By Ed Edelson
HealthDay Reporter
MONDAY, May 10 (HealthDay News) -- An analysis of studies has produced what its authors describe as a precise description of the beneficial effects of nut consumption on cholesterol and other heart-related fats.
It provides "the best evidence yet that eating nuts reduces LDL cholesterol and improves the blood lipids profile," said Dr. Joan Sabate, who chairs the nutrition department at the Loma Linda University School of Public Health in California and was a co-author of the report, published May 10 in Archives of Internal Medicine.
Sabate and fellow researchers at the university pooled data on 583 men and women who had participated in 25 nut consumption trials. The results showed that eating about 2.3 ounces of nuts a day -- a third of a cupful -- reduced total cholesterol levels by 5.1 percent and "bad" LDL cholesterol by 7.4 percent.
That amount of nut eating also improved the ratio of LDL cholesterol to "good" HDL cholesterol by 8.3 percent and caused a decrease of 10.2 percent in triglyceride levels among people with high levels of those blood fats.
Sabate is a leading figure in the somewhat limited field of nut nutrition. His first report on the beneficial effects, published in 1993, led to other studies that eventually prompted the U.S. Food and Drug Administration to issue a qualified health claim for nuts a decade later.
The 2003 FDA statement said that "scientific evidence suggests but does not prove that eating 1.5 ounces of most nuts per day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease."
On food labels, that claim is followed by a caution: "See nutrition information for fat content."
The FDA statement was issued in response to a petition filed by the International Tree Nut Council Research and Education Foundation, which supports the work done by Sabate and other nut nutrition researchers. The foundation helped fund the latest report.
The new study found that the benefits from eating nuts was greatest among thin people, those with high LDL cholesterol and those consuming a fat-rich diet.
But enthusiasm for nuts should be restrained, Sabate said. They are highly caloric, and thus can contribute to obesity. A 3-ounce-a-day limit was recommended.
Jeannie Gazzaniga-Moloo, a spokeswoman for the American Dietetic Association who is in private practice in Sacramento, Calif., said that "nuts can be a very healthy addition to any diet," but she recommends eating somewhat less of them.
She said she suggests that her clients consume about an ounce a day of nuts -- about 22 walnuts, for example, providing about 150 calories -- as part of their daily diet. "They are rich in protein and dietary fiber as well as numerous proteins and in various vitamins," Gazzaniga-Moloo said.
"They should eat the nuts they enjoy," she said. "They can try a variety."
Sabata said that the type of nuts eaten doesn't seem to matter. The study found essentially the same results for walnuts, almonds, peanuts, pecans, hazelnuts, macadamias and pistachios.
"Nuts are a matrix of healthy nutrients, and the most obvious reason for the cholesterol-lowering effect is their unsaturated fat content," Sabate said. "Nuts also contain fiber, vegetable protein, phytoesterols and other antioxidants."
The best evidence for the beneficial effect of nuts, though, has come from studies of walnuts and almonds, he added.
Friday, July 30, 2010
Saturday, July 24, 2010
Are you removing years from your life?
April 26, 2010 | 1:01 pm
From the Los Angeles Times:
You know that smoking is bad for your health. Ditto heavy drinking, a slovenly lifestyle or a preference for chili cheese fries over fruits and vegetables.
Epidemiologists have linked each of these behaviors to increased risk of heart disease, diabetes and stroke. But few people engage in only one unhealthy habit. (C’mon, what are you more likely to be snacking on while parked on the couch watching three consecutive NBA playoff games – carrot sticks and bottled water, or chips, guacamole and beer?) So an international group of researchers – including USC cancer epidemiologist Dr. Giske Ursin – studied the effect of all four bad behaviors at once.
What defines “bad”? Smokers fill that bill, while nonsmokers and former smokers did not. Men who consumed more than 21 8-gram servings of alcohol and women who drank more than 14 servings of alcohol were considered to have poor drinking behavior. Anyone who got less than 120 minutes of exercise each week was defined as having poor physical activity, and bad diets were those that contained fewer than 3 fruits or vegetables each day.
