiber layer thickness, as well as the electrical activity of the macula, in 13 female patients (mean age 28.6 years) with a diagnosis of anorexia nervosa (AN) – either of the calorie-restricting (n = 6) or binge-purge (n = 7) type, along with 20 healthy controls matched for age. Anorexic and bulimic patients had been diagnosed at least 8 years prior to the study and were in treatment at the time of the study, without current marked vitamin deficiencies [Br. J. Ophthalmol. 2010 [doi 10.1136/bjo.2009.177899]).

None of the anorexic or control patients had evidence of any visual failure; visual acuity for all remained normal. What the researchers found was subclinical damage to the structure of the anorexic women’s eyes. The anorexic women saw a mean foveal thickness of 140.04 mcm, compared with 150.85 in the control group. Retinal nerve fiber layers were also thinner – 116.42 mcm – in the superior area (vs. 123.15 in the control group) and 121.08 mcm in the inferior area (compared with 137.6 in the control group) around the optic nerve. With patients who self-induced vomiting, the damage was worse: in the left eye only, the calorie-restricting anorexics had a better foveal thickness (median 142 mcm) than did bulimics (median 134 mcm).

"Our results show that the retinal thickness of the macula is higher in restrictive-type anorectic patients than in binge-purge type patients, which means that the anatomical impairment of the fovea is greater in the AN binge-purge type, Dr. Moschos and colleagues wrote."

The possible reason for this, said Dr. Moschos in an interview, is that while calorie-restricting anorexics manage to obtain some vitamins, women who purge absorb fewer. "My opinion is that there is a correlation to vitamin deficiencies" over prolonged periods, she said.

Dr. Moschos and her colleagues noted that deficiencies of vitamin A in particular, a presumed culprit in one case study they cited of an anorexic with retinal lesions (J. Fr. Ophtalmol. 2007;30:15), were not seen among their subjects, whose own ocular changes, they speculated, were either caused by deficiencies of other nutrients or occurred in relation to dopamine, "an important neurotransmitter in the visual pathway."

The resxearchers mentioned several previous studies examining dopamine and physical changes to the retina. In people with Parkinson’s disease, "where there is a reduction in dopamine in the retina," they wrote, changes to retinal structure and function have been observed (Invest. Ophthalmol. Vis. Sci. 1990;31:2473-5).

And documented instances of impairment in visual discrimination learning among anorexics (Appetite 2003;40:85e9) "may be related to decreased appetitive function, possibly resulting from impaired dopaminergic neurotransmission, either as a result of food restriction or, more intriguingly, related to the underlying pathophysiology of AN itself," Dr. Moschos and her colleagues wrote.

The investigators acknowledged the limitations posed by the small size of their study, which is ongoing. Now, the group is extending the study to seek longer-term evidence of decline or even recovery in the young women’s maculae following treatment for their anorexia or bulimia. Currently, Dr. Moschos said, the wisdom that macular damage is irreversible stems from the fact that "what we know about maculae concerns much older people," than the anorexics in the study.

The study was funded by the University of Athens. Dr. Moschos and her colleagues reported no conflicts of interest.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

Being obese may significantly increase the risk of having a fatal coronary heart disease event independent of known obesity-affiliated cardiovascular risk factors such as high blood pressure and high cholesterol, investigators in Scotland have found.

By contrast, obesity alone was not seen as significantly increasing the risk of nonfatal CHD events.

The findings, derived from the long-term follow-up of a large pharmaceutical trial, and published Feb. 15 in the journal Heart (doi:10.1136/hrt.2010.211201), suggest that fatal and nonfatal CHD events could have separate causes – and that CHD death might not be preventable by mitigating traditional cardiovascular risk factors in obese men.

“It’s assumed that nonfatal and fatal events occur along an index of severity – but maybe there’s something different going on,” Dr. Jennifer Logue of the University of Glasgow, the study’s lead investigator, said in an interview.

With the fatal events, she said, “we found an almost 60% higher risk from obesity alone.” The risk was seen after modeling for obesity-associated cardiovascular risks such as high blood pressure and high cholesterol, along with factors such as smoking, low socioeconomic status, and medications.

