Naturopath Sentenced For Injecting Teen With Hydrogen Peroxide
O'Connell To Spend 13 Years In Prison
March 27, 2006
GOLDEN, Colo. -- The so-called holistic doctor who pleaded guilty in the death of a patient was sentenced Monday to 13 years in prison after a judge told him he had shown no remorse over the death of a 19-year-old cancer victim he was treating.
http://www.blogger.com/img/blank.gif
Brian O'Connell admitted last month to criminally negligent homicide for injecting 19-year-old Sean Flanagan with hydrogen peroxide. Flanagan suffered from Ewing's Sarcoma, a form of cancer, and had tried chemotherapy and radiation treatment to no avail.
Flanagan's family sent him to O'Connell, who practices using natural remedies. However, the family said that Flanagan died prematurely in 2003 because of O'Connell's treatments.
In court on Monday, O'Connell asked Jefferson County District Judge Margie Enquist for leniency, saying he didn't know what he was doing was wrong. He said he had changed and regretted Flanagan's death.
Enquist told O'Connell she didn't believe him, and sentenced him to just two years less than the maximum.
"You stand here today without remorse, without regret, and denying what you pled guilty to, and you still call yourself a victim," she said.
Flanagan's parents, Laura and David Flanagan, said the sentence was fair.
O'Connell showed no emotion when Enquist announced the sentence, but his wife, seated in the front row of the gallery, wept.
Defense attorney Richard Jaffe said no appeal was likely, but he said people who would have sought care from O'Connell were also victims.
"There are victims on the other side too that can't get treatment now," he said.
Jaffe presented about a dozen witnesses during the sentencing hearing who said O'Connell helped them fight conditions that did not respond to traditional medicine.
In February, O'Connell also admitted guilt to theft, perjury, criminally negligent homicide, illegal practice of medicine and third-degree assault.
O'Connell was in charge of Mountain Area Naturopathic Associates in Wheat Ridge. In his office he displayed numerous degrees and certifications claiming he was doctor and a naturopath. The Colorado Medical Board found that he had no license to practice medicine in Colorado and was not certified as any kind of health care worker.
O'Connell was treating Flanagan with a procedure known as ultraviolet blood irradiation, where his blood was removed from the body, passed under an ultraviolet light and then returned to the body. When he didn't respond well to that, O'Connell then treated Flanagan by injecting his blood with hydrogen peroxide. The next day he died.
Prosecutors argued that Flanagan's cause of death was listed as probable complications from the hydrogen peroxide treatment.
O'Connell also injected this hydrogen peroxide solution into a 17-year-old girl, which caused her to go into cardiac arrest...
Saturday, July 9, 2011
Wednesday, July 6, 2011
The hygiene hypothesis
The hygiene hypothesis
It suggests lack of early exposure to infectious agents can suppress development of the immune system
By Dr. Richard L. Gallo
Jan. 31, 2011
In 1998, researchers at the University of Georgia published a paperhttp://www.blogger.com/img/blank.gif that estimated about 5 million trillion bacterial cells reside on Earth. That’s a 5 with 30 zeros. That’s a lot of bacteria. Indeed, if each individual bacterium were a penny piled atop one another, it would take a trillion light-years to reach the end of the stack, which is far beyond the observable universe.
Some of these bacteria, Louis Pasteur and others duly discovered, cause disease, and so contemporary humans have long been urged, explicitly and otherwise, to fight back: Wash often. Stay clean. And don’t skimp on those alcohol-based hand-sanitizing gels, foams and lotions that reportedly kill 99 percent of all germs. Odds are there’s a dispenser near you right now.
But is cleanliness really next to goodliness?
Maybe not. There is compelling, growing evidence that being too clean might actually be bad for your health; that it results in increased sickness and the development of chronic immunological ailments that might not occur if we all dialed back on the Dial and dispensers.
This thinking is encapsulated in an idea called “the hygiene hypothesis,” which first emerged in the late-1980s. The hypothesis suggests that a lack of early childhood exposure to infectious agents and microorganisms (not just bacteria, but viruses and fungi, too) suppresses natural development of the immune system, resulting in increased susceptibility to infection and disease.
The hypothesis has been used to help explain why allergies like hay fever are less common in children from large families, even though presumably these kids are exposed to more infectious agents than those in smaller families. Epidemiologists have also noted that ailments like asthma and eczema (a kind of skin inflammation) are more prevalent in industrialized countries where personal cleanliness is emphasized.