After tracking nearly 5,000 British adults for 20 years, the researchers were able to correlate these behaviors with risk of disease and death. (In case you were wondering, men and women, average age 43.7, were equally lazy, but men were more likely to smoke, drink to excess and skip the fruits and veggies.)
The researchers found that Britons who indulged in all four bad behaviors were 3.49 times more likely to die over the course of the study than their countrymen (and women) who practiced clean living. That included a 3.14 times greater risk of death from cardiovascular disease; a 3.35 times greater risk of death from cancer; and a 4.29 times greater risk of death form any other cause.
Overall, 96% of those with healthy behaviors were alive at the end of the study, compared with 85% of those with the worst health habits. “The increase in mortality risk from no to 4 poor health behavior was equivalent to an increase in chronological age of about 12 years,” the researchers wrote.
The study will appear in Tuesday’s edition of Archives of Internal Medicine.
-- Karen Kaplan
From the Los Angeles Times:
You know that smoking is bad for your health. Ditto heavy drinking, a slovenly lifestyle or a preference for chili cheese fries over fruits and vegetables.
Epidemiologists have linked each of these behaviors to increased risk of heart disease, diabetes and stroke. But few people engage in only one unhealthy habit. (C’mon, what are you more likely to be snacking on while parked on the couch watching three consecutive NBA playoff games – carrot sticks and bottled water, or chips, guacamole and beer?) So an international group of researchers – including USC cancer epidemiologist Dr. Giske Ursin – studied the effect of all four bad behaviors at once.
What defines “bad”? Smokers fill that bill, while nonsmokers and former smokers did not. Men who consumed more than 21 8-gram servings of alcohol and women who drank more than 14 servings of alcohol were considered to have poor drinking behavior. Anyone who got less than 120 minutes of exercise each week was defined as having poor physical activity, and bad diets were those that contained fewer than 3 fruits or vegetables each day.
After tracking nearly 5,000 British adults for 20 years, the researchers were able to correlate these behaviors with risk of disease and death. (In case you were wondering, men and women, average age 43.7, were equally lazy, but men were more likely to smoke, drink to excess and skip the fruits and veggies.)
The researchers found that Britons who indulged in all four bad behaviors were 3.49 times more likely to die over the course of the study than their countrymen (and women) who practiced clean living. That included a 3.14 times greater risk of death from cardiovascular disease; a 3.35 times greater risk of death from cancer; and a 4.29 times greater risk of death form any other cause.
Overall, 96% of those with healthy behaviors were alive at the end of the study, compared with 85% of those with the worst health habits. “The increase in mortality risk from no to 4 poor health behavior was equivalent to an increase in chronological age of about 12 years,” the researchers wrote.
The study will appear in Tuesday’s edition of Archives of Internal Medicine.
-- Karen Kaplan
Friday, July 16, 2010
Companies Developing Systems to Help the Blind See Again
From the Wall Street Journal
By Jonathan Matsey
While the phrase bionic retinas may conjure images of Steve Austin in “The Six Million Dollar Man” or Geordi La Forge in “Star Trek: The Next Generation,” technology to create vision where none, or very little, exists, is not a television fantasy. Companies concentrating on damaged retinas look poised for success as the technology inches toward measurable achievement.
“We will be approved on the market in Europe this year,” said Bill Link, managing director at Versant Ventures, an investor in Second Sight Medical Products Inc.
Second Sight, based in Sylmar, Calif., is also looking at a U.S. Food and Drug Administration submission at the end of 2011, according to Link. The company has raised $16 million in venture capital.
Second Sight’s system uses a pair of glasses to send images to a receiver implanted on the retina. From there, the image is transmitted to the brain through the optic nerve. The device is targeted to patients who have lost most of their vision as a result of retinal degeneration and whose nerve connections are still intact.
A similar approach is being developed by Nano Retina Inc. of Herzliya Pituach, Israel, though Nano Retina aims for much greater visual clarity than Second Sight, it says. “We have a much higher resolution – about 1,000 pixels,” said Ra’anan Gefen, managing director of the company. “Second Sight is the most advanced (clinically) but on the other hand, it is really a limited device.”