“If you’ve got a middle-aged man in front of you with a [body mass index] of 35 – and that’s not an uncommon sight nowadays – yes, you can treat his blood pressure and cholesterol and help him stop smoking,” Dr. Logue said. “But his weight itself is still making him at significant risk.”

Dr. Logue and colleagues examined data from 6,082 men, with a mean age of 55, who had moderate hypercholesterolemia but who were without a history of diabetes or cardiovascular disease. The men had originally been enrolled in a manufacturer-sponsored, 5-year, randomized, placebo-controlled controlled trial to determine the effectiveness of the statin drug pravastatin in preventing cardiovascular events (N. Engl. J. Med. 1995; 333:1301-7), and the follow-up period ran to 15 years.

The pravastatin trial and the first 5 years of follow-up were funded by the drug’s manufacturer, Bristol Myers Squibb and Sankyo. The final years of follow-up and Dr. Logue and colleagues’ analysis were funded by the Scottish government and a grant from Scotland’s Chest, Heart and Stroke Association, respectively. Dr. Logue and colleagues declared no conflicts of interest.

The researchers excluded from their analysis men who had had a fatal or nonfatal CHD event in the first 2 years of the study, or those who had diabetes. A total of 1,027 nonfatal and 214 fatal CHD events were included in the analysis.

Dr. Logue and colleagues created two models in an attempt to isolate the role played by obesity alone in the fatal and nonfatal CHD events. One adjusted for age, sex, and statin treatment only. The other adjusted for these factors plus known cardiovascular risk factors, including blood pressure, elevated cholesterol, smoking status, high blood pressure, and use of a host of medications affecting blood pressure or the cardiovascular system. A standard social deprivation score, a measure of socioeconomic status, was also incorporated into the model.

The risk of fatal CHD events, the investigators found, was significantly increased in men with a body mass index of between 30 and 39.9 kg/m² in both the minimally adjusted model (HR 1.75) and the adjusted model (HR 1.60). Nonfatal CHD was not seen as independently increased by high BMI.

“This link was not seen for non-fatal CHD events and therefore, owing to large relative numbers of such events, also not seen for composite CHD events,” the investigators wrote in their analysis. “In other words, our data suggest that obesity may give greater risk for fatal CHD events than nonfatal events, even after accounting for classical CHD risk factors.”

The investigators cautioned that their results were not conclusive, but “should be considered hypothesis generating.”

Among the weaknesses of their study, they wrote, was the fact that it evaluated only men, and that the percentage of participants who were obese was relatively small, limiting its statistical power.

Among the study’s strengths, they wrote, was “the large cohort with a high number of events; this has allowed significant results to be generated while still allowing participants with events in the first 2 years to be excluded, along with those with known diabetes.” A further strength, they wrote, was having details of each death thanks to standardized government records. “Had we combined fatal and nonfatal CHD events we would have missed this important association.”

Dr. Logue and colleagues cited in their analysis a study highlighting inflammation as a possible culprit in fatal CHD events (PLoS Med. 2009 Aug. 6;6: e1000099) and another exploring the effects of adiposity on inflammation (J. Clin. Endocrinol. Metab. 2010;95:93-9).

“Recent work has shown that inflammatory markers, namely, IL-6, CRP and fibrinogen, are more strongly related to fatal than nonfatal cardiovascular events. As obesity is increasingly recognized as an inflammatory state, this is a potential etiological pathway to account for the increased risk of fatal CHD events seen with obesity,” the investigators wrote.

Dr. Logue said in an interview, however, that the culprit was far from clear. “It could be inflammation,” she said. “But there’s also upcoming evidence around structural changes to the heart caused by obesity, which could mean your heart can’t cope as well when you’re having a heart attack.” But more important in any case, she said, is to learn whether the risk of a fatal CHD event is mitigated by weight loss.

“I’d rather see the resources put into looking to see if we can get people’s weight down and preventing people getting to this weight in the first place,” Dr. Logue said.

The experimental drug apixaban has been shown to reduce the risk of stroke and systemic embolism by more than half, compared with aspirin, in people with atrial fibrillation who have failed or cannot take warfarin.

This effect was seen without a significant increase in the risk of major bleeding events, in a large randomized, placebo-controlled trial.