Though not conclusively proved, the hypothesis makes sense — at least as part of a larger explanation. Let’s look at the science.
One’s a crowd
If the world is fraught with bacteria, so too are you. Based solely on the average number of cells in a typical human being, we’re all more inhuman than human. Bacterial cells outnumber human cells 10 to 1. Your gut, for example, is a well-known bacterial repository, home to hundreds of trillions of individual microbes (somewhere between 300 and 1,000 species), many of which beneficially assist in necessary functions like digestion and immune response. Plus, they take up space that might otherwise be occupied by nastier, disease-causing pathogens.
Your skin is similarly populated. Recent studies have identified hundreds of species, many previously unknown. One estimate calculates the total number of skin-based bacteria on the average person at roughly 1,000,000,000,000. These bacteria live in colonies, each favoring a different environmental niche. The bacteria that prefer the crook of your elbow, for example, are different from those homesteading your forearm.
Swathed in our cloaks of microbial invisibility, some questions are nonetheless obvious: How do skin bacteria survive our constant assaults with soaps and antibiotics? And why don’t they make us sick more often?
In research published this year and last, my colleagues and I uncovered some of the answers. Our skin hums with constant communication and interaction between commensal or benign bacteria and skin cells. Certain species of superabundant Staphylococcus bacteria, for example, produce a molecule that inhibits the inflammation response (heat, redness, swelling) generated when you injure your skin. That’s a good thing. Some inflammation is vital to healing, but too much can be worse than the infection.
Why do Staphylococci do this? It’s hard to know for sure, but one possibility is that it’s an evolutionary adaptation, a neat trick bacteria have developed to reduce the chances that an inflammatory response will kill them. Another possibility is that we have evolved together and count on these bacteria to help us control the skin response. In return for this microbial good deed, we reward specific bacteria with a comfortable place to live.
Recently, we discovered that a specific type of Staphylococci — Staphylococcus epidermidis, the most common bacterial species cultured from human skin — produces antimicrobial molecules that kill some other kinds of bacteria, including its cousin, S. aureus, a more problematic bug that causes everything from pimples and boils to deadly pneumonia, meningitis and sepsis.
S. epidermidis not only makes antimicrobials, it also instructs human skin cells to make natural antimicrobials of their own, thus serving as both warning system and mentor. The result is a balanced relationship that benefits both human hosts and our commensal bacterial buddies.
Scorched skin policy
Overuse of antibiotic soaps and hand sanitizers upsets this happy homeostasis by essentially killing all bacteria, good and bad. The consequence of this scorched skin policy is that we kill the germs that sometimes contaminate our skin and make disease transmission more difficult, but also reduce the effectiveness of our skin’s antimicrobial defenses.
Wiping out all microbes means your skin is wide open to recolonization by all comers — commensals and pathogens. It may be a tossup which returns first and faster. Excessive cleanliness also removes natural oils that help keep skin supple and intact. Dry skin is more prone to cracking, which provides new entry points for bacteria and other agents. Some bacterial species that are harmless resting atop your skin are troublemakers inside it.
Of course, no one’s suggesting we abandon antimicrobial soaps, gels and lotions. In some situations and circumstances, such as hospitals and health care, they are essential. Every effort must be made to reduce exposure to pathogens. More broadly, people should continue to wash their hands regularly and diligently. (There’s an ongoing debate about whether daily washing beyond the wrists is necessary, but that’s a different story.)
As always, nature suggests a solution, albeit one that first requires us to more fully understand the complicated relationships between microbes and our health. Rather than regularly render our skin a sort of microbial dead zone, we could develop soaps and sanitizers that are more discriminating or which include ingredients that promote the return of bacteria like S. epidermidis or deter the development of conditions like eczema. We do a little bit of that now with soaps and lotions that contain compounds designed to help skin retain its oils and moisture.
Someday you might slather up with something that selectively kills and fertilizes, encouraging certain microbial species to take root and call you home, thus restoring balance to our natural ecology.
Richard L. Gallo, M.D., Ph.D., is a professor of medicine and pediatrics and chief of UC San Diego’s Division of Dermatology and the dermatology section of the Veterans Affairs San Diego Healthcare System.
It suggests lack of early exposure to infectious agents can suppress development of the immune system
By Dr. Richard L. Gallo
Jan. 31, 2011
In 1998, researchers at the University of Georgia published a paperhttp://www.blogger.com/img/blank.gif that estimated about 5 million trillion bacterial cells reside on Earth. That’s a 5 with 30 zeros. That’s a lot of bacteria. Indeed, if each individual bacterium were a penny piled atop one another, it would take a trillion light-years to reach the end of the stack, which is far beyond the observable universe.