According to Link, Second Sight’s first-generation device offers 16 pixels while a second-generation system will have 60. “They can read letters on a computer screen, they can tell light from dark, they can see a line on the ground,” said Link of people using Second Sight’s system.
Gefen, on the other hand, is more ambitious. “We will give them back vision so that they can see almost normally,” he said.
Gefen’s company was founded as a joint venture with nanotech company Zyvex Labs LLC of Richardson, Texas, and is backed by several million dollars from Rainbow Medical, an Israeli business accelerator, according to Rainbow Founding Partner Yossi Gross. Nano Retina is still a couple of years away from clinical studies, Gross said.
Costs for the two systems appear to be about the same. Link estimates Second Sight’s device will sell for $50,000 to $100,000 per system; Gefen says Nano Retina’s will cost around $60,000. Both companies said they expect much of that cost to be picked up by insurance companies. Link said his portfolio company is currently in discussion with potential payers.
Waiting in the wings is a third player – Optobionics Corp. – which had raised around $50 million from investors including Advanced Medical Optics Inc., Advanced Technology Ventures, Arch Venture Partners, Medtronic Inc. and Polaris Venture Partners and had taken its device through Phase II trials before hitting a snag in fund-raising for Phase III trials.
“There was no appetite to put in another $100 million,” said Alan Chow, chief executive of Optobionics. As a result, his company entered bankruptcy in 2007, recently relaunching after Chow bought the technology.
Unlike the other two companies, Optobionics is pursuing a trickier and more costly approach: restoring function to the damaged retina by using the device to stimulate the rods and cones, rather than using the system as an adjunct to the retina.
Chow said he is looking into ways to continue financing the Phase III development although he said it might not be through venture financing.
Despite the lengthy development times and funding challenges, those involved with the companies say they are motivated by the importance of their work. “Everybody says that this is a very ambitious project, but everybody admits that there is a real need here,” said Gross.
By Jonathan Matsey
While the phrase bionic retinas may conjure images of Steve Austin in “The Six Million Dollar Man” or Geordi La Forge in “Star Trek: The Next Generation,” technology to create vision where none, or very little, exists, is not a television fantasy. Companies concentrating on damaged retinas look poised for success as the technology inches toward measurable achievement.
“We will be approved on the market in Europe this year,” said Bill Link, managing director at Versant Ventures, an investor in Second Sight Medical Products Inc.
Second Sight, based in Sylmar, Calif., is also looking at a U.S. Food and Drug Administration submission at the end of 2011, according to Link. The company has raised $16 million in venture capital.
Second Sight’s system uses a pair of glasses to send images to a receiver implanted on the retina. From there, the image is transmitted to the brain through the optic nerve. The device is targeted to patients who have lost most of their vision as a result of retinal degeneration and whose nerve connections are still intact.
A similar approach is being developed by Nano Retina Inc. of Herzliya Pituach, Israel, though Nano Retina aims for much greater visual clarity than Second Sight, it says. “We have a much higher resolution – about 1,000 pixels,” said Ra’anan Gefen, managing director of the company. “Second Sight is the most advanced (clinically) but on the other hand, it is really a limited device.”
According to Link, Second Sight’s first-generation device offers 16 pixels while a second-generation system will have 60. “They can read letters on a computer screen, they can tell light from dark, they can see a line on the ground,” said Link of people using Second Sight’s system.
Gefen, on the other hand, is more ambitious. “We will give them back vision so that they can see almost normally,” he said.
Gefen’s company was founded as a joint venture with nanotech company Zyvex Labs LLC of Richardson, Texas, and is backed by several million dollars from Rainbow Medical, an Israeli business accelerator, according to Rainbow Founding Partner Yossi Gross. Nano Retina is still a couple of years away from clinical studies, Gross said.
Costs for the two systems appear to be about the same. Link estimates Second Sight’s device will sell for $50,000 to $100,000 per system; Gefen says Nano Retina’s will cost around $60,000. Both companies said they expect much of that cost to be picked up by insurance companies. Link said his portfolio company is currently in discussion with potential payers.