Findings from the study published online Feb. 10 in the New England Journal of Medicine (doi:10.1056/NEJMoa1007432) suggest that apixaban may be a safe alternative to vitamin K antagonists or clopidogrel and aspirin in this population.

Vitamin K antagonists such as warfarin can be problematic in people with atrial fibrillation, because of an unpredictable therapeutic effect and a need for frequent coagulation monitoring. The clopidogrel-aspirin combination reduces stroke risk but also increases major bleeding risk. Apixaban is a novel factor Xa inhibitor, part of a class of anticoagulant drugs developed from compounds identified in leeches and ticks.

For their research, funded by Bristol-Myers Squibb and Pfizer, which are jointly developing apixaban, Dr. Stuart J. Connolly of the Population Health Research Institute in Hamilton, Ont., and his colleagues conducted a study that comprised 5,599 patients aged 50 and older with atrial fibrillation who were at increased risk of stroke (determined as being age 75 or older, or having cardiovascular risk factors including diabetes, heart failure, or peripheral artery disease). The patients were randomized to receive a fixed dose of oral apixaban 5 mg or 2.5 mg, depending on age and body weight, twice daily (n = 2,808), or aspirin at a dose ranging from 81 to 324 mg/day (n = 2,791).

About 58% of study participants were men. Most of the aspirin subjects received doses of 162 mg or less, and the vast majority of the apixaban subjects received the higher dose. Forty percent of all participants had been treated previously with a vitamin K antagonist. The primary outcome of the trial was the occurrence of stroke or systemic embolism, and its primary safety outcome was the occurrence of major bleeding. Enrollment began in September 2007 and lasted until December 2009, with a mean follow-up of 1.1 years.

During the study period, 51 primary outcome events (1.6% per year) occurred in the apixaban arm and 113 (3.7% per year) in the aspirin arm (HR, 0.45 with apixaban; P less than .001). The annual rate of death from any cause was 3.5% in the apixaban arm and 4.4% in the aspirin arm (HR, 0.79; P = .07). Episodes of major bleeding were 44 (1.4% per year) with apixaban and 39 (1.2% per year) with aspirin (HR, 1.13; P = .57). Intracranial bleeding occurred in 11 and 13 patients in each group (HR, 0.85; P = .69).

In February 2010, the data safety monitoring board recommended termination of the study based on results from an interim analysis showing apixaban to be superior to aspirin in reducing stroke and systemic embolism. Data collection continued through May 28, 2010.

Conversely, in November 2010, a separate manufacturer-sponsored phase III apixaban study (n = 10,848), comparing the same 5-mg twice-daily dose to placebo in patients with acute coronary syndrome, was stopped because of an increase in major bleeding events that was not offset, the manufacturer reported, by a decrease in ischemic events. Trials comparing apixaban 2.5 mg twice daily with low-molecular-weight heparin following knee (Lancet 2010;375:807-15) and hip (N. Engl. J. Med. 2010;363:2487-98) surgeries did not show significant differences in bleeding events.

Dr. Connolly disclosed serving as a paid board member and receiving consulting fees or institutional grant support from Boehringer Ingelheim, Sanofi, Merck, and Bristol-Myers Squibb, among other pharmaceutical firms; of his 31 coauthors, nearly a third disclosed direct or indirect support from Bristol-Myers Squibb or Pfizer, and one was an employee of Bristol-Myers Squibb.

The experimental drug apixaban has been shown to reduce the risk of stroke and systemic embolism by more than half, compared with aspirin, in people with atrial fibrillation who have failed or cannot take warfarin.

This effect was seen without a significant increase in the risk of major bleeding events, in a large randomized, placebo-controlled trial.

Findings from the study published online Feb. 10 in the New England Journal of Medicine (doi:10.1056/NEJMoa1007432) suggest that apixaban may be a safe alternative to vitamin K antagonists or clopidogrel and aspirin in this population.

Vitamin K antagonists such as warfarin can be problematic in people with atrial fibrillation, because of an unpredictable therapeutic effect and a need for frequent coagulation monitoring. The clopidogrel-aspirin combination reduces stroke risk but also increases major bleeding risk. Apixaban is a novel factor Xa inhibitor, part of a class of anticoagulant drugs developed from compounds identified in leeches and ticks.