Some of these bacteria, Louis Pasteur and others duly discovered, cause disease, and so contemporary humans have long been urged, explicitly and otherwise, to fight back: Wash often. Stay clean. And don’t skimp on those alcohol-based hand-sanitizing gels, foams and lotions that reportedly kill 99 percent of all germs. Odds are there’s a dispenser near you right now.
But is cleanliness really next to goodliness?
Maybe not. There is compelling, growing evidence that being too clean might actually be bad for your health; that it results in increased sickness and the development of chronic immunological ailments that might not occur if we all dialed back on the Dial and dispensers.
This thinking is encapsulated in an idea called “the hygiene hypothesis,” which first emerged in the late-1980s. The hypothesis suggests that a lack of early childhood exposure to infectious agents and microorganisms (not just bacteria, but viruses and fungi, too) suppresses natural development of the immune system, resulting in increased susceptibility to infection and disease.
The hypothesis has been used to help explain why allergies like hay fever are less common in children from large families, even though presumably these kids are exposed to more infectious agents than those in smaller families. Epidemiologists have also noted that ailments like asthma and eczema (a kind of skin inflammation) are more prevalent in industrialized countries where personal cleanliness is emphasized.
Though not conclusively proved, the hypothesis makes sense — at least as part of a larger explanation. Let’s look at the science.
One’s a crowd
If the world is fraught with bacteria, so too are you. Based solely on the average number of cells in a typical human being, we’re all more inhuman than human. Bacterial cells outnumber human cells 10 to 1. Your gut, for example, is a well-known bacterial repository, home to hundreds of trillions of individual microbes (somewhere between 300 and 1,000 species), many of which beneficially assist in necessary functions like digestion and immune response. Plus, they take up space that might otherwise be occupied by nastier, disease-causing pathogens.
Your skin is similarly populated. Recent studies have identified hundreds of species, many previously unknown. One estimate calculates the total number of skin-based bacteria on the average person at roughly 1,000,000,000,000. These bacteria live in colonies, each favoring a different environmental niche. The bacteria that prefer the crook of your elbow, for example, are different from those homesteading your forearm.
Swathed in our cloaks of microbial invisibility, some questions are nonetheless obvious: How do skin bacteria survive our constant assaults with soaps and antibiotics? And why don’t they make us sick more often?
In research published this year and last, my colleagues and I uncovered some of the answers. Our skin hums with constant communication and interaction between commensal or benign bacteria and skin cells. Certain species of superabundant Staphylococcus bacteria, for example, produce a molecule that inhibits the inflammation response (heat, redness, swelling) generated when you injure your skin. That’s a good thing. Some inflammation is vital to healing, but too much can be worse than the infection.
Why do Staphylococci do this? It’s hard to know for sure, but one possibility is that it’s an evolutionary adaptation, a neat trick bacteria have developed to reduce the chances that an inflammatory response will kill them. Another possibility is that we have evolved together and count on these bacteria to help us control the skin response. In return for this microbial good deed, we reward specific bacteria with a comfortable place to live.
Recently, we discovered that a specific type of Staphylococci — Staphylococcus epidermidis, the most common bacterial species cultured from human skin — produces antimicrobial molecules that kill some other kinds of bacteria, including its cousin, S. aureus, a more problematic bug that causes everything from pimples and boils to deadly pneumonia, meningitis and sepsis.
S. epidermidis not only makes antimicrobials, it also instructs human skin cells to make natural antimicrobials of their own, thus serving as both warning system and mentor. The result is a balanced relationship that benefits both human hosts and our commensal bacterial buddies.
Scorched skin policy
Overuse of antibiotic soaps and hand sanitizers upsets this happy homeostasis by essentially killing all bacteria, good and bad. The consequence of this scorched skin policy is that we kill the germs that sometimes contaminate our skin and make disease transmission more difficult, but also reduce the effectiveness of our skin’s antimicrobial defenses.
Wiping out all microbes means your skin is wide open to recolonization by all comers — commensals and pathogens. It may be a tossup which returns first and faster. Excessive cleanliness also removes natural oils that help keep skin supple and intact. Dry skin is more prone to cracking, which provides new entry points for bacteria and other agents. Some bacterial species that are harmless resting atop your skin are troublemakers inside it.
