Kumar:
Wouldn't you like to see evidence of someone's "law" before you
consider it established?
In any case, cells obviously respond to stimuli, and the amount of
stimuli is important, just as the kind of stimulation. Also, in the
short term, "benefits" might be seen, but in the long term, serious
damage might be done (or something like cancer may result).
It is more useful to look at work that has actually been done. Below
is a report of one such study, from sciencedaily.com. They appear to
be missing the obvious point that it may be possible to avoid stressors
to begin with, and thus "stimulating" cells to produce more
antioxidants may not be necessary. Actually, it may be dangerous to do
this for more than a couple week or a month or so, but for some reason,
the researchers seem to get very excited, perhaps thinking they are the
next Einsteins, but then the long term results come in and they move on
to something else, realizing that their idea is a failure. This
happens over and over again, but they never seem to learn, perhaps
because the history of science is not of much interest to most
scientists. They always want to be "in the forefront," but the problem
is that the "forefront" has produced next to nothing over the last few
decades, at the very least.
1/25/2006
Researchers Discover New Way To Stimulate Brain To Release Antioxidants
A joint research effort between researchers at the Burnham Institute
for Medical Research in La Jolla, CA, and a team from Japan (Iwate
University, Osaka City University, Gifu University, Iwate Medical
University) has discovered a novel way to treat stroke and
neurodegenerative disorders. This approach works by inducing nerve
cells in the brain and the spine to release natural antioxidants that
protect nerve cells from stress and free radicals that lead to
neurodegenerative diseases. Until this discovery, researchers were
unable to induce release of these specific antioxidants directly in
nerve cells, at the site where damage and degeneration occurs.
In stroke and various neurodegenerative disorders, such as Alzheimer's
disease and Lou Gehrig's disease, glutamate, an amino acid found in
high quantities in the brain, is thought to accumulate. At normal
concentrations, glutamate acts as a neurotransmitter that nerves use to
communicate. However, at excessive levels glutamate is toxic, resulting
in over stimulation of nerve cells, known as excitotoxicity, and
causing excessive stress on the nerve cells eventually ending in cell
death. Studies described in this report suggest that NEPPs (short for
NEurite outgrowth-Promoting Prostaglandins), compounds that accumulate
in nerve cells, prevent nerve damage by activating the Keap1/Nrf2
pathway that regulates the production of antioxidants which relieve
cells of damaging free radicals that result from excitotoxicity.
"This is the first reported evidence that this protective response can
be activated directly in nerve cells to release antioxidants and
counter oxidative stress," said Stuart Lipton, M.D., Ph.D., Director of
the Del E. Webb Center for Neurosciences and Aging at the Burnham
Institute and senior author of the study. "These findings provide
support for further investigation of NEPP drugs to potentially treat
ischemic stroke, multiple sclerosis, Alzheimer's disease, Lou Gehrig's
disease and other neurodegenerative disorders."
Researchers found that NEPPs were able to activate a pathway in nerve
cells that is designed to protect against oxidative and nitrosative
stress (which produces free radicals) and excitotoxicity. This pathway,
known as Keap1/NrF2, regulates the production of natural antioxidants,
such as bilirubin, that can protect against oxidative stress resulting
from ischemic stroke and degenerative disorders.
