Many drugs damage mitochondria. And this subject is now getting more attention because of autism research.
So I thought I'd put this link up for interested readers.

Here is a very recent Science News discusses mitochondrial damage as a source of chronic illness.

http://www.sciencenews.org/view/feat...ndria_Gone_Bad


This makes more sense to me because what is coming out of the new research is that ANTIBIOTICS and other drugs (like statins), can damage mitochondria. The autism community has some interesting new studies showing vaccines may do this and antibiotic treatment for ear infections or other things that happen to little kids, often precede the appearance of autism.
The mitochondria in our cells are basically similar and actually derived FROM bacteria. So agents that KILL bacteria, may kill our mitochondria too.

example:
http://www.autism.com/medical/resear...ntibiotics.htm

There already is a supplement made by Dr. Bruce Ames who studies mito deterioration as a cause of aging:
Juvenon
http://www.bruceames.org/

I recall reading a mito website long ago that suggested a genetic weakness for this. In order to have a dramatic disorder one needs genes from both parents. But it has been suggested that people with one copy of the recessive gene may be more prone to damage from the environment and aging.

Thanks for that info, mrsD. (scary)

You are so much appreciated around here.

I am bumping this up because of this great new article about mitochondria.

This article really is interesting and poses the question of mito damage in many neurological disorders:

http://www.the-scientist.com/article...#ixzz1Lc4RYaHa

It was posted by olsen, a member of our PD forum here.

I really do think damaged mitochondria are at the heart of many forms of PN.

And, lots of it.
It's that two edged sword of dealing w/knowing what your medical issue is? And the 'insurance companies'. Thus the blessings of 'genetic profiling'. When your mitochondria 'change'? Does that alter ones' DNA? And HOW will this all be dealt with? Pn in a great example of how this mite happen, and in the whole process? Be excluded as a viable condition for treatment because IT IS GENETIC. Scary stuffs.
Like most here? My 'processes, neurologically' changed significantly, but I surely wasn't the one to cause it knowingly or willingly! IF as a result my 'genetic profiles changed'? Well, I'm not at fault and I'm in no breach of contract w/any insurer. Am I correct here?
Only issue now is...how far are they from the 'mouse model' to the human actual? 20- 50 years? I understand caution, but as more people w/PN can be excluded from some coverages, it's scary beyond the Twilight Zone.
Not to mention that testing for such things is likely pretty rich as well.
No peace for those in pain.
Thanks Mrs D, tho for bringing to light something astute and relevant [as always] to all of us!
A fan, as always. 's!!!!!!!!! - j

fascinating article. if correct or even partially correct, the implications are astounding.

This is, as another poster said, a fascinating article. Not being a medical professional but rather one who was of allied status, can't claim much knowledge about the mitochondria other than they are the tiny spark plugs within the cells.

But can say that one of the neuros I consulted last year during probably the most difficult time of my NLD SFN offered the possibility that it might could be the result of what he called "mitochondrial defect," although the Sjogren's researchers say SFN can also be an adjunct of primary Sjogren's, which I'm supposed to have. But who knows at this point whether or not the AI's might also be caused by faulty mitochondria?

Sheltiemom18

Hi Mrs. D, I tried to get into the site to read the article but it tells me I have to be a subscriber. Am I missing something?

Oh, I am a subscriber... but you know it is free. You could join,
just like Medscape. No money, nothing but some emails on the next issue.

I learned of this wonderful science site from olsen at PD forum.
So don't hesitate to join. It is safe to do so.

Our Copyright restrictions here do not allow us to copy full articles from most places.

So I cannot put it up here...some spots you do have to join.
Medscape is another with a very strict copyright.

I think you are right and the reason is:

"Muscle and nerve cells are big users of ATP. Nerve cells consume large amounts of glucose, which they use for production of ATP by aerobic respiration.

. . .

"In nerves, ATP is used mostly for active transport of sodium (Na+) and potassium (K+) ions but also drives secretion of neurotransmitter chemicals by the endomembrane system."

http://www.uwyo.edu/bio1000skh/lecture17.htm

I always wondered why my nerves didn't do their job properly when I was exhausted.

I wish I could see some research on exactly how much ATP nerves actually use.

---

Before I forget, here's something interesting on mitochondria:

"The long-term presence of excess cytokines is very damaging, and many scientific antennae are now tuned into cytokines as the factor which prevents mitochondria from repairing themselves. Major stimulants of excess cytokine production certainly include viruses and other infections, but once the infection has healed, cytokine production should cease. In M.E., arthritis and other chronic diseases for some reason it appears that it does not."

So before anyone spends a lot of money on mito support products, it may be worth getting a blood test first, esp. if anyone with CFS, or those who can't afford a slow recovery.

---

On a list of things Mg does, in a previous thread (on PD):

I wonder if this could explain the common problem of those with peripheral neuropathy, i.e., getting too hot, and failure to sweat.

Say the ATP breaks down as heat. Then it breaks down further, lacking the energy to complete the process of sweating to remove the heat, i.e., back-to-back failures.

I have a chronic problem of skin heating up where nerve damage apparently was done.

I don't see how the heat could be there, esp. as high as the temp gets, unless there's a lot of energy involved. It could also explain chronic fatigue, i.e., the conversion of ATP is chronically impaired, like an energy 'parasite.'