Of course, no one’s suggesting we abandon antimicrobial soaps, gels and lotions. In some situations and circumstances, such as hospitals and health care, they are essential. Every effort must be made to reduce exposure to pathogens. More broadly, people should continue to wash their hands regularly and diligently. (There’s an ongoing debate about whether daily washing beyond the wrists is necessary, but that’s a different story.)
As always, nature suggests a solution, albeit one that first requires us to more fully understand the complicated relationships between microbes and our health. Rather than regularly render our skin a sort of microbial dead zone, we could develop soaps and sanitizers that are more discriminating or which include ingredients that promote the return of bacteria like S. epidermidis or deter the development of conditions like eczema. We do a little bit of that now with soaps and lotions that contain compounds designed to help skin retain its oils and moisture.
Someday you might slather up with something that selectively kills and fertilizes, encouraging certain microbial species to take root and call you home, thus restoring balance to our natural ecology.
Richard L. Gallo, M.D., Ph.D., is a professor of medicine and pediatrics and chief of UC San Diego’s Division of Dermatology and the dermatology section of the Veterans Affairs San Diego Healthcare System.
Thursday, May 5, 2011
New drugs often marketed ahead of crucial data
Data that could save money and help doctors make smarter treatment decisions are often unavailable at the time new medicines hit the market, according to U.S. researchers.
New drugs often marketed ahead of crucial data
By Frederik Joelving
May 4, 2011
NEW YORK (Reuters Health) - Data that could save money and help doctors make smarter treatment decisions are often unavailable at the time new medicines hit the market, according to U.S. researchers.
In a study out Tuesday, they found nearly a third of new drug approvals from the Food and Drug Administration included no data on how well the medications compare with existing alternatives.
"Even when these things are accessible, it's hugely time-consuming to go through it," said Joshua Gagne, a pharmacist at Harvard Medical School in Boston.
That leaves insurers and healthcare providers at a loss when trying to find the best and cheapest drugs for their patients, Gagne, who led the new work, told Reuters Health.
In 2009, Congress earmarked $1.1 billion to support drug comparison research, which would help doctors choose between various drugs.
But that information is unlikely to appear until years after new medicines reach the market, because drugmakers only need to show their products work better than a sugar pill -- not how they compare to existing treatments.
"There is a gap between the time the drug hits the market and the time this information is generated," Gagne said.
With his colleagues, he went through public FDA data for 197 drugs approved between 2000 and 2010.
After excluding medications for diseases with no alternative treatments, 70 percent of the FDA approval packages contained some data on how the new products compared to existing ones.
Experts who spoke with Reuters Health were split in their reaction to the new study, published in the Journal of the American Medical Association.
Dr. Robert Temple, who directs FDA's Office of Medical Policy at the Center for Drug Evaluation and Research, said he was surprised by how many drugmakers had provided some comparative data, despite not being required to do so.
"Considering that there is absolutely no requirement, it is pretty impressive," he said in a phone interview.
Another expert took the opposite view.
"A third of new drugs that are approved have no comparative data at all," said Dr. Alec B. O'Connor of the University of Rochester School of Medicine and Dentistry in New York. "I think we'd all say that is sad."
He said he believes new drugs should always be tested against those already approved to treat a given disease.
In an earlier study, O'Connor had tried to compare the cost-effectiveness of different painkillers. But that turned out to be next to impossible, because almost no researchers had tested the drugs head-to-head.
"When a new drug becomes available, if it's not compared with a drug we already use, we don't know if it is better or worse -- we're just guessing. If you're a patient, I don't think you would want your doctor to be guessing," he told Reuters Health.
"You could save a lot of money if you had better comparative data at the time of approval," he added. "It's a win-win for patients, for doctors and for societal costs."
Meanwhile, Gagne and his team say the comparative FDA data, when it exists, should be made more accessible.
But according to an e-mail from Temple, of the FDA, that is not without problems.
"Comparative data are often too limited to allow a firm conclusion about comparative effectiveness (the size of studies that would be needed to rule out a small difference is usually daunting)," he told Reuters Health. "FDA would not want to suggest that a small study showing no difference between two treatments 'proves' equivalence, when the data fall well short of such proof."
SOURCE: bit.ly/j8dJ7p Journal of the American Medical Association, May 4, 2011.
New drugs often marketed ahead of crucial data
By Frederik Joelving
May 4, 2011
NEW YORK (Reuters Health) - Data that could save money and help doctors make smarter treatment decisions are often unavailable at the time new medicines hit the market, according to U.S. researchers.