For their research, funded by Bristol-Myers Squibb and Pfizer, which are jointly developing apixaban, Dr. Stuart J. Connolly of the Population Health Research Institute in Hamilton, Ont., and his colleagues conducted a study that comprised 5,599 patients aged 50 and older with atrial fibrillation who were at increased risk of stroke (determined as being age 75 or older, or having cardiovascular risk factors including diabetes, heart failure, or peripheral artery disease). The patients were randomized to receive a fixed dose of oral apixaban 5 mg or 2.5 mg, depending on age and body weight, twice daily (n = 2,808), or aspirin at a dose ranging from 81 to 324 mg/day (n = 2,791).

About 58% of study participants were men. Most of the aspirin subjects received doses of 162 mg or less, and the vast majority of the apixaban subjects received the higher dose. Forty percent of all participants had been treated previously with a vitamin K antagonist. The primary outcome of the trial was the occurrence of stroke or systemic embolism, and its primary safety outcome was the occurrence of major bleeding. Enrollment began in September 2007 and lasted until December 2009, with a mean follow-up of 1.1 years.

During the study period, 51 primary outcome events (1.6% per year) occurred in the apixaban arm and 113 (3.7% per year) in the aspirin arm (HR, 0.45 with apixaban; P less than .001). The annual rate of death from any cause was 3.5% in the apixaban arm and 4.4% in the aspirin arm (HR, 0.79; P = .07). Episodes of major bleeding were 44 (1.4% per year) with apixaban and 39 (1.2% per year) with aspirin (HR, 1.13; P = .57). Intracranial bleeding occurred in 11 and 13 patients in each group (HR, 0.85; P = .69).

In February 2010, the data safety monitoring board recommended termination of the study based on results from an interim analysis showing apixaban to be superior to aspirin in reducing stroke and systemic embolism. Data collection continued through May 28, 2010.

Conversely, in November 2010, a separate manufacturer-sponsored phase III apixaban study (n = 10,848), comparing the same 5-mg twice-daily dose to placebo in patients with acute coronary syndrome, was stopped because of an increase in major bleeding events that was not offset, the manufacturer reported, by a decrease in ischemic events. Trials comparing apixaban 2.5 mg twice daily with low-molecular-weight heparin following knee (Lancet 2010;375:807-15) and hip (N. Engl. J. Med. 2010;363:2487-98) surgeries did not show significant differences in bleeding events.

Dr. Connolly disclosed serving as a paid board member and receiving consulting fees or institutional grant support from Boehringer Ingelheim, Sanofi, Merck, and Bristol-Myers Squibb, among other pharmaceutical firms; of his 31 coauthors, nearly a third disclosed direct or indirect support from Bristol-Myers Squibb or Pfizer, and one was an employee of Bristol-Myers Squibb.

The experimental drug apixaban has been shown to reduce the risk of stroke and systemic embolism by more than half, compared with aspirin, in people with atrial fibrillation who have failed or cannot take warfarin.

This effect was seen without a significant increase in the risk of major bleeding events, in a large randomized, placebo-controlled trial.

Findings from the study published online Feb. 10 in the New England Journal of Medicine (doi:10.1056/NEJMoa1007432) suggest that apixaban may be a safe alternative to vitamin K antagonists or clopidogrel and aspirin in this population.

Vitamin K antagonists such as warfarin can be problematic in people with atrial fibrillation, because of an unpredictable therapeutic effect and a need for frequent coagulation monitoring. The clopidogrel-aspirin combination reduces stroke risk but also increases major bleeding risk. Apixaban is a novel factor Xa inhibitor, part of a class of anticoagulant drugs developed from compounds identified in leeches and ticks.

For their research, funded by Bristol-Myers Squibb and Pfizer, which are jointly developing apixaban, Dr. Stuart J. Connolly of the Population Health Research Institute in Hamilton, Ont., and his colleagues conducted a study that comprised 5,599 patients aged 50 and older with atrial fibrillation who were at increased risk of stroke (determined as being age 75 or older, or having cardiovascular risk factors including diabetes, heart failure, or peripheral artery disease). The patients were randomized to receive a fixed dose of oral apixaban 5 mg or 2.5 mg, depending on age and body weight, twice daily (n = 2,808), or aspirin at a dose ranging from 81 to 324 mg/day (n = 2,791).