Waiting in the wings is a third player – Optobionics Corp. – which had raised around $50 million from investors including Advanced Medical Optics Inc., Advanced Technology Ventures, Arch Venture Partners, Medtronic Inc. and Polaris Venture Partners and had taken its device through Phase II trials before hitting a snag in fund-raising for Phase III trials.
“There was no appetite to put in another $100 million,” said Alan Chow, chief executive of Optobionics. As a result, his company entered bankruptcy in 2007, recently relaunching after Chow bought the technology.
Unlike the other two companies, Optobionics is pursuing a trickier and more costly approach: restoring function to the damaged retina by using the device to stimulate the rods and cones, rather than using the system as an adjunct to the retina.
Chow said he is looking into ways to continue financing the Phase III development although he said it might not be through venture financing.
Despite the lengthy development times and funding challenges, those involved with the companies say they are motivated by the importance of their work. “Everybody says that this is a very ambitious project, but everybody admits that there is a real need here,” said Gross.
Thursday, July 8, 2010
Arteries Age Twice as Fast in Smokers
By Ed Edelson
HealthDay Reporter
MONDAY, April 26 (HealthDay News) -- It's well-known that smoking is bad for the heart and other parts of the body, and researchers now have chronicled in detail one reason why -- because continual smoking causes progressive stiffening of the arteries.
In fact, smokers' arteries stiffen with age at about double the speed of those of nonsmokers, Japanese researchers have found.
Stiffer arteries are prone to blockages that can cause heart attacks, strokes and other problems.
"We've known that arteries become more stiff in time as one ages," said Dr. William B. Borden, a preventive cardiologist and assistant professor of medicine at Weill Cornell Medical Center in New York City. "This shows that smoking accelerates the process. But it also adds more information in terms of the role smoking plays as a cause of cardiovascular disease."
For the study, researchers at Tokyo Medical University measured the brachial-ankle pulse wave velocity, the speed with which blood pumped from the heart reaches the nearby brachial artery, the main blood vessel of the upper arm, and the faraway ankle. Blood moves slower through stiff arteries, so a bigger time difference means stiffer blood vessels.
Looking at more than 2,000 Japanese adults, the researchers found that the annual change in that velocity was greater in smokers than nonsmokers over the five to six years of the study.
Smokers' large- and medium-sized arteries stiffened at twice the rate of nonsmokers', according to the report released online April 26 in the Journal of the American College of Cardiology by the team from Tokyo and the University of Texas at Austin.
That's no big surprise, said Borden, noting there's definitely a dose-response relationship. "The more smoking, the more arterial stiffening there is per day."
The study authors measured stiffening by years, not by day, but the damaging effect of smoking was clear over the long run.
The finding gives doctors one more argument to use in their continuing effort to get smokers to quit, said Dr. David Vorchheimer, associate professor of medicine and cardiology at Mount Sinai Medical Center in New York City.
"One of the challenges that physicians face when trying to get people to stop smoking is the argument, 'Well, I've been smoking for years and nothing has happened to me yet,'" Vorchheimer said. "What this study emphasizes is that the damage is cumulative. The fact that you've gotten away with it so far doesn't mean you'll get away with it forever."
The stiffening of arteries is "one of the earliest and most subtle changes that occur" in smokers' bodies, Vorchheimer said. "Some people's arteries can be safe for a few years. The good thing about that is the possibility that the damage will heal if you give up smoking."
Another notable aspect of the study was the analysis of the effect of smoking on C-reactive protein, a molecular marker of inflammation that appears to play a role in cardiovascular disease. The study found no relationship between blood levels of C-reactive protein and arterial stiffening.
That finding adds one more piece to the puzzle of C-reactive protein and cardiovascular disease that researchers are trying to assemble, Borden said. "We're still trying to understand the role of CRP, whether it's a cause or a marker of other factors that lead to cardiovascular disease," he said.
HealthDay Reporter
MONDAY, April 26 (HealthDay News) -- It's well-known that smoking is bad for the heart and other parts of the body, and researchers now have chronicled in detail one reason why -- because continual smoking causes progressive stiffening of the arteries.
In fact, smokers' arteries stiffen with age at about double the speed of those of nonsmokers, Japanese researchers have found.