In a study out Tuesday, they found nearly a third of new drug approvals from the Food and Drug Administration included no data on how well the medications compare with existing alternatives.
"Even when these things are accessible, it's hugely time-consuming to go through it," said Joshua Gagne, a pharmacist at Harvard Medical School in Boston.
That leaves insurers and healthcare providers at a loss when trying to find the best and cheapest drugs for their patients, Gagne, who led the new work, told Reuters Health.
In 2009, Congress earmarked $1.1 billion to support drug comparison research, which would help doctors choose between various drugs.
But that information is unlikely to appear until years after new medicines reach the market, because drugmakers only need to show their products work better than a sugar pill -- not how they compare to existing treatments.
"There is a gap between the time the drug hits the market and the time this information is generated," Gagne said.
With his colleagues, he went through public FDA data for 197 drugs approved between 2000 and 2010.
After excluding medications for diseases with no alternative treatments, 70 percent of the FDA approval packages contained some data on how the new products compared to existing ones.
Experts who spoke with Reuters Health were split in their reaction to the new study, published in the Journal of the American Medical Association.
Dr. Robert Temple, who directs FDA's Office of Medical Policy at the Center for Drug Evaluation and Research, said he was surprised by how many drugmakers had provided some comparative data, despite not being required to do so.
"Considering that there is absolutely no requirement, it is pretty impressive," he said in a phone interview.
Another expert took the opposite view.
"A third of new drugs that are approved have no comparative data at all," said Dr. Alec B. O'Connor of the University of Rochester School of Medicine and Dentistry in New York. "I think we'd all say that is sad."
He said he believes new drugs should always be tested against those already approved to treat a given disease.
In an earlier study, O'Connor had tried to compare the cost-effectiveness of different painkillers. But that turned out to be next to impossible, because almost no researchers had tested the drugs head-to-head.
"When a new drug becomes available, if it's not compared with a drug we already use, we don't know if it is better or worse -- we're just guessing. If you're a patient, I don't think you would want your doctor to be guessing," he told Reuters Health.
"You could save a lot of money if you had better comparative data at the time of approval," he added. "It's a win-win for patients, for doctors and for societal costs."
Meanwhile, Gagne and his team say the comparative FDA data, when it exists, should be made more accessible.
But according to an e-mail from Temple, of the FDA, that is not without problems.
"Comparative data are often too limited to allow a firm conclusion about comparative effectiveness (the size of studies that would be needed to rule out a small difference is usually daunting)," he told Reuters Health. "FDA would not want to suggest that a small study showing no difference between two treatments 'proves' equivalence, when the data fall well short of such proof."
SOURCE: bit.ly/j8dJ7p Journal of the American Medical Association, May 4, 2011.
Friday, April 29, 2011
$50 eye drug found equal to $2,000 dose
$50 eye drug found equal to $2,000 dose
Study may alter patient choices
By Deborah Kotz
Boston Globe
April 29, 2011
An expensive eye injection that’s approved to treat macular degeneration — the most common cause of age-related blindness — works no better than a much cheaper drug at preventing vision loss. That’s the finding of a long-awaited study published online yesterday by the New England Journal of Medicine.
The study, involving more than 1,200 patients with the “wet’’ form of macular degeneration, found no difference between those who were randomly treated for one year with the more expensive drug Lucentis — which costs about $2,000 a dose — and the cheaper drug Avastin, which costs $50.
“Lucentis and Avastin were equivalent for visual acuity,’’ said study leader Dr. Daniel Martin, chair of ophthalmology at the Cleveland Clinic Cole Eye Institute during a press conference. “When we looked at the number of letters gained or lost on an eye chart, the lost or gained lines of vision, the two drugs are virtually identical.’’
For about five years, doctors have been treating most macular degeneration patients “off-label’’ with Avastin (bevacizumab), which is primarily a cancer treatment, since it’s chemically similar to Lucentis (ranibizumab). (They use a fraction of the dose given cancer patients.) But there was always uncertainty as to whether it was just as safe and effective. Experts say the new study indicates that it is...
Study may alter patient choices
By Deborah Kotz
Boston Globe
April 29, 2011
An expensive eye injection that’s approved to treat macular degeneration — the most common cause of age-related blindness — works no better than a much cheaper drug at preventing vision loss. That’s the finding of a long-awaited study published online yesterday by the New England Journal of Medicine.
