By Maggie Fox, Health and Science Editor - Mon Dec 10, 5:15 PM PST
WASHINGTON (Reuters) - People who eat a lot of red meat and processed meats have a higher risk of several types of cancer, including lung cancer and colorectal cancer, U.S. researchers reported on Monday.
The work is the first big study to show a link between meat and lung cancer. It also shows that people who eat a lot of meat have a higher risk of liver and esophageal cancer and that men raise their risk of pancreatic cancer by eating red meat.
"A decrease in the consumption of red and processed meat could reduce the incidence of cancer at multiple sites," Dr. Amanda Cross and colleagues at the U.S. National Cancer Institute wrote in their report, published in the Public Library of Science journal PLoS Medicine.
The researchers studied 500,000 people aged 50 to 71 who took part in a diet and health study done in conjunction with the AARP, formerly the American Association for Retired Persons.
After eight years, 53,396 cases of cancer were diagnosed.
"Statistically significant elevated risks (ranging from 20 percent to 60 percent) were evident for esophageal, colorectal, liver, and lung cancer, comparing individuals in the highest with those in the lowest quintile of red meat intake," the researchers wrote.
The people in the top 20 percent of eating processed meat had a 20 percent higher risk of colorectal cancer -- mostly rectal cancer -- and a 16 percent higher risk for lung cancer.
"Furthermore, red meat intake was associated with an elevated risk for cancers of the esophagus and liver," the researchers wrote.
These differences held even when smoking was accounted for.
"Red meat intake was not associated with gastric or bladder cancer, leukemia, lymphoma, or melanoma," added the researchers, whose study is freely available on the Internet at http://medicine.plosjournals.org/perlserv/?request=get-document& doi=10.1371/journal.pmed.0040325.
Red meat was defined as all types of beef, pork and lamb. Processed meat included bacon, red meat sausage, poultry sausage, luncheon meats, cold cuts, ham and most types of hot dogs including turkey dogs.
Meats can cause cancer by several routes, the researchers noted. "For example, they are both sources of saturated fat and iron, which have independently been associated with carcinogenesis," the researchers wrote.
Meat is also a source of several chemicals known to cause DNA mutations, including N-nitroso compounds (NOCs), heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs).
Jeanine Genkinger of Georgetown University in Washington, D.C., and Anita Koushik of the University of Montreal said the findings fit in with other research.
"Meat consumption in relation to cancer risk has been reported in over a hundred epidemiological studies from many countries with diverse diets," they wrote in a commentary.
Tuesday, December 11, 2007
Monday, December 10, 2007
Study Shows Why the Flu Likes Winter
y GINA KOLATA
Published: December 5, 2007
Researchers in New York believe they have solved one of the great mysteries of the flu: Why does the infection spread primarily in the winter months?
Skip to next paragraph
Related
Times Health Guide: The Flu
The answer, they say, has to do with the virus itself. It is more stable and stays in the air longer when air is cold and dry, the exact conditions for much of the flu season.
“Influenza virus is more likely to be transmitted during winter on the way to the subway than in a warm room,” said Peter Palese, a flu researcher who is professor and chairman of the microbiology department at Mount Sinai School of Medicine in New York and the lead author of the flu study.
Dr. Palese published details of his findings in the Oct. 19 issue of PLoS Pathogens. The crucial hint that allowed him to do his study came from a paper published in the aftermath of the 1918 flu pandemic, when doctors were puzzling over why and how the virus had spread so quickly and been so deadly.
As long as flu has been recognized, people have asked, Why winter? The very name, “influenza,” is an Italian word that some historians proposed, originated in the mid-18th century as influenza di freddo, or “influence of the cold.”
Flu season in northern latitudes is from November to March, the coldest months. In southern latitudes, it is from May until September. In the tropics, there is not much flu at all and no real flu season.
There was no shortage of hypotheses. Some said flu came in winter because people are indoors; and children are in school, crowded together, getting the flu and passing it on to their families.
Others proposed a diminished immune response because people make less vitamin D or melatonin when days are shorter. Others pointed to the direction of air currents in the upper atmosphere. But many scientists were not convinced.
“We know one of the largest factors is kids in school — most of the major epidemics are traced to children,” said Dr. Jonathan McCullers, a flu researcher at St. Jude Children’s Research Hospital in Memphis. “But that still does not explain wintertime. We don’t see flu in September and October.”