Stiffer arteries are prone to blockages that can cause heart attacks, strokes and other problems.
"We've known that arteries become more stiff in time as one ages," said Dr. William B. Borden, a preventive cardiologist and assistant professor of medicine at Weill Cornell Medical Center in New York City. "This shows that smoking accelerates the process. But it also adds more information in terms of the role smoking plays as a cause of cardiovascular disease."
For the study, researchers at Tokyo Medical University measured the brachial-ankle pulse wave velocity, the speed with which blood pumped from the heart reaches the nearby brachial artery, the main blood vessel of the upper arm, and the faraway ankle. Blood moves slower through stiff arteries, so a bigger time difference means stiffer blood vessels.
Looking at more than 2,000 Japanese adults, the researchers found that the annual change in that velocity was greater in smokers than nonsmokers over the five to six years of the study.
Smokers' large- and medium-sized arteries stiffened at twice the rate of nonsmokers', according to the report released online April 26 in the Journal of the American College of Cardiology by the team from Tokyo and the University of Texas at Austin.
That's no big surprise, said Borden, noting there's definitely a dose-response relationship. "The more smoking, the more arterial stiffening there is per day."
The study authors measured stiffening by years, not by day, but the damaging effect of smoking was clear over the long run.
The finding gives doctors one more argument to use in their continuing effort to get smokers to quit, said Dr. David Vorchheimer, associate professor of medicine and cardiology at Mount Sinai Medical Center in New York City.
"One of the challenges that physicians face when trying to get people to stop smoking is the argument, 'Well, I've been smoking for years and nothing has happened to me yet,'" Vorchheimer said. "What this study emphasizes is that the damage is cumulative. The fact that you've gotten away with it so far doesn't mean you'll get away with it forever."
The stiffening of arteries is "one of the earliest and most subtle changes that occur" in smokers' bodies, Vorchheimer said. "Some people's arteries can be safe for a few years. The good thing about that is the possibility that the damage will heal if you give up smoking."
Another notable aspect of the study was the analysis of the effect of smoking on C-reactive protein, a molecular marker of inflammation that appears to play a role in cardiovascular disease. The study found no relationship between blood levels of C-reactive protein and arterial stiffening.
That finding adds one more piece to the puzzle of C-reactive protein and cardiovascular disease that researchers are trying to assemble, Borden said. "We're still trying to understand the role of CRP, whether it's a cause or a marker of other factors that lead to cardiovascular disease," he said.
Saturday, July 3, 2010
Grapes could reduce diabetes and heart disease
By Richard Alleyne, Science Correspondent for the UK Telegraph
Published: 2:54PM BST 26 Apr 2010
The fruit lowered blood pressure, improved heart function and reduced other risk factors for heart disease and metabolic syndrome, it was claimed.
American researchers found this could be due to phytochemicals – naturally occurring antioxidants – that grapes contain.
Following animal tests, the research revealed a grape-enriched diet preventing risk factors for metabolic syndrome, a condition which is often a precursor to type 2 diabetes.
Mixing a blend of green, red and black grapes into the diets of laboratory rats as part of a high-fat, American style diet, they were compared with a test group fed with a similar diet full of fat and sugars.
After three months, the rats that received the grape-enriched diet had lower blood pressure, better heart function, and reduced indicators of inflammation in the heart and the blood than rats who received no grape powder.
Rats also had lower triglycerides and improved glucose tolerance.
Heart surgeon Dr Steven Bolling said: "The possible reasoning behind the lessening of metabolic syndrome is that the phytochemicals were active in protecting the heart cells from the damaging effects of metabolic syndrome.
"In the rats, inflammation of the heart and heart function was maintained far better.
"Although there's not a particular direct correlation between this study and what humans should do, it's very interesting to postulate that a diet higher in phytochemical-rich fruits, such as grapes, may benefit humans."
Although he added those wanting to lower blood pressure and reduce the risk of diabetes should follow some tried-and-true advice such as eating a healthy diet low in saturated fat, trans fat and cholesterol, maintain a desirable weight and exercise more.
The findings are published at the Experimental Biology convention in California.