About 58% of study participants were men. Most of the aspirin subjects received doses of 162 mg or less, and the vast majority of the apixaban subjects received the higher dose. Forty percent of all participants had been treated previously with a vitamin K antagonist. The primary outcome of the trial was the occurrence of stroke or systemic embolism, and its primary safety outcome was the occurrence of major bleeding. Enrollment began in September 2007 and lasted until December 2009, with a mean follow-up of 1.1 years.

During the study period, 51 primary outcome events (1.6% per year) occurred in the apixaban arm and 113 (3.7% per year) in the aspirin arm (HR, 0.45 with apixaban; P less than .001). The annual rate of death from any cause was 3.5% in the apixaban arm and 4.4% in the aspirin arm (HR, 0.79; P = .07). Episodes of major bleeding were 44 (1.4% per year) with apixaban and 39 (1.2% per year) with aspirin (HR, 1.13; P = .57). Intracranial bleeding occurred in 11 and 13 patients in each group (HR, 0.85; P = .69).

In February 2010, the data safety monitoring board recommended termination of the study based on results from an interim analysis showing apixaban to be superior to aspirin in reducing stroke and systemic embolism. Data collection continued through May 28, 2010.

Conversely, in November 2010, a separate manufacturer-sponsored phase III apixaban study (n = 10,848), comparing the same 5-mg twice-daily dose to placebo in patients with acute coronary syndrome, was stopped because of an increase in major bleeding events that was not offset, the manufacturer reported, by a decrease in ischemic events. Trials comparing apixaban 2.5 mg twice daily with low-molecular-weight heparin following knee (Lancet 2010;375:807-15) and hip (N. Engl. J. Med. 2010;363:2487-98) surgeries did not show significant differences in bleeding events.

Dr. Connolly disclosed serving as a paid board member and receiving consulting fees or institutional grant support from Boehringer Ingelheim, Sanofi, Merck, and Bristol-Myers Squibb, among other pharmaceutical firms; of his 31 coauthors, nearly a third disclosed direct or indirect support from Bristol-Myers Squibb or Pfizer, and one was an employee of Bristol-Myers Squibb.

Nearly 1.3 million Europeans will die from cancer this year, according to epidemiologists who predict that age-standardized death rates for most cancers will have dropped or remained flat since 2007 with the exception of lung cancer in women.

Based on a close analysis of continuing trends in the European Union, an estimated 1,281,436 E.U. residents – 721,252 men and 560,184 women of all ages – will die of cancer in 2011, they said. Overall, E.U. cancer deaths have will have dropped 7% in men and 6% in women over 5 years, from 153.8 per 100,000 to 142.8 per 100,000 in men, and from 90.7 to 85.3 in women, they say – a continuation of longer-term patterns of decline.

For their research, published Feb. 9 in Annals of Oncology (Annals Oncol. 2011 Feb. 9 [doi:10.1093/annonc/mdq774]), epidemiologist Dr. Carlo La Vecchia of the University of Milan, along with Dr. Fabio Levi of Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland, and colleagues, examined World Health Organization mortality records to identify deaths from stomach, colorectal, pancreatic, lung, breast, uterine, cervical, and prostate cancers, along with leukemia deaths and total cancer deaths, for all EU countries besides Cyprus between 1970 and 2007.

They also used the most recent national cancer-death data available (the oldest from 2005 and the newest from 2008) for France, Germany, Italy, Poland, Spain, and the United Kingdom, Europe’s six most populous countries.

Dr. La Vecchia, Dr. Levi, and colleagues identified a downward trend in mortality for all cancers studied, except for pancreatic cancer, which was predicted to remain flat for men and increase very slightly among women in 2011, they said. They also noted that the one former Eastern bloc country, Poland, among the six populous countries studied, had higher overall death rates and less impressive declines than did the others. For example, estimated mortality rates for uterine cancer in Poland were three times higher than those projected for Germany: 7.9 and 2.6 per 100,000 women, respectively.