As for the crowding argument, Dr. McCullers said, “That never made sense.” People work all year round and crowd into buses and subways and planes no matter what the season.
“We needed some actual data,” Dr. McCullers added.
But getting data was surprisingly difficult, Dr. Palese said.
The ideal study would expose people to the virus under different conditions and ask how likely they were to become infected. Such a study, Dr. Palese said, would not be permitted because there would be no benefit to the individuals.
There were no suitable test animals. Mice can be infected with the influenza virus but do not transmit it. Ferrets can be infected and transmit the virus, but they are somewhat large, they bite and they are expensive, so researchers would rather not work with them.
To his surprise, Dr. Palese stumbled upon a solution that appeared to be a good second best.
Reading a paper published in 1919 in the Journal of the American Medical Association on the flu epidemic at Camp Cody in New Mexico, he came upon a key passage: “It is interesting to note that very soon after the epidemic of influenza reached this camp, our laboratory guinea pigs began to die.” At first, the study’s authors wrote, they thought the animals had died from food poisoning. But, they continued, “a necropsy on a dead pig revealed unmistakable signs of pneumonia.”
Dr. Palese bought some guinea pigs and exposed them to the flu virus. Just as the paper suggested, they got the flu and spread it among themselves. So Dr. Palese and his colleagues began their experiments.
By varying air temperature and humidity in the guinea pigs’ quarters, they discovered that transmission was excellent at 41 degrees. It declined as the temperature rose until, by 86 degrees, the virus was not transmitted at all.
The virus was transmitted best at a low humidity, 20 percent, and not transmitted at all when the humidity reached 80 percent.
The animals also released viruses nearly two days longer at 41 degrees than at a typical room temperature of 68 degrees.
Flu viruses spread through the air, unlike cold viruses, Dr. Palese said, which primarily spread by direct contact when people touch surfaces that had been touched by someone with a cold or shake hands with someone who is infected, for example.
Flu viruses are more stable in cold air, and low humidity also helps the virus particles remain in the air. That is because the viruses float in the air in little respiratory droplets, Dr. Palese said. When the air is humid, those droplets pick up water, grow larger and fall to the ground.
But Dr. Palese does not suggest staying in a greenhouse all winter to avoid the flu. The best strategy, he says, is a flu shot.
It is unclear why infected animals released viruses for a longer time at lower temperatures. There was no difference in their immune response, but one possibility is that their upper airways are cooler, making the virus residing there more stable.
Flu researchers said they were delighted to get some solid data at last on flu seasonality.
“It was great work, and work that needed to be done,” said Dr. Terrence Tumpe, a senior microbiologist at the Centers for Disease Control and Prevention.
Dr. McCullers said he was pleased to see something convincing on the flu season question.
“It was a really interesting paper, the first really scientific approach, to answer a classic question that we’ve been debating for years and years,” he said.
As for Dr. Palese, he was glad he spotted the journal article that mentioned guinea pigs.
“Sometimes it pays to read the old literature,” he said.
Published: December 5, 2007
Researchers in New York believe they have solved one of the great mysteries of the flu: Why does the infection spread primarily in the winter months?
Skip to next paragraph
Related
Times Health Guide: The Flu
The answer, they say, has to do with the virus itself. It is more stable and stays in the air longer when air is cold and dry, the exact conditions for much of the flu season.
“Influenza virus is more likely to be transmitted during winter on the way to the subway than in a warm room,” said Peter Palese, a flu researcher who is professor and chairman of the microbiology department at Mount Sinai School of Medicine in New York and the lead author of the flu study.
Dr. Palese published details of his findings in the Oct. 19 issue of PLoS Pathogens. The crucial hint that allowed him to do his study came from a paper published in the aftermath of the 1918 flu pandemic, when doctors were puzzling over why and how the virus had spread so quickly and been so deadly.
As long as flu has been recognized, people have asked, Why winter? The very name, “influenza,” is an Italian word that some historians proposed, originated in the mid-18th century as influenza di freddo, or “influence of the cold.”
Flu season in northern latitudes is from November to March, the coldest months. In southern latitudes, it is from May until September. In the tropics, there is not much flu at all and no real flu season.
There was no shortage of hypotheses. Some said flu came in winter because people are indoors; and children are in school, crowded together, getting the flu and passing it on to their families.