Published: 2:54PM BST 26 Apr 2010
The fruit lowered blood pressure, improved heart function and reduced other risk factors for heart disease and metabolic syndrome, it was claimed.
American researchers found this could be due to phytochemicals – naturally occurring antioxidants – that grapes contain.
Following animal tests, the research revealed a grape-enriched diet preventing risk factors for metabolic syndrome, a condition which is often a precursor to type 2 diabetes.
Mixing a blend of green, red and black grapes into the diets of laboratory rats as part of a high-fat, American style diet, they were compared with a test group fed with a similar diet full of fat and sugars.
After three months, the rats that received the grape-enriched diet had lower blood pressure, better heart function, and reduced indicators of inflammation in the heart and the blood than rats who received no grape powder.
Rats also had lower triglycerides and improved glucose tolerance.
Heart surgeon Dr Steven Bolling said: "The possible reasoning behind the lessening of metabolic syndrome is that the phytochemicals were active in protecting the heart cells from the damaging effects of metabolic syndrome.
"In the rats, inflammation of the heart and heart function was maintained far better.
"Although there's not a particular direct correlation between this study and what humans should do, it's very interesting to postulate that a diet higher in phytochemical-rich fruits, such as grapes, may benefit humans."
Although he added those wanting to lower blood pressure and reduce the risk of diabetes should follow some tried-and-true advice such as eating a healthy diet low in saturated fat, trans fat and cholesterol, maintain a desirable weight and exercise more.
The findings are published at the Experimental Biology convention in California.
Friday, June 4, 2010
Gene therapy used to treat total color blindness in dogs
By Jacques Von Lunen, Special to The Oregon...
April 22, 2010, 12:37PM
Researchers at the University of Pennsylvania have successfully used gene therapy to treat a congenital eye disease that affects dogs and people.
The disease, achromatopsia, also called total color blindness, affects the function of the small cones in the retina that receive light. Proper function of the cones is essential for color and daytime vision. About one in 30,000-50,000 humans is afflicted with the disease.
Although achromatopsia is quite rare, its treatment is thought to function as a model for other, more common, diseases that affect the retinal cones.
The observed results of the study suggest the dogs' retinal cells and visual pathways were able to process the input from the restored cones.
This video filmed by the researchers shows how dogs with the disease could easily make their way through a darkened obstacle course, but had significant trouble navigating the same course in bright light. Dogs treated with the gene therapy walked the course with the same speed as healthy dogs.
The gene therapy targets mutations of a gene known as CNGB3, the most common cause of achromatopsia in humans. Dogs are the only large animal with CNGB3-achromatopsia.
The treatment cured young dogs and was effective for the 33 months of the study, which led researchers to believe that it is permanent. The success rate for dogs 54 weeks or older was lower than that for younger dogs.
Many vision-impairing disorders in humans result from genetic defects. So far, mutations have been identified in approximately 150 genes. This wealth of genetic information and the development of gene-transfer technologies make successful treatment of these disorders a real possibility for the first time.
-- Jacques Von Lunen
April 22, 2010, 12:37PM
Researchers at the University of Pennsylvania have successfully used gene therapy to treat a congenital eye disease that affects dogs and people.
The disease, achromatopsia, also called total color blindness, affects the function of the small cones in the retina that receive light. Proper function of the cones is essential for color and daytime vision. About one in 30,000-50,000 humans is afflicted with the disease.
Although achromatopsia is quite rare, its treatment is thought to function as a model for other, more common, diseases that affect the retinal cones.
The observed results of the study suggest the dogs' retinal cells and visual pathways were able to process the input from the restored cones.
This video filmed by the researchers shows how dogs with the disease could easily make their way through a darkened obstacle course, but had significant trouble navigating the same course in bright light. Dogs treated with the gene therapy walked the course with the same speed as healthy dogs.
The gene therapy targets mutations of a gene known as CNGB3, the most common cause of achromatopsia in humans. Dogs are the only large animal with CNGB3-achromatopsia.
The treatment cured young dogs and was effective for the 33 months of the study, which led researchers to believe that it is permanent. The success rate for dogs 54 weeks or older was lower than that for younger dogs.