The European patterns reported stand in contrast to new global trends published in a Feb 4 report by the American Cancer Society (Global Cancer Facts & Figures 2nd Edition), which highlights an increasing portion of cancer deaths in developing countries attributable to lifestyle changes such as smoking, unhealthy diet, and physical inactivity as opposed to infections such as hepatitis B virus (HBV), human immunodeficiency virus, human papillomavirus, and helicobacter pylori. For example, male lung cancer mortality, which is declining in Europe, has been increasing in China and other countries in Asia and Africa. And breast cancer (likely reflective of changes in reproductive patterns, obesity, physical inactivity, and delayed breast cancer screening) now leads in cancer deaths among women in developing countries, as opposed to cervical cancer, according to the ACS report.

Yet even within Europe, divides persist along national and economic lines. In a report presented to the European Parliament Feb. 9 by the European Society for Pediatric Oncology, investigators found that Eastern European countries with a heavy oncology burden tended not to collaborate in research with countries with better-developed research structures, and that pediatric cancer patients suffered as a result.

Dr. La Vecchia said in an interview that Poland’s high mortality, related to drug access and quality of treatment, was representative of other former Eastern bloc countries in the European Union. "It’s a complex problem of medical culture and organization," he said. "All central and eastern Europe countries have this problem, but there is room of improvement even in the wealthier countries."

Female lung cancer was one area that needed desperate attention throughout the European Union, Dr. La Vecchia said. While deaths from breast cancer in women are likely to continue to fall, the trend in female lung cancer deaths is rising everywhere but the United Kingdom, which at 20.33 per 100,000 women still has the highest female lung cancer mortality in the European Union, followed by Poland at 16.6 per 100,000. In both countries, more women will die from lung cancer than from breast cancer in 2011, the investigators predicted.

Overall, lung cancer deaths among E.U. women will increase from 12.55 per 100,000 in 2007 to 13.12 in 2011, the investigators predicted, while rates among men have fallen. "This suggests that the lung cancer epidemic in European women is still expanding, and the rate may ultimately approach 14 to 15 per 100,000 in 2015," the investigators wrote.

"This is essentially attributable to smoking," Dr. La Vecchia said. Bans on indoor smoking are now widespread in Western Europe, but "these have only been adopted over the last 5 years, so while you see some impact on cardiovascular disease, you don’t see any important change in cancer yet in the short term." Women, he said, are simply not quitting fast enough: "We need to concentrate on convincing women to stop smoking."

The investigators noted in their analysis that among the study’s weaknesses was the fact that its predictions were short term and could be affected by unexpected events. Also, they wrote, "These predictions are based on the most recent trends in available data." However, "if a change, or even a reversal of trends, has taken place in the last 2 or 3 years," they cautioned, the regression model would not have picked it up.

The study by Dr. La Vecchia, Dr. Levi, and colleagues was funded by the Swiss Cancer League and the Italian Association for Cancer Research. The authors reported having no conflicts of interest.

Nearly 1.3 million Europeans will die from cancer this year, according to epidemiologists who predict that age-standardized death rates for most cancers will have dropped or remained flat since 2007 with the exception of lung cancer in women.

Based on a close analysis of continuing trends in the European Union, an estimated 1,281,436 E.U. residents – 721,252 men and 560,184 women of all ages – will die of cancer in 2011, they said. Overall, E.U. cancer deaths have will have dropped 7% in men and 6% in women over 5 years, from 153.8 per 100,000 to 142.8 per 100,000 in men, and from 90.7 to 85.3 in women, they say – a continuation of longer-term patterns of decline.

For their research, published Feb. 9 in Annals of Oncology (Annals Oncol. 2011 Feb. 9 [doi:10.1093/annonc/mdq774]), epidemiologist Dr. Carlo La Vecchia of the University of Milan, along with Dr. Fabio Levi of Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland, and colleagues, examined World Health Organization mortality records to identify deaths from stomach, colorectal, pancreatic, lung, breast, uterine, cervical, and prostate cancers, along with leukemia deaths and total cancer deaths, for all EU countries besides Cyprus between 1970 and 2007.

They also used the most recent national cancer-death data available (the oldest from 2005 and the newest from 2008) for France, Germany, Italy, Poland, Spain, and the United Kingdom, Europe’s six most populous countries.

