Health and Fitness Blog

SEOUL (Reuters) -
South Korea plans to help obese children pay for health club membership and other activities that can help them lose weight, an official said on Wednesday.

Health ministry official Chun Myung-sook said the rate of childhood obesity had tripled over the past three years due to a changing diet higher in fatty foods and a more sedentary lifestyle.

Under the government plan, elementary school students whose body mass index indicates obesity will be able to receive up to 40,000 won ($33.58) a month to help them bring their weight down.

“Kids won’t be able to waste the money on eating sweets. We will give them electronic vouchers that can only be used in designated places,” Chun said.

Costs to the government and the economy related to childhood obesity were 2 trillion won in 2006, the ministry said, making the voucher program cost effective.

(Reporting by Kim Junghyun and Jon Herskovitz; Editing by Jonathan Hopfner)

Source

SEOUL (Reuters) -
South Korea plans to help obese children pay for health club membership and other activities that can help them lose weight, an official said on Wednesday.

Health ministry official Chun Myung-sook said the rate of childhood obesity had tripled over the past three years due to a changing diet higher in fatty foods and a more sedentary lifestyle.

Under the government plan, elementary school students whose body mass index indicates obesity will be able to receive up to 40,000 won ($33.58) a month to help them bring their weight down.

“Kids won’t be able to waste the money on eating sweets. We will give them electronic vouchers that can only be used in designated places,” Chun said.

Costs to the government and the economy related to childhood obesity were 2 trillion won in 2006, the ministry said, making the voucher program cost effective.

(Reporting by Kim Junghyun and Jon Herskovitz; Editing by Jonathan Hopfner)

Source

TUESDAY, Sept. 30 (HealthDay News) — Drugs used to treat obesity may
be effective against a wide range of viral infections such as the flu,
hepatitis, and even HIV, say researchers from the University of Rochester
Medical Center and Princeton University.

In cellular metabolism, glucose can be converted into fatty acids — a
process known as fatty acid biosynthesis. Fatty acid biosynthesis is not
essential in humans, but many viruses use these fatty acids to build their
viral envelopes, or outer coatings, which help the viruses penetrate and
infect human cells.

For the new study, published Sept. 28 in the journal Nature
Biotechnology, the researchers developed techniques to monitor cell
metabolism as human cells become infected by a virus called human
cytomegalovirus (HCMV). HCMV serves as a model for the processes that
occur in many enveloped viral infections and in cancer.

“Using new fluxomic techniques, our study reveals that viral infection
takes control of cellular metabolism and drives, among other things,
marked increases in fatty acid synthesis,” study author John Munger,
assistant professor of biochemistry and biophysics at the University of
Rochester Medical Center, said in a medical center news release. “We also
found that if you target these increases in fatty acid metabolism using
existing anti-obesity and anti-metabolism drugs, you inhibit viral
replication.”

Using their technique, the researchers tracked isotope-labeled glucose
as it spread during cellular metabolism. They measured the impact that
infection with HCMV had on the speed at which the labeled glucose
spread.

To determine whether interfering with fatty acid biosynthesis could
stop viral replication, the researchers studied the effects of drugs that
inhibit acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), which
are enzymes that build fatty acids. These drugs are currently used to
treat obesity and high cholesterol.

Treatment with 5-tetradecyloxy-2-furoic acid (TOFA), an ACC inhibitor,
resulted in a more than thousand-fold reduction in HCMV replication. And
treatment with C75 (trans-4-carboxy-5-octyl-3-methylene-butyrolactone), an
inhibitor of FAS, resulted in a more than 100-fold reduction in the virus’
replication.

To see if the drugs would impact the replication of other enveloped
viruses, the researchers measured the replication of influenza A in the
presence of the same drug. They found similar reductions in
replication.

“Recent studies have shown that fatty acid biosynthesis is important
for the replication of diverse enveloped viruses,” said Munger. “The
replication of both hepatitis C and HIV, for example, has been linked
recently with lipid synthesis, reinforcing our approach and its
importance. Lastly, viral infection also clearly upregulates glycolysis, a
marker for tumor growth, which is just the latest in the longstanding
connection between viruses and cancer. Hopefully, our work will at some
point provide insight into the metabolic manipulations seen in cancer as
well.”

More information

The American Society for Microbiology has more about viruses.

Source

TUESDAY, Sept. 30 (HealthDay News) — Drugs used to treat obesity may
be effective against a wide range of viral infections such as the flu,
hepatitis, and even HIV, say researchers from the University of Rochester
Medical Center and Princeton University.

