Vitamin C Cures Fast Aging Mice from Cancer,
Diabetes, Heart Failure, High Cholesterol
Clearly indicates that healthy individuals do not
require a large amount of vitamin C in order to increase their lifespan,
scientist says
Jan.
4, 2010 Vitamin C has been found to cure mice from abnormalities
caused by Werner syndrome (accelerated aging) gene, including cancer,
obesity, diabetes, heart failure and high cholesterol in new research
published in the FASEB Journal.
In the research report in the January 2010 issue, a
team of Canadian scientists show that vitamin C stops and even reverses
accelerated aging in a mouse model of Werner's syndrome, but the
discovery may also be applicable to other progeroid syndromes.
People with Werner's syndrome begin to show signs
of accelerated aging in their 20s and develop age-related diseases and
generally die before the age of 50.
"Our study clearly indicates that a healthy
organism or individuals with no health problems do not require a large
amount of vitamin C in order to increase their lifespan, especially if
they have a balanced diet and they exercise," said Michel Lebel, Ph.D.,
co-author of the study from the Centre de Recherche en Cancerologie in
Quebec, Canada.
"An organism or individual with a mutation in the
WRN gene or any gene affected by the WRN protein, and thus predisposes
them to several age-related diseases, may benefit from a diet with the
appropriate amount of vitamin C."
Scientists treated both normal mice and mice with a
mutation in the gene responsible for Werner's syndrome (WRN gene) with
vitamin C in drinking water.
Before treatment, the mice with a mutated WRN gene
were fat, diabetic, and developing heart disease and cancer. After
treatment, the mutant mice were as healthy as the normal mice and lived
a normal lifespan.
Progeroid syndromes (PSs) constitute a group of
disorders characterized by clinical features mimicking physiological
aging at an early age. In some of these syndromes, biological hallmarks
of aging are also present, whereas in others, a link with physiological
aging, if any, remains to be elucidated. These syndromes are clinically
and genetically heterogeneous and most of them, including Werner
syndrome and Hutchinson-Gilford progeria, are known as 'segmental aging
syndromes', as they do not feature all aspects usually associated to
physiological aging. However, all the characterized PSs enter in the
field of rare monogenic disorders and several causative genes have been
identified.
Vitamin C also improved how the mice stored and
burned fat, decreased tissue inflammation and decreased oxidative stress
in the WRN mice.
The healthy mice did not appear to benefit from
vitamin C.
"Vitamin C has become one of the most misunderstood
substances in our medicine cabinets and food," said Gerald Weissmann,
M.D., Editor-in-Chief of the FASEB Journal.
"This study and others like it help explain how and
why this chemical can help to defend some, but certainly not all, people
from premature senescence (aging)."
Source:
The FASEB Journal (http://www.fasebj.org)
is published by the Federation of the American Societies for
Experimental Biology (FASEB). The journal has been recognized by the
Special Libraries Association as one of the top 100 most influential
biomedical journals of the past century and is the most cited biology
journal worldwide according to the Institute for Scientific Information.
FASEB comprises 22 nonprofit societies with more than 80,000 members,
making it the largest coalition of biomedical research associations in
the United States. FASEB advances health and welfare by promoting
progress and education in biological and biomedical sciences through
service to its member societies and collaborative advocacy.
Details: Laurent Massip, Chantal Garand, Eric R.
Paquet, Victoria C. Cogger, Jennifer N. O'Reilly, Leslee Tworek, Avril
Hatherell, Carla G. Taylor, Eric Thorin, Peter Zahradka, David G. Le
Couteur, and Michel Lebel. Vitamin C restores healthy aging in a mouse
model for Werner syndrome. FASEB J. 2010 24: 158-172.
http://www.fasebj.org/cgi/content/abstract/24/1/158