Dr. La Vecchia, Dr. Levi, and colleagues identified a downward trend in mortality for all cancers studied, except for pancreatic cancer, which was predicted to remain flat for men and increase very slightly among women in 2011, they said. They also noted that the one former Eastern bloc country, Poland, among the six populous countries studied, had higher overall death rates and less impressive declines than did the others. For example, estimated mortality rates for uterine cancer in Poland were three times higher than those projected for Germany: 7.9 and 2.6 per 100,000 women, respectively.

The European patterns reported stand in contrast to new global trends published in a Feb 4 report by the American Cancer Society (Global Cancer Facts & Figures 2nd Edition), which highlights an increasing portion of cancer deaths in developing countries attributable to lifestyle changes such as smoking, unhealthy diet, and physical inactivity as opposed to infections such as hepatitis B virus (HBV), human immunodeficiency virus, human papillomavirus, and helicobacter pylori. For example, male lung cancer mortality, which is declining in Europe, has been increasing in China and other countries in Asia and Africa. And breast cancer (likely reflective of changes in reproductive patterns, obesity, physical inactivity, and delayed breast cancer screening) now leads in cancer deaths among women in developing countries, as opposed to cervical cancer, according to the ACS report.

Yet even within Europe, divides persist along national and economic lines. In a report presented to the European Parliament Feb. 9 by the European Society for Pediatric Oncology, investigators found that Eastern European countries with a heavy oncology burden tended not to collaborate in research with countries with better-developed research structures, and that pediatric cancer patients suffered as a result.

Dr. La Vecchia said in an interview that Poland’s high mortality, related to drug access and quality of treatment, was representative of other former Eastern bloc countries in the European Union. "It’s a complex problem of medical culture and organization," he said. "All central and eastern Europe countries have this problem, but there is room of improvement even in the wealthier countries."

Female lung cancer was one area that needed desperate attention throughout the European Union, Dr. La Vecchia said. While deaths from breast cancer in women are likely to continue to fall, the trend in female lung cancer deaths is rising everywhere but the United Kingdom, which at 20.33 per 100,000 women still has the highest female lung cancer mortality in the European Union, followed by Poland at 16.6 per 100,000. In both countries, more women will die from lung cancer than from breast cancer in 2011, the investigators predicted.

Overall, lung cancer deaths among E.U. women will increase from 12.55 per 100,000 in 2007 to 13.12 in 2011, the investigators predicted, while rates among men have fallen. "This suggests that the lung cancer epidemic in European women is still expanding, and the rate may ultimately approach 14 to 15 per 100,000 in 2015," the investigators wrote.

"This is essentially attributable to smoking," Dr. La Vecchia said. Bans on indoor smoking are now widespread in Western Europe, but "these have only been adopted over the last 5 years, so while you see some impact on cardiovascular disease, you don’t see any important change in cancer yet in the short term." Women, he said, are simply not quitting fast enough: "We need to concentrate on convincing women to stop smoking."

The investigators noted in their analysis that among the study’s weaknesses was the fact that its predictions were short term and could be affected by unexpected events. Also, they wrote, "These predictions are based on the most recent trends in available data." However, "if a change, or even a reversal of trends, has taken place in the last 2 or 3 years," they cautioned, the regression model would not have picked it up.

The study by Dr. La Vecchia, Dr. Levi, and colleagues was funded by the Swiss Cancer League and the Italian Association for Cancer Research. The authors reported having no conflicts of interest.

Nearly 1.3 million Europeans will die from cancer this year, according to epidemiologists who predict that age-standardized death rates for most cancers will have dropped or remained flat since 2007 with the exception of lung cancer in women.

Based on a close analysis of continuing trends in the European Union, an estimated 1,281,436 E.U. residents – 721,252 men and 560,184 women of all ages – will die of cancer in 2011, they said. Overall, E.U. cancer deaths have will have dropped 7% in men and 6% in women over 5 years, from 153.8 per 100,000 to 142.8 per 100,000 in men, and from 90.7 to 85.3 in women, they say – a continuation of longer-term patterns of decline.