In cellular metabolism, glucose can be converted into fatty acids — a
process known as fatty acid biosynthesis. Fatty acid biosynthesis is not
essential in humans, but many viruses use these fatty acids to build their
viral envelopes, or outer coatings, which help the viruses penetrate and
infect human cells.

For the new study, published Sept. 28 in the journal Nature
Biotechnology, the researchers developed techniques to monitor cell
metabolism as human cells become infected by a virus called human
cytomegalovirus (HCMV). HCMV serves as a model for the processes that
occur in many enveloped viral infections and in cancer.

“Using new fluxomic techniques, our study reveals that viral infection
takes control of cellular metabolism and drives, among other things,
marked increases in fatty acid synthesis,” study author John Munger,
assistant professor of biochemistry and biophysics at the University of
Rochester Medical Center, said in a medical center news release. “We also
found that if you target these increases in fatty acid metabolism using
existing anti-obesity and anti-metabolism drugs, you inhibit viral
replication.”

Using their technique, the researchers tracked isotope-labeled glucose
as it spread during cellular metabolism. They measured the impact that
infection with HCMV had on the speed at which the labeled glucose
spread.

To determine whether interfering with fatty acid biosynthesis could
stop viral replication, the researchers studied the effects of drugs that
inhibit acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), which
are enzymes that build fatty acids. These drugs are currently used to
treat obesity and high cholesterol.

Treatment with 5-tetradecyloxy-2-furoic acid (TOFA), an ACC inhibitor,
resulted in a more than thousand-fold reduction in HCMV replication. And
treatment with C75 (trans-4-carboxy-5-octyl-3-methylene-butyrolactone), an
inhibitor of FAS, resulted in a more than 100-fold reduction in the virus’
replication.

To see if the drugs would impact the replication of other enveloped
viruses, the researchers measured the replication of influenza A in the
presence of the same drug. They found similar reductions in
replication.

“Recent studies have shown that fatty acid biosynthesis is important
for the replication of diverse enveloped viruses,” said Munger. “The
replication of both hepatitis C and HIV, for example, has been linked
recently with lipid synthesis, reinforcing our approach and its
importance. Lastly, viral infection also clearly upregulates glycolysis, a
marker for tumor growth, which is just the latest in the longstanding
connection between viruses and cancer. Hopefully, our work will at some
point provide insight into the metabolic manipulations seen in cancer as
well.”

More information

The American Society for Microbiology has more about viruses.

Source

TUESDAY, Sept. 30 (HealthDay News) — Researchers have uncovered
a genetic link between obesity and the risk for colon cancer. The
discovery could lead to greater accuracy in predicting who is at risk for
the disease, experts say.

Research has suggested that colon cancer risk rises with increasing
weight, but this finding points to a genetic reason for the link.

“We have discovered that a genetic variant of the adiponectin gene,
called ADIPOQ, is associated with colon cancer risk,” said lead researcher
Dr. Boris Pasche, director of the division of hematology and oncology at
the Comprehensive Cancer Center of the University of Alabama at
Birmingham. “This genetic variant may identify individuals who have a
higher risk to develop colorectal cancer,” he said.

The report was published in the Oct. 1 issue of the Journal of the
American Medical Association.

For the study, Pasche’s team focused on ADIPOQ. This gene promotes the
formation of a fat hormone called adiponectin. People who inherit a common
variant of the gene have up to a 30 percent lower risk of colon cancer
compared with people without this gene variant, the study found.

On the other hand, the researchers believe that people who do
not have this gene variant, or those who have high levels of
adiponectin in their blood, may be at a slightly increased risk for colon
cancer and could benefit from early screening for the disease.

“Adiponectin, a hormone exclusively secreted by the adipose [fat]
tissue, is now genetically linked with colorectal cancer,” Pasche said.
“This is the first evidence that genetic variants of a ‘fat hormone’
affect risk of colorectal cancer,” he said.

Whether people without this gene variant can reduce their risk of colon
cancer through diet and exercise isn’t clear, the researchers noted.

“This adds a little bit more to our understanding of one place where
genetics plays a role in prostate cancer development,” said Dr. Durado
Brooks, director of colon and prostate cancer prevention programs at the
American Cancer Society. “It helps point us in some more specific
directions; it adds another piece to the puzzle,” he said.

Brooks does not believe that the finding is definitive, however. “It
supports some of the other work that has already been done, identifying
this particular gene region with colorectal cancer,” he said.