Others proposed a diminished immune response because people make less vitamin D or melatonin when days are shorter. Others pointed to the direction of air currents in the upper atmosphere. But many scientists were not convinced.
“We know one of the largest factors is kids in school — most of the major epidemics are traced to children,” said Dr. Jonathan McCullers, a flu researcher at St. Jude Children’s Research Hospital in Memphis. “But that still does not explain wintertime. We don’t see flu in September and October.”
As for the crowding argument, Dr. McCullers said, “That never made sense.” People work all year round and crowd into buses and subways and planes no matter what the season.
“We needed some actual data,” Dr. McCullers added.
But getting data was surprisingly difficult, Dr. Palese said.
The ideal study would expose people to the virus under different conditions and ask how likely they were to become infected. Such a study, Dr. Palese said, would not be permitted because there would be no benefit to the individuals.
There were no suitable test animals. Mice can be infected with the influenza virus but do not transmit it. Ferrets can be infected and transmit the virus, but they are somewhat large, they bite and they are expensive, so researchers would rather not work with them.
To his surprise, Dr. Palese stumbled upon a solution that appeared to be a good second best.
Reading a paper published in 1919 in the Journal of the American Medical Association on the flu epidemic at Camp Cody in New Mexico, he came upon a key passage: “It is interesting to note that very soon after the epidemic of influenza reached this camp, our laboratory guinea pigs began to die.” At first, the study’s authors wrote, they thought the animals had died from food poisoning. But, they continued, “a necropsy on a dead pig revealed unmistakable signs of pneumonia.”
Dr. Palese bought some guinea pigs and exposed them to the flu virus. Just as the paper suggested, they got the flu and spread it among themselves. So Dr. Palese and his colleagues began their experiments.
By varying air temperature and humidity in the guinea pigs’ quarters, they discovered that transmission was excellent at 41 degrees. It declined as the temperature rose until, by 86 degrees, the virus was not transmitted at all.
The virus was transmitted best at a low humidity, 20 percent, and not transmitted at all when the humidity reached 80 percent.
The animals also released viruses nearly two days longer at 41 degrees than at a typical room temperature of 68 degrees.
Flu viruses spread through the air, unlike cold viruses, Dr. Palese said, which primarily spread by direct contact when people touch surfaces that had been touched by someone with a cold or shake hands with someone who is infected, for example.
Flu viruses are more stable in cold air, and low humidity also helps the virus particles remain in the air. That is because the viruses float in the air in little respiratory droplets, Dr. Palese said. When the air is humid, those droplets pick up water, grow larger and fall to the ground.
But Dr. Palese does not suggest staying in a greenhouse all winter to avoid the flu. The best strategy, he says, is a flu shot.
It is unclear why infected animals released viruses for a longer time at lower temperatures. There was no difference in their immune response, but one possibility is that their upper airways are cooler, making the virus residing there more stable.
Flu researchers said they were delighted to get some solid data at last on flu seasonality.
“It was great work, and work that needed to be done,” said Dr. Terrence Tumpe, a senior microbiologist at the Centers for Disease Control and Prevention.
Dr. McCullers said he was pleased to see something convincing on the flu season question.
“It was a really interesting paper, the first really scientific approach, to answer a classic question that we’ve been debating for years and years,” he said.
As for Dr. Palese, he was glad he spotted the journal article that mentioned guinea pigs.
“Sometimes it pays to read the old literature,” he said.
Wednesday, November 14, 2007
Breast-Feeding Cuts Food Allergy Risk
WEDNESDAY, Nov. 14 (HealthDay News) -- Breast-feeding in the first three months of life appears to help shield children from developing food allergies.
ADVERTISEMENT
That's just one of a number of findings on food allergies scheduled to be presented this week at the annual meeting of the American College of Allergy, Asthma and Immunology in Dallas.
Research has determined a possible role for food allergy prevention strategies in high-risk children, including maternal food avoidance in pregnancy, breast-feeding, maternal food avoidance while breast-feeding, use of hyper-allergenic formulas, delayed introduction of allergenic foods and probiotics, noted one expert.
"A review of 18 studies demonstrates a significant protective effect of exclusive breast-feeding for at least three months for children with high risk for atopy (genetic tendency to develop allergic diseases) against the development of atopic dermatitis and early childhood asthma-like symptoms," Dr. Robert Wood, international health director for pediatric allergy and immunology at Johns Hopkins School of Medicine, said in a prepared statement.