Many vision-impairing disorders in humans result from genetic defects. So far, mutations have been identified in approximately 150 genes. This wealth of genetic information and the development of gene-transfer technologies make successful treatment of these disorders a real possibility for the first time.
-- Jacques Von Lunen
Friday, May 21, 2010
"Nanotechnology-Based" Vaccine Successfully Reverses Type 1 Diabetes In Mice.
By Serena Gordon
HealthDay Reporter
THURSDAY, April 8 (HealthDay News) -- Canadian researchers have successfully reversed type 1 diabetes in mice using a new vaccine technology that appears to solely target the immune system cells responsible for the disease.
"The body has built-in mechanisms that try to counter disease progression, and we now have a mechanism that can be [used] to selectively blunt an immune response without causing a systemic response," said the study's senior author, Dr. Pere Santamaria, a professor at the Julia McFarlane Diabetes Research Centre at the University of Calgary in Alberta.
What's more, Santamaria said, the technique developed for the diabetes vaccine may be applicable to other autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis.
So far, the research has only been conducted in mice. "We don't yet know if it will work in humans, but we're very excited and think this offers hope," said Santamaria.
Type 1 diabetes is an autoimmune disease. That means that the body's immune system, which usually targets invading unwanted cells, such as bacteria, mistakenly destroys healthy cells. In the case of type 1 diabetes, the immune system destroys the insulin-producing beta cells in the pancreas. This knocks out the body's ability to produce insulin, the hormone that helps convert blood sugar to energy for cells in the body. So, people with type 1 diabetes must inject insulin multiple times a day, every day, to stay alive.
"Autoimmune diseases, like type 1 diabetes, multiple sclerosis and rheumatoid arthritis, are caused by an overactive immune system. Normally, the immune system helps us fend off cancer and infection, but in some people, it becomes overaggressive," Santamaria explained.
Although there are medications available that can dampen the entire immune response, these medications can create additional problems, such as an increased risk of cancer and serious infection.
However, the Canadian researchers discovered that the body doesn't just allow the autoimmune aggression to go unchecked. There is a counter-mechanism that produces immune system cells to try to fight the rogue immune cells that are creating the damage in type 1 diabetes.
But these cells -- know as memory-like autoregulatory T cells -- aren't as strong as the rogue cells and so they quickly become overwhelmed.
Using a "nanotechnology-based" vaccine, the researchers were able to boost the effects of the weaker immune cells, which allowed them to stop the damaging immune cells from attacking. The vaccine consists of nanoparticles -- spheres thousands of times smaller than a single cell of the body -- "coated" with antigens that bind to molecules used to stimulate certain T cells.
"With this nanovaccine, we engage the weak immune cells and make them multiply and divide, and then they can counter the autoimmune response without impairing systemic immunity," said Santamaria.
Instead of directly attacking the stronger cells, the autoregulatory T cells turn off the signal that tells the stronger immune cells to attack, effectively stopping the destruction of the beta cells.
Santamaria said it's not clear yet if this vaccine would be a one-time treatment, or would need to be administered periodically. He said it's likely additional treatment might be necessary.
Santamaria said the next step in his work is to produce the drug in a version that can be used in clinical trials on humans.
Teodora Staeva, director of Immune Therapies for the Juvenile Diabetes Research Foundation International, called the new research "a very novel therapeutic approach that seems to have great potential."
"A lot of work remains to be done. This therapy has the promise of being safer -- although that has to be proven in toxicology studies -- because it specifically targets the cells that are causing the problems," Staeva said.
Staeva said that if this vaccine proves itself in human studies, it has the potential to help both newly diagnosed type 1 diabetics and those who've had the disease for years. But, she said, in people who've had type 1 for a long time, beta cell transplantation might be necessary.
Results of the study were published online April 8 and are to appear in the April 23 print version of the journal Immunity.
More information
Learn more about type 1 diabetes and the role of the immune system from the Juvenile Diabetes Research Foundation.