The finding does help clarify one element linking obesity and colon
cancer, but “there is no clinical application to this finding in the
immediate future,” Brooks said. “I don’t think we would alter any
recommendation, other than encouraging people to maintain a healthy
weight.”

Dr. Georgia Wiesner, a cancer geneticist at University Hospitals‘ Case
Medical Center in Cleveland, agreed.

“I’d love to say that any time we find a new gene that identifies risk
or alters risk we would be able to put that into a new drug treatment or
at least identify people who are more at risk,” Wiesner said. “But in this
study, it might just tease out the pathogenesis of disease,” she said.

It’s already known that people who are obese have a higher risk for
colon cancer, Wiesner said. “I don’t know that telling somebody they might
have a specific marker is really going to alter what they are going to
do,” she said. “It doesn’t mean that these people don’t need regular
screening.”

More information

For more on colon cancer, visit the American Cancer Society.

Source

TUESDAY, Sept. 30 (HealthDay News) — Researchers have uncovered
a genetic link between obesity and the risk for colon cancer. The
discovery could lead to greater accuracy in predicting who is at risk for
the disease, experts say.

Research has suggested that colon cancer risk rises with increasing
weight, but this finding points to a genetic reason for the link.

“We have discovered that a genetic variant of the adiponectin gene,
called ADIPOQ, is associated with colon cancer risk,” said lead researcher
Dr. Boris Pasche, director of the division of hematology and oncology at
the Comprehensive Cancer Center of the University of Alabama at
Birmingham. “This genetic variant may identify individuals who have a
higher risk to develop colorectal cancer,” he said.

The report was published in the Oct. 1 issue of the Journal of the
American Medical Association.

For the study, Pasche’s team focused on ADIPOQ. This gene promotes the
formation of a fat hormone called adiponectin. People who inherit a common
variant of the gene have up to a 30 percent lower risk of colon cancer
compared with people without this gene variant, the study found.

On the other hand, the researchers believe that people who do
not have this gene variant, or those who have high levels of
adiponectin in their blood, may be at a slightly increased risk for colon
cancer and could benefit from early screening for the disease.

“Adiponectin, a hormone exclusively secreted by the adipose [fat]
tissue, is now genetically linked with colorectal cancer,” Pasche said.
“This is the first evidence that genetic variants of a ‘fat hormone’
affect risk of colorectal cancer,” he said.

Whether people without this gene variant can reduce their risk of colon
cancer through diet and exercise isn’t clear, the researchers noted.

“This adds a little bit more to our understanding of one place where
genetics plays a role in prostate cancer development,” said Dr. Durado
Brooks, director of colon and prostate cancer prevention programs at the
American Cancer Society. “It helps point us in some more specific
directions; it adds another piece to the puzzle,” he said.

Brooks does not believe that the finding is definitive, however. “It
supports some of the other work that has already been done, identifying
this particular gene region with colorectal cancer,” he said.

The finding does help clarify one element linking obesity and colon
cancer, but “there is no clinical application to this finding in the
immediate future,” Brooks said. “I don’t think we would alter any
recommendation, other than encouraging people to maintain a healthy
weight.”

Dr. Georgia Wiesner, a cancer geneticist at University Hospitals‘ Case
Medical Center in Cleveland, agreed.

“I’d love to say that any time we find a new gene that identifies risk
or alters risk we would be able to put that into a new drug treatment or
at least identify people who are more at risk,” Wiesner said. “But in this
study, it might just tease out the pathogenesis of disease,” she said.

It’s already known that people who are obese have a higher risk for
colon cancer, Wiesner said. “I don’t know that telling somebody they might
have a specific marker is really going to alter what they are going to
do,” she said. “It doesn’t mean that these people don’t need regular
screening.”

More information

For more on colon cancer, visit the American Cancer Society.

Source

TUESDAY, Sept. 30 (HealthDay News) — Drugs used to treat obesity may
be effective against a wide range of viral infections such as the flu,
hepatitis, and even HIV, say researchers from the University of Rochester
Medical Center and Princeton University.

In cellular metabolism, glucose can be converted into fatty acids — a
process known as fatty acid biosynthesis. Fatty acid biosynthesis is not
essential in humans, but many viruses use these fatty acids to build their
viral envelopes, or outer coatings, which help the viruses penetrate and
infect human cells.