The study, involving more than 1,200 patients with the “wet’’ form of macular degeneration, found no difference between those who were randomly treated for one year with the more expensive drug Lucentis — which costs about $2,000 a dose — and the cheaper drug Avastin, which costs $50.
“Lucentis and Avastin were equivalent for visual acuity,’’ said study leader Dr. Daniel Martin, chair of ophthalmology at the Cleveland Clinic Cole Eye Institute during a press conference. “When we looked at the number of letters gained or lost on an eye chart, the lost or gained lines of vision, the two drugs are virtually identical.’’
For about five years, doctors have been treating most macular degeneration patients “off-label’’ with Avastin (bevacizumab), which is primarily a cancer treatment, since it’s chemically similar to Lucentis (ranibizumab). (They use a fraction of the dose given cancer patients.) But there was always uncertainty as to whether it was just as safe and effective. Experts say the new study indicates that it is...
Monday, April 18, 2011
ACS President Resigns Over Controversial Editorial
ACS President Resigns Over Controversial Editorial
By Emily P. Walker
MedPage Today
April 18, 2011
The president-elect of the American College of Surgeons has resigned in light of backlash over an editorial he penned on the mood-enhancing effects semen has on women,
The ACS announced the resignation of Lazar Greenfield, MD, in an email sent to its members on Sunday.
In the article, Greenfield, an emeritus professor of surgery at the University of Michigan, cited research from the Archives of Sexual Behavior and wrote, "Female college students having unprotected sex were significantly less depressed than were those whose partners used condoms."
The article offended many in the surgeons' group, and some said it was sexist and perpetuates the boys club mentality of surgery.
Greenfield expressed his "deep regret" and then his resignation to the group's Board of Regents, which met Sunday to consider the status of the 78-year-old surgeon.
Writing in the Valentine's Day editorial, which was published in Surgery News -- and has since been retracted -- Greenfield discussed research that suggests semen includes mood enhancers including oxytocin and serotonin (and a sleep enhancer, melatonin).
He concluded: "So there's a deeper bond between men and women than St. Valentine would have suspected, and now we know there's a better gift for that day than chocolates."
The ACS received "numerous communications from the surgical community about the editorial," wrote the group's president, L. D. Britt, MD, along with Carlos Pellegrini, MD, chairman of the Board of Regents, and David Hoyt, MD, executive director.
At least one female ACS member, Colleen Brophy, MD, a professor of surgery at Vanderbilt University, resigned from the ACS over the editorial.
Writing in a letter to the Board, Brophy said the editorial is "just a symptom of a bigger issue," and that that college needs to be more transparent in choosing its leaders and conducting business.
"The fact that Dr. Greenfield apologized for me, for my 'taking offense' to his op ed without any insight into the implications that a physician leader advocated for unprotected sex, disturbs me," she wrote.
In a brief email to MedPage Today, Greenfield dismissed the claim that his editorial pointed to a larger sexist culture in surgery.
ACS officials acknowledged the contributions of Greenfield, including his invention of the "Greenfield Filter" a device placed in the inferior vena cava of patients who are particularly vulnerable to pulmonary embolism, to prevent venous emboli from entering the pulmonary circulation.
"We wish to honor Dr. Greenfield and celebrate his inestimable contributions to the College and the surgical community," the ACS officials wrote. "We also know that at this critical juncture for surgery and health care in America, it is important that the American College of Surgeons not be distracted by any issues that would diminish its focus on improving care of the surgical patient."
The group announced it would appoint a woman, Patricia Numann, MD, a retired surgeon from SUNY Upstate Medical Center, as the next president-elect...
By Emily P. Walker
MedPage Today
April 18, 2011
The president-elect of the American College of Surgeons has resigned in light of backlash over an editorial he penned on the mood-enhancing effects semen has on women,
The ACS announced the resignation of Lazar Greenfield, MD, in an email sent to its members on Sunday.
In the article, Greenfield, an emeritus professor of surgery at the University of Michigan, cited research from the Archives of Sexual Behavior and wrote, "Female college students having unprotected sex were significantly less depressed than were those whose partners used condoms."
The article offended many in the surgeons' group, and some said it was sexist and perpetuates the boys club mentality of surgery.
Greenfield expressed his "deep regret" and then his resignation to the group's Board of Regents, which met Sunday to consider the status of the 78-year-old surgeon.
Writing in the Valentine's Day editorial, which was published in Surgery News -- and has since been retracted -- Greenfield discussed research that suggests semen includes mood enhancers including oxytocin and serotonin (and a sleep enhancer, melatonin).