SOURCES: Pere Santamaria, M.D., Ph.D., professor, Julia McFarlane Diabetes Research Centre, University of Calgary, Alberta; Teodora Staeva, Ph.D., director, immune therapies, Juvenile Diabetes Research Foundation, New York City; April 23, 2010, Immunity
Last Updated: April 08, 2010
Copyright © 2010 HealthDay. All rights reserved.
HealthDay Reporter
THURSDAY, April 8 (HealthDay News) -- Canadian researchers have successfully reversed type 1 diabetes in mice using a new vaccine technology that appears to solely target the immune system cells responsible for the disease.
"The body has built-in mechanisms that try to counter disease progression, and we now have a mechanism that can be [used] to selectively blunt an immune response without causing a systemic response," said the study's senior author, Dr. Pere Santamaria, a professor at the Julia McFarlane Diabetes Research Centre at the University of Calgary in Alberta.
What's more, Santamaria said, the technique developed for the diabetes vaccine may be applicable to other autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis.
So far, the research has only been conducted in mice. "We don't yet know if it will work in humans, but we're very excited and think this offers hope," said Santamaria.
Type 1 diabetes is an autoimmune disease. That means that the body's immune system, which usually targets invading unwanted cells, such as bacteria, mistakenly destroys healthy cells. In the case of type 1 diabetes, the immune system destroys the insulin-producing beta cells in the pancreas. This knocks out the body's ability to produce insulin, the hormone that helps convert blood sugar to energy for cells in the body. So, people with type 1 diabetes must inject insulin multiple times a day, every day, to stay alive.
"Autoimmune diseases, like type 1 diabetes, multiple sclerosis and rheumatoid arthritis, are caused by an overactive immune system. Normally, the immune system helps us fend off cancer and infection, but in some people, it becomes overaggressive," Santamaria explained.
Although there are medications available that can dampen the entire immune response, these medications can create additional problems, such as an increased risk of cancer and serious infection.
However, the Canadian researchers discovered that the body doesn't just allow the autoimmune aggression to go unchecked. There is a counter-mechanism that produces immune system cells to try to fight the rogue immune cells that are creating the damage in type 1 diabetes.
But these cells -- know as memory-like autoregulatory T cells -- aren't as strong as the rogue cells and so they quickly become overwhelmed.
Using a "nanotechnology-based" vaccine, the researchers were able to boost the effects of the weaker immune cells, which allowed them to stop the damaging immune cells from attacking. The vaccine consists of nanoparticles -- spheres thousands of times smaller than a single cell of the body -- "coated" with antigens that bind to molecules used to stimulate certain T cells.
"With this nanovaccine, we engage the weak immune cells and make them multiply and divide, and then they can counter the autoimmune response without impairing systemic immunity," said Santamaria.
Instead of directly attacking the stronger cells, the autoregulatory T cells turn off the signal that tells the stronger immune cells to attack, effectively stopping the destruction of the beta cells.
Santamaria said it's not clear yet if this vaccine would be a one-time treatment, or would need to be administered periodically. He said it's likely additional treatment might be necessary.
Santamaria said the next step in his work is to produce the drug in a version that can be used in clinical trials on humans.
Teodora Staeva, director of Immune Therapies for the Juvenile Diabetes Research Foundation International, called the new research "a very novel therapeutic approach that seems to have great potential."
"A lot of work remains to be done. This therapy has the promise of being safer -- although that has to be proven in toxicology studies -- because it specifically targets the cells that are causing the problems," Staeva said.
Staeva said that if this vaccine proves itself in human studies, it has the potential to help both newly diagnosed type 1 diabetics and those who've had the disease for years. But, she said, in people who've had type 1 for a long time, beta cell transplantation might be necessary.
Results of the study were published online April 8 and are to appear in the April 23 print version of the journal Immunity.
More information
Learn more about type 1 diabetes and the role of the immune system from the Juvenile Diabetes Research Foundation.
SOURCES: Pere Santamaria, M.D., Ph.D., professor, Julia McFarlane Diabetes Research Centre, University of Calgary, Alberta; Teodora Staeva, Ph.D., director, immune therapies, Juvenile Diabetes Research Foundation, New York City; April 23, 2010, Immunity
Last Updated: April 08, 2010
Copyright © 2010 HealthDay. All rights reserved.
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