For the new study, published Sept. 28 in the journal Nature
Biotechnology, the researchers developed techniques to monitor cell
metabolism as human cells become infected by a virus called human
cytomegalovirus (HCMV). HCMV serves as a model for the processes that
occur in many enveloped viral infections and in cancer.

“Using new fluxomic techniques, our study reveals that viral infection
takes control of cellular metabolism and drives, among other things,
marked increases in fatty acid synthesis,” study author John Munger,
assistant professor of biochemistry and biophysics at the University of
Rochester Medical Center, said in a medical center news release. “We also
found that if you target these increases in fatty acid metabolism using
existing anti-obesity and anti-metabolism drugs, you inhibit viral
replication.”

Using their technique, the researchers tracked isotope-labeled glucose
as it spread during cellular metabolism. They measured the impact that
infection with HCMV had on the speed at which the labeled glucose
spread.

To determine whether interfering with fatty acid biosynthesis could
stop viral replication, the researchers studied the effects of drugs that
inhibit acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), which
are enzymes that build fatty acids. These drugs are currently used to
treat obesity and high cholesterol.

Treatment with 5-tetradecyloxy-2-furoic acid (TOFA), an ACC inhibitor,
resulted in a more than thousand-fold reduction in HCMV replication. And
treatment with C75 (trans-4-carboxy-5-octyl-3-methylene-butyrolactone), an
inhibitor of FAS, resulted in a more than 100-fold reduction in the virus’
replication.

To see if the drugs would impact the replication of other enveloped
viruses, the researchers measured the replication of influenza A in the
presence of the same drug. They found similar reductions in
replication.

“Recent studies have shown that fatty acid biosynthesis is important
for the replication of diverse enveloped viruses,” said Munger. “The
replication of both hepatitis C and HIV, for example, has been linked
recently with lipid synthesis, reinforcing our approach and its
importance. Lastly, viral infection also clearly upregulates glycolysis, a
marker for tumor growth, which is just the latest in the longstanding
connection between viruses and cancer. Hopefully, our work will at some
point provide insight into the metabolic manipulations seen in cancer as
well.”

More information

The American Society for Microbiology has more about viruses.

Source

TUESDAY, Sept. 30 (HealthDay News) — Researchers have uncovered
a genetic link between obesity and the risk for colon cancer. The
discovery could lead to greater accuracy in predicting who is at risk for
the disease, experts say.

Research has suggested that colon cancer risk rises with increasing
weight, but this finding points to a genetic reason for the link.

“We have discovered that a genetic variant of the adiponectin gene,
called ADIPOQ, is associated with colon cancer risk,” said lead researcher
Dr. Boris Pasche, director of the division of hematology and oncology at
the Comprehensive Cancer Center of the University of Alabama at
Birmingham. “This genetic variant may identify individuals who have a
higher risk to develop colorectal cancer,” he said.

The report was published in the Oct. 1 issue of the Journal of the
American Medical Association.

For the study, Pasche’s team focused on ADIPOQ. This gene promotes the
formation of a fat hormone called adiponectin. People who inherit a common
variant of the gene have up to a 30 percent lower risk of colon cancer
compared with people without this gene variant, the study found.

On the other hand, the researchers believe that people who do
not have this gene variant, or those who have high levels of
adiponectin in their blood, may be at a slightly increased risk for colon
cancer and could benefit from early screening for the disease.

“Adiponectin, a hormone exclusively secreted by the adipose [fat]
tissue, is now genetically linked with colorectal cancer,” Pasche said.
“This is the first evidence that genetic variants of a ‘fat hormone’
affect risk of colorectal cancer,” he said.

Whether people without this gene variant can reduce their risk of colon
cancer through diet and exercise isn’t clear, the researchers noted.

“This adds a little bit more to our understanding of one place where
genetics plays a role in prostate cancer development,” said Dr. Durado
Brooks, director of colon and prostate cancer prevention programs at the
American Cancer Society. “It helps point us in some more specific
directions; it adds another piece to the puzzle,” he said.

Brooks does not believe that the finding is definitive, however. “It
supports some of the other work that has already been done, identifying
this particular gene region with colorectal cancer,” he said.

The finding does help clarify one element linking obesity and colon
cancer, but “there is no clinical application to this finding in the
immediate future,” Brooks said. “I don’t think we would alter any
recommendation, other than encouraging people to maintain a healthy
weight.”

Dr. Georgia Wiesner, a cancer geneticist at University Hospitals‘ Case
Medical Center in Cleveland, agreed.