He offered a number of recommendations for children at high risk of allergic diseases:
* Women should avoid peanuts and tree nuts during pregnancy and while breast-feeding.
* Mothers should supplement breast-feeding with a hypoallergenic formula (extensively or partially hydrolyzed).
* Delay feeding these children solid foods until they're six months old.
* Delay introduction of milk and egg until age 1 and peanut and tree nuts until age 3.
* Start early intervention when signs of food allergy appear (secondary prevention).
In a planned presentation about allergies and dietary restrictions, another expert noted that a person may have an allergy to one member of a food family, but may be able to eat other members of the same food family.
For example, one study on nine common fish found cross-reactivity and allergenicity were highest among cod, salmon and pollack and lowest among halibut, flounder, tuna and mackerel. Another study on edible nuts found cross-reactivity was strong among walnut, pecan and hazelnut; moderate among cashew, pistachio, Brazil nut and almond; and extremely low between peanut and tree nuts.
"You may be allergic to a particular part of a food, but not to another part," Dr. Sami Bahna, chief of allergy and immunology at Louisiana State University in Shreveport, said in a prepared statement.
Another expert said doctors need to consider food allergy as a potential cause of gastrointestinal or dermatological symptoms in patients.
"The eosinophilic gastrointestinal disorders (EGID) which may affect the esophagus, stomach, colon and rectum are mostly chronic and recurrent disorders that adversely impact quality of life for patients and families," Dr. Amal Assa'ad, director of the Food Allergy & Eosinophilic Disorders Clinic at Cincinnati Children's Medical Center, said in a prepared statement.
"Patients with EGID have a high rate of sensitization to food and environmental allergens, and many of them have a high rate of clinical symptoms with various food ingestions. A subset of patients respond to removal of major food allergens from their diet," Assa'ad said.
"EGID management often requires multiple specialists, including the primary physician, allergy and immunology, gastroenterology, nutrition and psychology," she noted.
ADVERTISEMENT
That's just one of a number of findings on food allergies scheduled to be presented this week at the annual meeting of the American College of Allergy, Asthma and Immunology in Dallas.
Research has determined a possible role for food allergy prevention strategies in high-risk children, including maternal food avoidance in pregnancy, breast-feeding, maternal food avoidance while breast-feeding, use of hyper-allergenic formulas, delayed introduction of allergenic foods and probiotics, noted one expert.
"A review of 18 studies demonstrates a significant protective effect of exclusive breast-feeding for at least three months for children with high risk for atopy (genetic tendency to develop allergic diseases) against the development of atopic dermatitis and early childhood asthma-like symptoms," Dr. Robert Wood, international health director for pediatric allergy and immunology at Johns Hopkins School of Medicine, said in a prepared statement.
He offered a number of recommendations for children at high risk of allergic diseases:
* Women should avoid peanuts and tree nuts during pregnancy and while breast-feeding.
* Mothers should supplement breast-feeding with a hypoallergenic formula (extensively or partially hydrolyzed).
* Delay feeding these children solid foods until they're six months old.
* Delay introduction of milk and egg until age 1 and peanut and tree nuts until age 3.
* Start early intervention when signs of food allergy appear (secondary prevention).
In a planned presentation about allergies and dietary restrictions, another expert noted that a person may have an allergy to one member of a food family, but may be able to eat other members of the same food family.
For example, one study on nine common fish found cross-reactivity and allergenicity were highest among cod, salmon and pollack and lowest among halibut, flounder, tuna and mackerel. Another study on edible nuts found cross-reactivity was strong among walnut, pecan and hazelnut; moderate among cashew, pistachio, Brazil nut and almond; and extremely low between peanut and tree nuts.
"You may be allergic to a particular part of a food, but not to another part," Dr. Sami Bahna, chief of allergy and immunology at Louisiana State University in Shreveport, said in a prepared statement.
Another expert said doctors need to consider food allergy as a potential cause of gastrointestinal or dermatological symptoms in patients.
"The eosinophilic gastrointestinal disorders (EGID) which may affect the esophagus, stomach, colon and rectum are mostly chronic and recurrent disorders that adversely impact quality of life for patients and families," Dr. Amal Assa'ad, director of the Food Allergy & Eosinophilic Disorders Clinic at Cincinnati Children's Medical Center, said in a prepared statement.
