Strawberries May Delay Onset of Huntington's Disease

by VR Sreeraman on  November 17, 2010 at 2:03 PM

Diet & Nutrition News

  

In a new study, scientists found that strawberries and other fruits and vegetables slows the onset of motor problems and delays
death in three models of Huntington's disease.

Researchers at the Salk Institute for Biological Studies studied Fisetin, a naturally occurring compound found in many fruits and
vegetables, and its role in treating Huntington's and other neurodegenerative conditions.

Huntington's disease (HD) is an inherited disorder that destroys neurons in certain parts of the brain and slowly erodes victims'
ability to walk, talk and reason.

It is caused by a kind of genetic stutter, which leads to the expansion of a trinucleotide repeat in the huntingtin protein. When the
length of the repeated section reaches a certain threshold, the bearer develops Huntington's disease.

Pamela Maher and her team began their study by looking at a nerve cell line that could be made to express a mutant form of the
Huntington protein. Without treatment, about 50 percent of these cells will die within a few days. Adding fisetin, however,
prevented cell death.

Next, Maher tested fisetin in fruit flies overexpressing mutant Huntington in neurons in the brain. The affected flies don't live as long
as normal flies and also have defective eye development. When they were fed fisetin, however, the HD flies maintained their life
span and had fewer eye defects.

The team also found that mutant mice that were fed fisetin experienced a delay in the onset of motor defects, and their life span
was extended by about 30 percent.

Read more: Strawberries May Delay Onset of Huntington's Disease http://www.medindia.net/news/Strawberries-May-Delay-Onset-

of-Huntingtons-Disease-76817-1.htm#ixzz15XZ8zxIt
Diets Fail Due to Greediness Gene
by Kathy Jones on  November 16, 2010 at 9:35 PM

Diet & Nutrition News

A new study says that the 'greediness gene' in you causes diets to fail even before they start.

Briton researchers from Oxford University and the Medical Research Council have shown that a rogue gene
linked to obesity makes us fat by boosting appetite.

The find may pave way for drugs that take the edge off appetite, melting away 'muffin tops' and pruning pot
bellies.

The researchers found a gene called FTO, which was the first widespread genetic flaw to be linked to obesity.
In a previous study, those who carried two rogue copies of the rogue DNA increased their risk of obesity by 70
per cent and diabetes by 50 per cent.

49 per cent who inherit just one flawed FTO gene are 30 per cent more likely to be obese than those with two
normal copies of the gene.

"For the first time we have provided convincing proof that the FTO gene causes obesity," The Daily Mail
quoted researcher Chris Church as saying.

"The next step is to understand how it does this, for instance whether it increases appetite by influencing our
brain or alters messages from our fat stores and other tissues," he added.

The research is reported in the journal Nature Genetics.

Source-ANI
Obesity 'Virus' Spreads Like Common Cold, Scientists Say

Monday, January 26, 2009

 Reuters

A passenger waits for a delayed flight at Heathrow Airport in London.

Obesity can be "caught" as easily as a common cold from other people's coughs, sneezes and dirty hands, scientists said Monday.

The condition has been linked to a highly-infectious virus which causes sniffles and sore throats.

Nikhil Dhurandhar, an associate professor at The Pennington Biomedical Research Center, in Baton Rouge, La., said the virus, known
as AD-36, infects the lungs then whisks around the body, forcing fat cells to multiply and also causing sore throats.

"When this virus goes to fat tissue it replicates, making more copies of itself and in the process increases the number of new fat
cells, which may explain why the fat tissue expands and why people get fat when they are infected with this virus," Dhurandhar said.

In one test, a third of obese people had the rare and highly contagious virus compared to just 11 percent of thinner people. Weight
gain can last three months until the body has built up resistance to the bug.

New research supports earlier theories from studies on weight gain; evidence in tests on mice and chickens shows the bug could
cause overweight people to gain weight.

"People could be fat for reasons other than viral infections, so it’s pointless for fat people to try to avoid infection," said Dhurandhar.

The study also reveals research claiming dieters always feel hungry because humans have a "natural body weight" and they will
always suffer hunger pangs.

The Pennington Biomedical Research Center, a campus of the Louisiana State University system, conducts both clinical and basic
research. Its mission is to promote healthier lives through research and education in nutrition

and preventive medicine.

Adenovirus serotype 36
From Wikipedia, the free encyclopedia
  (Redirected from Obesity virus)
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Adenovirus serotype 36
Virus classification
Group: Group I (dsDNA)
Family: Adenoviridae
Genus: Mastadenovirus
Human adenovirus D
Species:
(HAdV-D)

Human adenovirus 36 (HAdV-36) or Ad-36 or Adv36 is one of 52 types of adenoviruses known to infect
humans. AD-36 was first isolated in 1978 from the feces of a girl suffering from diabetes and enteritis, and has
long been recognized as a cause of respiratory and eye infections in humans. It was first shown to be associated
with obesity in chickens by Dr. Nikhil Dhurandhar.[3][4]

There has been a positive correlation between body fat and the presence of AD-36 antibodies in the blood/
Previous research showed that chicken or mice injected with similar types of viruses show a statistically
significant weight gain.

To date, AD-36 is the only human adenovirus that has been linked with human obesity, present in 30% of obese
humans and 11% of nonobese humans. In addition, a study of obese Americans indicates that about 30% of the
obese individuals and only 5% of non-obese individuals have antibodies to Ad-36. Another study determined
that children with the virus averaged 52 pounds heavier than those with no signs of it and obese children with
the virus averaged 35 pounds heavier than obese children with no trace of the virus. AD-36 also causes obesity
in chickens, mice, rats, and monkeys.AD-36 infection can induce cellular differentiation of 3T3-L1
preadipocytes and stem cells derived from human adipose tissue
November 9th, 2010

Lip-Licking Self Destruction…

If your lips are dry or chapped you’d think that licking them would be a reasonable solution.

What you may not know is that licking your lips does more harm than good.

Common issues for lip-lickers…

Digestion of your own skin

Saliva contains digestive enzymes which help begin breaking down the foods we eat.  When in contact with the
lips it can begin to eat away at the skin and cause irritation around the corners of the mouth.

The reason the lips are sensitive to this is because unlike most of the skin on the body, the lips don’t produce
“sebum” – an oily substance that acts as a line of defence.  This is where chap-stick comes in.

Increased Dryness

 You’d think that licking the lips would, at least temporarily, moisturize the lips…

What ends up happening instead is the opposite – increased dryness!

Why increased dryness?

When licking the lips, the water on the surface begins to evaporate.  In the evaporation process additional
moisture from within the lips ends up being drawn out. The result – Lips that are even more dry.  

With drier lips we instinctively lick our lips again and again… at this point we are stuck deep in a vicious circle
of dryness.

Sources: Medicineonline