For their research, published Feb. 9 in Annals of Oncology (Annals Oncol. 2011 Feb. 9 [doi:10.1093/annonc/mdq774]), epidemiologist Dr. Carlo La Vecchia of the University of Milan, along with Dr. Fabio Levi of Centre Hospitalier Universitaire Vaudois and University of Lausanne, Switzerland, and colleagues, examined World Health Organization mortality records to identify deaths from stomach, colorectal, pancreatic, lung, breast, uterine, cervical, and prostate cancers, along with leukemia deaths and total cancer deaths, for all EU countries besides Cyprus between 1970 and 2007.

They also used the most recent national cancer-death data available (the oldest from 2005 and the newest from 2008) for France, Germany, Italy, Poland, Spain, and the United Kingdom, Europe’s six most populous countries.

Dr. La Vecchia, Dr. Levi, and colleagues identified a downward trend in mortality for all cancers studied, except for pancreatic cancer, which was predicted to remain flat for men and increase very slightly among women in 2011, they said. They also noted that the one former Eastern bloc country, Poland, among the six populous countries studied, had higher overall death rates and less impressive declines than did the others. For example, estimated mortality rates for uterine cancer in Poland were three times higher than those projected for Germany: 7.9 and 2.6 per 100,000 women, respectively.

The European patterns reported stand in contrast to new global trends published in a Feb 4 report by the American Cancer Society (Global Cancer Facts & Figures 2nd Edition), which highlights an increasing portion of cancer deaths in developing countries attributable to lifestyle changes such as smoking, unhealthy diet, and physical inactivity as opposed to infections such as hepatitis B virus (HBV), human immunodeficiency virus, human papillomavirus, and helicobacter pylori. For example, male lung cancer mortality, which is declining in Europe, has been increasing in China and other countries in Asia and Africa. And breast cancer (likely reflective of changes in reproductive patterns, obesity, physical inactivity, and delayed breast cancer screening) now leads in cancer deaths among women in developing countries, as opposed to cervical cancer, according to the ACS report.

Yet even within Europe, divides persist along national and economic lines. In a report presented to the European Parliament Feb. 9 by the European Society for Pediatric Oncology, investigators found that Eastern European countries with a heavy oncology burden tended not to collaborate in research with countries with better-developed research structures, and that pediatric cancer patients suffered as a result.

Dr. La Vecchia said in an interview that Poland’s high mortality, related to drug access and quality of treatment, was representative of other former Eastern bloc countries in the European Union. "It’s a complex problem of medical culture and organization," he said. "All central and eastern Europe countries have this problem, but there is room of improvement even in the wealthier countries."

Female lung cancer was one area that needed desperate attention throughout the European Union, Dr. La Vecchia said. While deaths from breast cancer in women are likely to continue to fall, the trend in female lung cancer deaths is rising everywhere but the United Kingdom, which at 20.33 per 100,000 women still has the highest female lung cancer mortality in the European Union, followed by Poland at 16.6 per 100,000. In both countries, more women will die from lung cancer than from breast cancer in 2011, the investigators predicted.

Overall, lung cancer deaths among E.U. women will increase from 12.55 per 100,000 in 2007 to 13.12 in 2011, the investigators predicted, while rates among men have fallen. "This suggests that the lung cancer epidemic in European women is still expanding, and the rate may ultimately approach 14 to 15 per 100,000 in 2015," the investigators wrote.

"This is essentially attributable to smoking," Dr. La Vecchia said. Bans on indoor smoking are now widespread in Western Europe, but "these have only been adopted over the last 5 years, so while you see some impact on cardiovascular disease, you don’t see any important change in cancer yet in the short term." Women, he said, are simply not quitting fast enough: "We need to concentrate on convincing women to stop smoking."

The investigators noted in their analysis that among the study’s weaknesses was the fact that its predictions were short term and could be affected by unexpected events. Also, they wrote, "These predictions are based on the most recent trends in available data." However, "if a change, or even a reversal of trends, has taken place in the last 2 or 3 years," they cautioned, the regression model would not have picked it up.

The study by Dr. La Vecchia, Dr. Levi, and colleagues was funded by the Swiss Cancer League and the Italian Association for Cancer Research. The authors reported having no conflicts of interest.