"Patients with EGID have a high rate of sensitization to food and environmental allergens, and many of them have a high rate of clinical symptoms with various food ingestions. A subset of patients respond to removal of major food allergens from their diet," Assa'ad said.
"EGID management often requires multiple specialists, including the primary physician, allergy and immunology, gastroenterology, nutrition and psychology," she noted.
Monday, July 23, 2007
Study Links Diet Soft Drinks With Cardiac Risk
By Ed Edelson
HealthDay Reporter 1 hour, 31 minutes ago
MONDAY, July 23 (HealthDay News) -- Drinking more than one soda a day -- even if it's the sugar-free diet kind -- is associated with an increased incidence of metabolic syndrome, a cluster of risk factors linked to the development of diabetes and cardiovascular disease, a study finds.
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The link to diet soda found in the study was "striking" but not entirely a surprise, said Dr. Ramachandran Vasan, study senior author and professor of medicine at Boston University School of Medicine. There had been some hints of it in earlier studies, he said.
"But this is the first study to show the association in a prospective fashion and in a large population," Vasan said.
That population consisted of more than 6,000 participants in the Framingham Heart Study, which has been following residents of a Massachusetts town since 1948. When the soda portion of the study began, all participants were free of metabolic syndrome, a collection of risk factors including high blood pressure, elevated levels of the blood fats called triglycerides, low levels of the artery-protecting HDL cholesterol, high fasting blood sugar levels and excessive waist circumference. Metabolic syndrome is the presence of three or more of these risk factors.
Over the four years of the study, people who consumed more than one soft drink of any kind a day were 44 percent more likely to develop metabolic syndrome than those who didn't drink a soda a day.
The findings are published in the July 24 issue of the journal Circulation.
A variety of explanations, none proven, have been proposed for the link between diet soft drink consumption and metabolic syndrome, Vasan said. That association was evident even when the researchers accounted for other factors, such as levels of saturated fat and fiber in the diet, total calorie intake, smoking and physical activity.
One theory is that the high sweetness of all soft drinks makes a person more prone to eat sugary, fattening foods. Another is that the caramel content of soft drinks promotes metabolic changes that lead to insulin resistance. "These are hotly debated by nutritional experts," Vasan said.
Vasan, who noted that he is not a nutritional expert, said he leans toward the theory that "this is a marker of dietary behavior" -- that people who like to drink sweet soda also like to eat the kind of foods that cardiac nutritionists warn against.
"But we cannot infer causality," Vasan said, meaning there is no proof that soda itself is the villain. "We have an association. Maybe it is a causal one or maybe it is a marker of something else."
Carefully controlled animal studies might resolve the cause-and-effect issue, he said.
Dr. Elizabeth G. Nabel, director of the U.S. National Heart, Lung, and Blood Institute, which funds the Framingham Heart Study, said in a prepared statement: "Other studies have shown that the extra calories and sugar in soft drinks contribute to weight gain, and therefore heart disease risk. This study echoes those findings by extending the link to all soft drinks and the metabolic syndrome."
HealthDay Reporter 1 hour, 31 minutes ago
MONDAY, July 23 (HealthDay News) -- Drinking more than one soda a day -- even if it's the sugar-free diet kind -- is associated with an increased incidence of metabolic syndrome, a cluster of risk factors linked to the development of diabetes and cardiovascular disease, a study finds.
ADVERTISEMENT
The link to diet soda found in the study was "striking" but not entirely a surprise, said Dr. Ramachandran Vasan, study senior author and professor of medicine at Boston University School of Medicine. There had been some hints of it in earlier studies, he said.
"But this is the first study to show the association in a prospective fashion and in a large population," Vasan said.
That population consisted of more than 6,000 participants in the Framingham Heart Study, which has been following residents of a Massachusetts town since 1948. When the soda portion of the study began, all participants were free of metabolic syndrome, a collection of risk factors including high blood pressure, elevated levels of the blood fats called triglycerides, low levels of the artery-protecting HDL cholesterol, high fasting blood sugar levels and excessive waist circumference. Metabolic syndrome is the presence of three or more of these risk factors.
Over the four years of the study, people who consumed more than one soft drink of any kind a day were 44 percent more likely to develop metabolic syndrome than those who didn't drink a soda a day.
The findings are published in the July 24 issue of the journal Circulation.
