Aging and disease(s) cause mitochondrial damage. The powerhouses of our cells (many more than one per cell) are damaged.Here's some recent research (also research Dr. Bruce Ames):
Mice Study May Show How Human Cells Age
By WILLIAM McCALL, AP
(May 26) -- Scientists in Sweden say aging begins in a fundamental way - in the accumulation of tiny changes to a mysterious genetic component in cells called mitochondrial DNA.
Researchers describe the study as the first experimental evidence of this theory - at least in laboratory mice. They believe the finding could explain how humans age and how the body's systems begin to misfire, although more tests must bear them out. The mouse results appear in the current issue of the journal Nature.
"It seems to be a universal phenomenon in mammals that you have this damage to mitochondrial DNA as you get older," said the study's senior author, Nils-Goran Larsson at the Karolinska Institute in Stockholm.
"But I and many others thought this was just a secondary phenomenon," Larsson said. "I think the importance of our paper is that we actually show these mutations can indeed cause several changes associated with aging."
Other scientists say the Swedish experiments clearly show that a high rate of mutation in mitochondrial DNA has an effect on aging.
"But that does not mean all aging is caused by mutations in mitochondrial DNA," said David Finkelstein of the National Institute on Aging, part of the National Institutes of Health.
In the experiments, the Swedish team used mice bred with a defective version of an *enzyme* responsible for maintaining mitochondrial DNA.
Mitochondria are tiny biochemical power plants in cells that convert food into energy. Mitochondria contain strands of their own DNA that are separate from the cell nucleus where the body's genes reside.
The deterioration in the experimental mice started at 25 weeks - young adulthood in normal mice. They prematurely experienced a range of familiar age-related complaints, including baldness, osteoporosis, anemia, curvature of the spine and reduced fertility.
The lifespan of the experimental mice was markedly reduced, with the median age of death at 48 weeks. The oldest of the experimental mice died before 61 weeks.
In normal mice, early aging signs appear at about 40 weeks. Emaciation and other signs of old age accumulate by 1.5 years, and lab mice typically live a little over 2 years.
In an accompanying commentary in Nature, George Martin and Lawrence Loeb of the University of Washington said the results are also consistent with the theory that so-called "free radicals" play a role in aging.
Free radicals typically are oxygen molecules that lack an electron, often setting up a corrosive chain reaction that can damage other cells.
Regardless of how aging begins, researchers said the steps to extend a healthy, youthful life are familiar and simple.
"Watch what you eat, exercise, don't smoke, keep your mind active," Finkelstein said, "and you're more likely to live longer."
05/26/04
Mg controls OVER 350 enzymes.
What can repair this mDNA? Perhaps:
Protein Kinase it appears is DNA dependent...and
. The physical integrity of the DNA helix appears to be dependent on Mg2+
a. Mg2+ ion decreases the number DNA replication errors
b. Mg2+ ion stimulates DNA repair
c. Most of the known enzymes involved in repairing DNA lesions are dependent on Mg2+ at varying degrees
http://www.mdschoice.com/elements/elements/major_minerals/magnesium.htm
Re: free radicals:
``Visual defects are common in surviving preterm infants. Increased levels of harmful neurochemical mediators that have been reported in these conditions include ***oxygen free radicals, excitatory amino acids, tumor necrosis factor-alpha (TNF-a) and in thromboxane A2 (TXA2) which are aggravated in magnesium deficiency and may be ameliorated by magnesium.''
http://www.barttersite.com/mgpreemies.htm
It is known that ketones can shut down an enzyme called phosphofructokinase (6) . This enzyme plays a critical role in glycolysis, a process that may be the only source of energy for cancer cells.
Without sufficient energy, cells cannot produce sufficient ATP. This creates a build-up of free radicals that can lead to apoptosis. Normal cells are not necessarily affected in the same manner because they derive most of their daily energy needs from the Krebs cycle (7) .
http://www.apjohncancerinstitute.org/caatdoctorprotocol1.htm
When I went to verify the above website, it was not available. However, the following 2 websites provide similar information.
www.apjohncancerinstitute.org/newsletter-old2.htm
http://www.lowcarbluxury.com/newsletter/lclnewsvol03-no04-pg2.html
http://www.barttersite.com/mgpreemies.htm
I respectfully disagree with this statement:
"the immune system is confused somehow, and mistakes its own cells for the foreign invader, or because the immune system is overrevved in trying to attack an invader, and overdoes it."
I believe the body is chosing a particular pathway to the degree necessary to try to prolong the person's life.
When we alter that pathway, instead of boosting/supporting our own immune system...the troubles compound.
Because my sister has elevated TNF alpha and because she was on countless abx. for so long ("Couldn't possibly still be infected") ...her doctor has diagnosed her as having an "autoimmune disease".
And he's a "reputable" doctor in a major city...