He concluded: "So there's a deeper bond between men and women than St. Valentine would have suspected, and now we know there's a better gift for that day than chocolates."
The ACS received "numerous communications from the surgical community about the editorial," wrote the group's president, L. D. Britt, MD, along with Carlos Pellegrini, MD, chairman of the Board of Regents, and David Hoyt, MD, executive director.
At least one female ACS member, Colleen Brophy, MD, a professor of surgery at Vanderbilt University, resigned from the ACS over the editorial.
Writing in a letter to the Board, Brophy said the editorial is "just a symptom of a bigger issue," and that that college needs to be more transparent in choosing its leaders and conducting business.
"The fact that Dr. Greenfield apologized for me, for my 'taking offense' to his op ed without any insight into the implications that a physician leader advocated for unprotected sex, disturbs me," she wrote.
In a brief email to MedPage Today, Greenfield dismissed the claim that his editorial pointed to a larger sexist culture in surgery.
ACS officials acknowledged the contributions of Greenfield, including his invention of the "Greenfield Filter" a device placed in the inferior vena cava of patients who are particularly vulnerable to pulmonary embolism, to prevent venous emboli from entering the pulmonary circulation.
"We wish to honor Dr. Greenfield and celebrate his inestimable contributions to the College and the surgical community," the ACS officials wrote. "We also know that at this critical juncture for surgery and health care in America, it is important that the American College of Surgeons not be distracted by any issues that would diminish its focus on improving care of the surgical patient."
The group announced it would appoint a woman, Patricia Numann, MD, a retired surgeon from SUNY Upstate Medical Center, as the next president-elect...
Wednesday, April 6, 2011
U.S. researchers develop new drug shrinking cancer in animals
U.S. researchers develop new drug shrinking cancer in animals
2011 April 07
xinhuanet.com
A study led by researchers at the University of Michigan (U-M) showed in animal studies that new cancer drug compounds they developed shrank tumors, with few side effects.
The study, done in two mouse models of human cancer, looked at two compounds designed to activate a protein that kills cancer cells. The protein, p53, is inactivated in a significant number of human cancers. In some cases, it is because another protein, MDM2, binds to p53 and blocks its tumor suppresser function. This allows the tumor to grow unchecked. The new compounds block MDM2 from binding to p53, consequently activating p53.
"For the first time, we showed that activation of p53 by our highly potent and optimized MDM2 inhibitors can achieve complete tumor regression in a mouse model of human cancer," says lead study author Shaomeng Wang, director of the Cancer Drug Discovery Program at the U-M Comprehensive Cancer Center.
Wang presented the study Wednesday at the American Association for Cancer Research 102nd annual meeting.
Many traditional cancer drugs also activate p53 but they do so by causing DNA damage in both tumor cells and normal cells, causing side effects. These new MDM2 inhibitors activate p53 while avoiding the DNA damage common with other drugs. In this study, which was done in collaboration with Ascenta Therapeutics and Sanonfi-Aventis, researchers showed that these new drugs shrank tumors without significant side effects.
Because p53 is involved in all types of human cancer, the new drug has potential to be used in multiple types of cancer. Further, the researchers also identified certain markers in tumors that predict which ones will be particularly sensitive to the MDM2 inhibitor, which would allow physicians to target the drug only to patients most likely to benefit.
2011 April 07
xinhuanet.com
A study led by researchers at the University of Michigan (U-M) showed in animal studies that new cancer drug compounds they developed shrank tumors, with few side effects.
The study, done in two mouse models of human cancer, looked at two compounds designed to activate a protein that kills cancer cells. The protein, p53, is inactivated in a significant number of human cancers. In some cases, it is because another protein, MDM2, binds to p53 and blocks its tumor suppresser function. This allows the tumor to grow unchecked. The new compounds block MDM2 from binding to p53, consequently activating p53.
"For the first time, we showed that activation of p53 by our highly potent and optimized MDM2 inhibitors can achieve complete tumor regression in a mouse model of human cancer," says lead study author Shaomeng Wang, director of the Cancer Drug Discovery Program at the U-M Comprehensive Cancer Center.
Wang presented the study Wednesday at the American Association for Cancer Research 102nd annual meeting.
Many traditional cancer drugs also activate p53 but they do so by causing DNA damage in both tumor cells and normal cells, causing side effects. These new MDM2 inhibitors activate p53 while avoiding the DNA damage common with other drugs. In this study, which was done in collaboration with Ascenta Therapeutics and Sanonfi-Aventis, researchers showed that these new drugs shrank tumors without significant side effects.