“I’d love to say that any time we find a new gene that identifies risk
or alters risk we would be able to put that into a new drug treatment or
at least identify people who are more at risk,” Wiesner said. “But in this
study, it might just tease out the pathogenesis of disease,” she said.

It’s already known that people who are obese have a higher risk for
colon cancer, Wiesner said. “I don’t know that telling somebody they might
have a specific marker is really going to alter what they are going to
do,” she said. “It doesn’t mean that these people don’t need regular
screening.”

More information

For more on colon cancer, visit the American Cancer Society.

Source

WASHINGTON (AFP) -
The discovery of a genetic link between obesity and colon cancer may pave the way for more effective screening tests for the disease, according to a study published Tuesday.

Researchers found that people who inherit a variation of a gene called ADIPOQ, which results in the formation of a fat hormone called adiponectin, are 30 percent less likely to develop colon cancer.

People identified without this gene variant, or who have excessive blood levels of the fat hormone, would therefore benefit from early colon examinations, said Boris Pasche, professor at the University of Alabama Comprehensive Cancer Center and lead author of the study.

“Our hope is that we can significantly improve the screening and early detection for this disease, and open new avenues for better understanding the genetic and lifestyle factors that influence colon cancer risk,” said Pasche.

A third of people with colon cancer have a family history of the disease, he said.

Scientists have already proven a link between obesity and genetics, and that colon cancer is influenced by genetics.

The latest study, published in the Journal of the American Medical Association, is the first to prove a three-way connection between genetics, obesity and colon cancer risk.

The study showed that test subjects who did not have the genetic variation could reduce their risk through physical exercise and dieting to lose weight.

Colon cancer is the third deadliest cancer in the United States.

Nearly 150,000 Americans are diagnosed each year, and 50,000 of those diagnosed die from the disease, according to estimates from the American Cancer Society.

Source

Hurricanes Gustav, Ike and other disasters have long-reaching affects; 57.7 million Americans experience a mental health disorder in any given year; the National Alliance on Mental Illness and other organizations, including Allsup, are raising awareness during Mental Illness Awareness Week

Belleville, IL (Vocus/PRWEB ) September 25, 2008 — It is the storm damage that people often don’t talk about–mental disorders such as depression, anxiety and post-traumatic stress disorder that strike in the wake of a catastrophic experience.

Mental Illness Awareness Week poster

Post-trauma mental conditions are one of many mental disorders that affect some 57.7 million Americans in any given year, according to the National Alliance on Mental Illness, which is observing Mental Illness Awareness Week, Oct. 5-11, 2008. Organizations, including Allsup, which represents people nationwide for Social Security Disability Insurance benefits, are helping to raise awareness about mental illnesses and the help available to people and their families.

Anxiety disorders, including post-traumatic stress disorder (PTSD), panic disorder and phobias, affect about 40 million people, NAMI reports. One in five veterans of Iraq and Afghanistan (almost 300,000 troops) will experience major depression or PTSD when they return home. Other types of mental disorders also affect millions of people, including 5.7 million with bipolar disorder and 2.4 million who have schizophrenia.

“People living with mental illnesses often are among the most vulnerable in our society. Unfortunately, they also are often overlooked during disasters,” said NAMI executive director Michael J. Fitzpatrick, who recently announced the creation of a NAMI Hurricane Relief Fund to help individuals and families affected by hurricanes Gustav and Ike.

NAMI makes a number of resources and support available through its Web site, including:

• About Medications: Find details on specific medications, dosages and treatment information.
• State & Local NAMIs: Get contact information for local associations through a state-by-state guide.
• Support Programs: Find support and build connections through peer-to-peer, family and caregiver offerings.

One of the most significant facts about mental illness is that two-thirds of people living with a condition do not receive treatment. During Mental Illness Awareness Week, the association is emphasizing the theme, “Building Community. Taking Action.”

Mental illness can affect anyone at any time, and the benefit for individuals and their families comes from realizing that mental health is a part of everyone’s well-being and healthcare.

Allsup is observing Mental Illness Awareness Week with free posters available to hospitals, clinics and other community groups by calling Karen Hercules-Doerr at (800) 854-1418, ext. 5770.

Media contact:
National Alliance on Mental Illness
Christine Armstrong
(703) 524-7600
christinea@nami.org
www.nami.org

Free posters:
Allsup
Karen Hercules-Doerr
(800) 854-1418, ext. 5770
k.hercules-doerr@allsupinc.com
http://www.allsupcares.com

Source