A variety of explanations, none proven, have been proposed for the link between diet soft drink consumption and metabolic syndrome, Vasan said. That association was evident even when the researchers accounted for other factors, such as levels of saturated fat and fiber in the diet, total calorie intake, smoking and physical activity.
One theory is that the high sweetness of all soft drinks makes a person more prone to eat sugary, fattening foods. Another is that the caramel content of soft drinks promotes metabolic changes that lead to insulin resistance. "These are hotly debated by nutritional experts," Vasan said.
Vasan, who noted that he is not a nutritional expert, said he leans toward the theory that "this is a marker of dietary behavior" -- that people who like to drink sweet soda also like to eat the kind of foods that cardiac nutritionists warn against.
"But we cannot infer causality," Vasan said, meaning there is no proof that soda itself is the villain. "We have an association. Maybe it is a causal one or maybe it is a marker of something else."
Carefully controlled animal studies might resolve the cause-and-effect issue, he said.
Dr. Elizabeth G. Nabel, director of the U.S. National Heart, Lung, and Blood Institute, which funds the Framingham Heart Study, said in a prepared statement: "Other studies have shown that the extra calories and sugar in soft drinks contribute to weight gain, and therefore heart disease risk. This study echoes those findings by extending the link to all soft drinks and the metabolic syndrome."
Sunday, July 22, 2007
Plastic Hemoglobin May Help Save Trauma Victims, Soldiers
Dr Lance Twyman, professor of chemistry at Sheffield University has developed a synthetic form of hemoglobin that may save thousands of lives each year.
They say that the artificial blood is light to carry, does not need to be kept cool and can be kept for longer.
The new blood is made up of plastic molecules that have an iron atom at their core, like haemoglobin, that can carry oxygen through the body.
The scientists said the artificial blood could be cheap to produce and they were looking for extra funding to develop a final prototype that would be suitable for biological testing.
Dr Lance Twyman, of the university's Department of Chemistry, said: "We are very excited about the potential for this product and about the fact that this could save lives.
"Many people die from superficial wounds when they are trapped in an accident or are injured on the battlefield and can't get blood before they get to hospital.
"This product can be stored a lot more easily than blood, meaning large quantities could be carried easily by ambulances and the armed forces."
A sample of the artificial blood prototype will be on display at the Science Museum in London from 22 May as part of an exhibition about the history of plastics.
They say that the artificial blood is light to carry, does not need to be kept cool and can be kept for longer.
The new blood is made up of plastic molecules that have an iron atom at their core, like haemoglobin, that can carry oxygen through the body.
The scientists said the artificial blood could be cheap to produce and they were looking for extra funding to develop a final prototype that would be suitable for biological testing.
Dr Lance Twyman, of the university's Department of Chemistry, said: "We are very excited about the potential for this product and about the fact that this could save lives.
"Many people die from superficial wounds when they are trapped in an accident or are injured on the battlefield and can't get blood before they get to hospital.
"This product can be stored a lot more easily than blood, meaning large quantities could be carried easily by ambulances and the armed forces."
A sample of the artificial blood prototype will be on display at the Science Museum in London from 22 May as part of an exhibition about the history of plastics.
Wednesday, June 6, 2007
Teams mimic stem cells using skin cells
NEW YORK - In a leap forward for stem cell research, three independent teams of scientists reported Wednesday that they have produced the equivalent of embryonic stem cells in mice using skin cells without the controversial destruction of embryos.
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If the same could be done with human skin cells — a big if — the procedure could lead to breakthrough medical treatments without the contentious ethical and political debates surrounding the use of embryos.
Experts were impressed by the achievement.
"I think it's one of the most exciting things that has come out about embryonic stem cells, period," said researcher Dr. Asa Abeliovich of Columbia University in New York, who didn't participate in the work. "It's very convincing that it's real."
But he and others cautioned that it will take further study to see whether this scientific advance can be harnessed for creating new human therapies. For one thing, the procedure used to get the mouse skin cells to mimic embryonic stem cells wouldn't be suitable. And it's simply not known whether the mouse results can be reproduced with human cells.
"We have a long way to go," said John Gearhart of Johns Hopkins University, a stem cell researcher who also wasn't involved in the new work.
In any case, scientists said, the advance does not mean that research that involves getting stem cells from human embryos should now be abandoned. "We simply don't know which approach ... will work the best," said researcher Konrad Hochedlinger of the Harvard Stem Cell Institute, who led one of the three teams.