Because p53 is involved in all types of human cancer, the new drug has potential to be used in multiple types of cancer. Further, the researchers also identified certain markers in tumors that predict which ones will be particularly sensitive to the MDM2 inhibitor, which would allow physicians to target the drug only to patients most likely to benefit.
Friday, March 25, 2011
Social Networks Prevent Dementia in Women
June 6, 2008
Social Networks Prevent Dementia in Women, Kaiser Permanente Study Finds
Kaiser Permanente press release
A strong social network of family and friends is associated with a lower risk of dementia, says a Kaiser Permanente study published in the July issue of the American Journal of Public Health. This is the latest in a series of studies that Kaiser Permanente is conducting on the causes and prevention of dementia.
The five-year study from the Kaiser Permanente Southern California Department of Research & Evaluation followed 2,249 women 78 years or older who had not been diagnosed with dementia and found that women with large social networks were about 26 percent less likely to develop dementia when compared to those women with smaller networks.
"There are a variety of ways that a large social network can facilitate cognitive health but the possible influence on the brain is indirect and largely unknown. Future studies will need to examine which specific aspects of social network are associated with dementia risk. We also need to identify and describe what synthetic social networks may be created that serve to augment or substitute social networks for the elderly who are more socially isolated." said Dr. Valerie Crooks, lead author and research scientist at Kaiser Permanente Southern California Department of Research & Evaluation in Pasadena.
"This well done study significantly adds to the growing body of information that lifestyle, cognitive activity and social connectivity appear to reduce the risk of dementia and help maintain a healthy brain and my advice to older adults is to maintain and even increase their social ties", said Dr. Richard Della Penna, medical director, Kaiser Permanente Aging Network and national Elder Care Clinical Lead for the Care Management Institute.
As many as 5 million Americans are living with Alzheimer's disease, the most common form of dementia. This study provides longitudinal evidence that having larger social networks does have a protective association on the development of dementia in very elderly women.
"The Alzheimer's Association supports the adoption of a brain-healthy lifestyle and encourages all people to remain mentally, socially and physically engaged," said William Thies, PhD, vice president of Medical and Scientific Relations at the Alzheimer's Association. "There is a growing body of scientific evidence that suggests staying socially active, in combination with other activities like managing medical risks, exercising and maintaining a healthy diet, may reduce the risk of Alzheimer's or other dementia."
This study was funded by the National Institute on Aging.
Social Networks Prevent Dementia in Women, Kaiser Permanente Study Finds
Kaiser Permanente press release
A strong social network of family and friends is associated with a lower risk of dementia, says a Kaiser Permanente study published in the July issue of the American Journal of Public Health. This is the latest in a series of studies that Kaiser Permanente is conducting on the causes and prevention of dementia.
The five-year study from the Kaiser Permanente Southern California Department of Research & Evaluation followed 2,249 women 78 years or older who had not been diagnosed with dementia and found that women with large social networks were about 26 percent less likely to develop dementia when compared to those women with smaller networks.
"There are a variety of ways that a large social network can facilitate cognitive health but the possible influence on the brain is indirect and largely unknown. Future studies will need to examine which specific aspects of social network are associated with dementia risk. We also need to identify and describe what synthetic social networks may be created that serve to augment or substitute social networks for the elderly who are more socially isolated." said Dr. Valerie Crooks, lead author and research scientist at Kaiser Permanente Southern California Department of Research & Evaluation in Pasadena.
"This well done study significantly adds to the growing body of information that lifestyle, cognitive activity and social connectivity appear to reduce the risk of dementia and help maintain a healthy brain and my advice to older adults is to maintain and even increase their social ties", said Dr. Richard Della Penna, medical director, Kaiser Permanente Aging Network and national Elder Care Clinical Lead for the Care Management Institute.
As many as 5 million Americans are living with Alzheimer's disease, the most common form of dementia. This study provides longitudinal evidence that having larger social networks does have a protective association on the development of dementia in very elderly women.
"The Alzheimer's Association supports the adoption of a brain-healthy lifestyle and encourages all people to remain mentally, socially and physically engaged," said William Thies, PhD, vice president of Medical and Scientific Relations at the Alzheimer's Association. "There is a growing body of scientific evidence that suggests staying socially active, in combination with other activities like managing medical risks, exercising and maintaining a healthy diet, may reduce the risk of Alzheimer's or other dementia."
This study was funded by the National Institute on Aging.
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