Embryonic stem cells are prized because they can develop into all types of tissue. So experts believe they might be used for transplant therapies in people who are paralyzed or have illnesses ranging from diabetes to Parkinson's disease.
To harvest human embryonic stem cells, embryos must be destroyed, an action many people oppose.
Scientists have long hoped to find a way to reprogram ordinary body cells to act like stem cells, avoiding the use of embryos altogether. The new mouse studies seem to have accomplished that. Past experiments seeking alternative routes to getting stem cells have generally involved tampering with an embryo or egg.
At a press conference Wednesday, Hochedlinger and a member of a second team said their work was not an attempt to evade the ethical objections to embryo destruction. Instead, they said, the goal was to learn how cell reprogramming works.
But in a telephone interview, a prominent critic of embryonic stem cell research welcomed the new work on ethical terms.
"This is what we were looking for people to explore because it may provide all the advantages of embryonic stem cells without the moral problem," said Richard Doerflinger, deputy director of pro-life activities for the U.S. Conference of Catholic Bishops. "So I'm very encouraged."
Hochedlinger and colleagues present their work in the inaugural issue of the journal Cell Stem Cell. (The first word in the journal's name refers to its publisher, Cell Press).
The other two teams reported their results Wednesday on the Web site of the journal Nature. Rudolf Jaenisch of the Whitehead Institute in Cambridge, Mass., is the senior author of one paper, and the work behind the other paper was led by Shinya Yamanaka of Kyoto University in Japan.
The new work builds on a landmark paper Yamanaka published last August. He found that by slipping four genes into mouse skin cells called fibroblasts, he could make the altered cells behave much like embryonic stem cells in lab tests.
But these so-called "iPS" cells still showed significant differences from embryonic stem cells. The three new papers report on creating iPS cells that proved virtually identical to stem cells in a variety of lab tests.
The technique used in the mouse studies could promote cancer in any patients getting therapy based on iPS cells, so researchers emphasized that a new approach that avoids that hazard would have to be developed.
Gearhart called that a major issue to be resolved. In addition, he said, scientists still must show that these cells can give rise to many cell types in the lab, as embryonic stem cells can.
And all this must be accomplished in human cells — a difficult task, he said, because introducing genes into human cells is a major challenge.
If the technique can be harnessed for people, the iPS cells and the tissue they develop into would provide a genetic match to the person who donated the skin cells. That would make them suitable for transplant to that person, theoretically without fear of rejection.
ADVERTISEMENT
If the same could be done with human skin cells — a big if — the procedure could lead to breakthrough medical treatments without the contentious ethical and political debates surrounding the use of embryos.
Experts were impressed by the achievement.
"I think it's one of the most exciting things that has come out about embryonic stem cells, period," said researcher Dr. Asa Abeliovich of Columbia University in New York, who didn't participate in the work. "It's very convincing that it's real."
But he and others cautioned that it will take further study to see whether this scientific advance can be harnessed for creating new human therapies. For one thing, the procedure used to get the mouse skin cells to mimic embryonic stem cells wouldn't be suitable. And it's simply not known whether the mouse results can be reproduced with human cells.
"We have a long way to go," said John Gearhart of Johns Hopkins University, a stem cell researcher who also wasn't involved in the new work.
In any case, scientists said, the advance does not mean that research that involves getting stem cells from human embryos should now be abandoned. "We simply don't know which approach ... will work the best," said researcher Konrad Hochedlinger of the Harvard Stem Cell Institute, who led one of the three teams.
Embryonic stem cells are prized because they can develop into all types of tissue. So experts believe they might be used for transplant therapies in people who are paralyzed or have illnesses ranging from diabetes to Parkinson's disease.
To harvest human embryonic stem cells, embryos must be destroyed, an action many people oppose.
Scientists have long hoped to find a way to reprogram ordinary body cells to act like stem cells, avoiding the use of embryos altogether. The new mouse studies seem to have accomplished that. Past experiments seeking alternative routes to getting stem cells have generally involved tampering with an embryo or egg.
At a press conference Wednesday, Hochedlinger and a member of a second team said their work was not an attempt to evade the ethical objections to embryo destruction. Instead, they said, the goal was to learn how cell reprogramming works.
But in a telephone interview, a prominent critic of embryonic stem cell research welcomed the new work on ethical terms.
"This is what we were looking for people to explore because it may provide all the advantages of embryonic stem cells without the moral problem," said Richard Doerflinger, deputy director of pro-life activities for the U.S. Conference of Catholic Bishops. "So I'm very encouraged."
Hochedlinger and colleagues present their work in the inaugural issue of the journal Cell Stem Cell. (The first word in the journal's name refers to its publisher, Cell Press).
The other two teams reported their results Wednesday on the Web site of the journal Nature. Rudolf Jaenisch of the Whitehead Institute in Cambridge, Mass., is the senior author of one paper, and the work behind the other paper was led by Shinya Yamanaka of Kyoto University in Japan.
The new work builds on a landmark paper Yamanaka published last August. He found that by slipping four genes into mouse skin cells called fibroblasts, he could make the altered cells behave much like embryonic stem cells in lab tests.
But these so-called "iPS" cells still showed significant differences from embryonic stem cells. The three new papers report on creating iPS cells that proved virtually identical to stem cells in a variety of lab tests.
The technique used in the mouse studies could promote cancer in any patients getting therapy based on iPS cells, so researchers emphasized that a new approach that avoids that hazard would have to be developed.
Gearhart called that a major issue to be resolved. In addition, he said, scientists still must show that these cells can give rise to many cell types in the lab, as embryonic stem cells can.
And all this must be accomplished in human cells — a difficult task, he said, because introducing genes into human cells is a major challenge.
If the technique can be harnessed for people, the iPS cells and the tissue they develop into would provide a genetic match to the person who donated the skin cells. That would make them suitable for transplant to that person, theoretically without fear of rejection.
Wednesday, April 11, 2007
No genetic link found for heart risk, study says
CHICAGO (Reuters) - Genetic testing failed to find any gene mutations that predict a higher risk of heart disease, a study released on Tuesday said.
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Scientists at Yale University worked up the genetic profiles of nearly 1,500 people to examine 85 genes that smaller, earlier studies suggested might confer susceptibility to heart problems.
More than half the patients had come to a hospital having suffered a heart attack or other acute symptoms, while the others had experienced no heart trouble.
Only one genetic variation showed even a modest association to heart problems in the study, which was published in the
Journal of the American Medical Association.
"We therefore conclude that our findings, in this large sample ... cannot support that this panel of gene variants contains bona fide (heart disease) risk factors," study author Dr. Thomas Morgan wrote. Morgan is now at Washington University in St. Louis.
A significant proportion of pregnant women opt for genetic testing to determine if the fetus will develop an array of potential ailments such as cystic fibrosis or a form of mental retardation.
Increasingly, genetic testing is also being performed later in life to detect if a person has a higher risk of contracting diseases such as Alzheimer's or inherited breast cancer.
The availability of genetic testing also raises complex ethical questions, such as who should know about a person's risk and what should be done about it.
"Our findings come at a critical juncture in complex disease genetics," Morgan wrote, adding that several clinics offer genetic tests for several of the gene mutations his study examined.
"However, our findings suggest that such clinical genetic testing is premature and underscore the importance of robust replication studies of reported associations prior to their application to clinical care," he added.
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Scientists at Yale University worked up the genetic profiles of nearly 1,500 people to examine 85 genes that smaller, earlier studies suggested might confer susceptibility to heart problems.
More than half the patients had come to a hospital having suffered a heart attack or other acute symptoms, while the others had experienced no heart trouble.
Only one genetic variation showed even a modest association to heart problems in the study, which was published in the
Journal of the American Medical Association.
"We therefore conclude that our findings, in this large sample ... cannot support that this panel of gene variants contains bona fide (heart disease) risk factors," study author Dr. Thomas Morgan wrote. Morgan is now at Washington University in St. Louis.
A significant proportion of pregnant women opt for genetic testing to determine if the fetus will develop an array of potential ailments such as cystic fibrosis or a form of mental retardation.
Increasingly, genetic testing is also being performed later in life to detect if a person has a higher risk of contracting diseases such as Alzheimer's or inherited breast cancer.
The availability of genetic testing also raises complex ethical questions, such as who should know about a person's risk and what should be done about it.
"Our findings come at a critical juncture in complex disease genetics," Morgan wrote, adding that several clinics offer genetic tests for several of the gene mutations his study examined.
"However, our findings suggest that such clinical genetic testing is premature and underscore the importance of robust replication studies of reported associations prior to their application to clinical care," he added.
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