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-   -   Mitochondria: (https://www.neurotalk.org/peripheral-neuropathy/80999-mitochondria.html)

mrsD 03-12-2009 09:11 AM

Mitochondria:
 
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.

DM 03-12-2009 09:30 AM

Thanks for that info, mrsD. (scary)

You are so much appreciated around here.

mrsD 05-06-2011 06:14 PM

New article:
 
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.

dahlek 05-06-2011 09:29 PM

Mrs D? As always this IS food for thought!
 
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. :hug::hug::hug::hug:'s!!!!!!!!! - j

echoes long ago 05-07-2011 07:27 PM

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

Sheltiemom18 05-09-2011 01:33 PM

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

mrsD 05-15-2011 01:17 PM

More on mitochondrial damage:
 
Here is another very interesting article:

http://www.sciencedaily.com/releases...0512161938.htm

It focuses on Parkinson's damage, but it contains interesting other information about neurons and how mitochondria function inside them.

And also offers a solution of sorts:
Glutathione and NAC (n-acetyl cysteine).

Glutathinone was mentioned on Dr. Jay Cohen's website as a possible treatment for fluoroquinolone antibiotic damage causing PN.

Nervous 05-21-2011 10:38 PM

So, are we adding glutathione to our list of recommended supplements? If so, in what form? That article said that glutathione was not well-absorbed by mouth and that taking precursors so the body could produce its own glutathione was only a theory.

mrsD 05-22-2011 07:34 AM

Glutathione does not work by mouth...it is destroyed in the stomach.

Supplements to encourage the body to make more are the way to go. n-acetyl cysteine is one--abbreviated as NAC. This is not expensive either.

The person on Dr. Cohen's website went to a holistic doctor and had IV infusions containing glutathione, and that way it improved his fluoroquinolone induced mito damage and his PN.

http://medicationsense.com/articles/...ity070508.html

Glutathione is made in the liver.

Here is a more complete article on it:
http://en.wikipedia.org/wiki/Glutathione

NeuroLogic 12-17-2011 07:35 PM

"Mitochondrial dysfunction is a common cause of peripheral neuropathies."

http://www.jneurosci.org/content/31/28/10128.abstract

My mitochondrial dysfunction is getting worse. In the last week my fingers, toes, and nose have all suddenly become cold very often. Room temp. is 24C and they feel the same as they did when the previous week when it was 19C. They don't heat up easily or quickly. RT needs to be 25-26C for fingers, toes, and nose to not feel cold. The problem is at 26C my scalp starts to feel as if it's burning. So there's a very narrow temp. range I can be comfortable at (0.5-1 degree window). Now I'll wake up at night and my feet will be cold. I'll add a thick blanket, but they won't heat up, and I can't get back to sleep. Which just makes my energy lower and mito function worse.

I'm going to load up on mito supplements.

mrsD 12-18-2011 07:58 AM

I personally believe the mitochondria are damaged mostly by antibiotics.
This is where much of the research is.

Many antibiotic drugs kill bacteria, and mitochondria are actually bacteria who live in our cells, as symbiotes... some ancient plan where they joined with other cells to provide energy for the organism.

But toxins may poison them too. Once a cell cannot make energy it stops functioning properly.

Free radical damage also is implicated. This is why antioxidants work for aging and PN I think. Oxidation by oxygen free radicals.

Thanks for the article. It really helps to have a mental picture or framework to see how PN problems really are. Otherwise it seems rather nebulous IMO.

Here is a link showing what Schwann cells are:
http://en.wikipedia.org/wiki/Schwann_cell

NeuroLogic 12-20-2011 05:29 AM

I have a new theory on peripheral neuropathy.

I used to think the hyperexcitability of nerves was caused by magnesium deficiency; i.e., not enough Mg to pump the Ca out. So I kept taking Mg... but the nerves didn't quieten down, making me wonder if the Ca was still not getting expelled quickly, therefore continuing to fire ad infinitum.

I just read that you need ATP to get that Mg pump working. So even if you have plenty of Mg to drive out the Ca, it's not going to move properly without the 'batteries' (ATP) to power the pump properly?

I also read that up to 30% of the mitochondrial energy is used to run that pump. As long as the mito furnaces aren't doing their job, Mg supplements are in vain or to some extent ineffective. You have to start with fixing the furnace.

To me it seems the symptoms of too high Ca and PN can be very similar.

It seems the best rehab order is:

1) Fix mitochondrial function;

2) Increase Mg;

3) Monitor Ca (make sure it's not too high);

4) Take all the usual PN/nerve supplements.

(Low mito will limit supplement absorption?)

hopeful 12-20-2011 05:51 PM

Quote:

Originally Posted by mrsD (Post 768332)
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.

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?:)

mrsD 12-20-2011 05:57 PM

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.

mrsD 12-20-2011 06:20 PM

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.

hopeful 12-21-2011 12:39 PM

Quote:

Originally Posted by mrsD (Post 834093)
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.

Thanks I subscribed!:)

fabdou 12-21-2011 01:45 PM

This is a very interesting topic. In addition to antibiotics, it may also explain how statins can produce PN. Is it possible/likely that mito damage from statins and other toxins could produce clinical sxs in a shorter time period than that seen with more chronic causes of PN, like CMT?

My neurologist believes I have CMT despite a negative genetic workup and negative family hx (and negative extensive workup for any other cause of PN) He says my muscle atrophy/ EMG findings are consistent with something that took years to develop. I disagree because I have lost mass and strength only since being on statins for 5 yrs. Could mito damage cause a similar clinical presentation over a shorter period of time and mimic CMT in its clinical presentation?

mrsD 12-21-2011 02:10 PM

I believe that a most recent theory of statins damage, is
failure to remyelinate the damage caused by other things.
There have been studies on animals showing CNS remyelination failure too.

fabdou 12-21-2011 02:13 PM

So are you saying that statins would not be a primary cause, but would impair the healing of damage from another process?

mrsD 12-21-2011 02:21 PM

Only that particular study points to remyelination problems.

I don't think we see even acknowledgment of damage in US because of Big Pharma blocking that data.

http://www.ncbi.nlm.nih.gov/pubmed/19349355

This is only one theory... I think after the statins go generic we
will see much more.

Kitt 12-21-2011 09:18 PM

Quote:

Originally Posted by fabdou (Post 834333)
This is a very interesting topic. In addition to antibiotics, it may also explain how statins can produce PN. Is it possible/likely that mito damage from statins and other toxins could produce clinical sxs in a shorter time period than that seen with more chronic causes of PN, like CMT?

My neurologist believes I have CMT despite a negative genetic workup and negative family hx (and negative extensive workup for any other cause of PN) He says my muscle atrophy/ EMG findings are consistent with something that took years to develop. I disagree because I have lost mass and strength only since being on statins for 5 yrs. Could mito damage cause a similar clinical presentation over a shorter period of time and mimic CMT in its clinical presentation?

Here is an interesting site. Statins are contraindicated for people who have CMT.

http://help4cmt.com/articles/?id=35&...terol-with-cmt

The general population can also have trouble with statins such as muscle pain, weakness, etc. I know people who have experienced this. This site might help and there are many sites out there.

http://www.mayoclinic.com/health/sta...ffects/MY00205

Despite the fact that you have had a negative genetic workup and a negative family history, you still could have a type of CMT. Symptoms can vary greatly even within the same family. They can be hardly having any symptoms that are noticeable at all. There could be a spontaneous mutation which is rare.

NeuroLogic 12-22-2011 12:24 AM

I just heard about PQQ, which a search on this board indicated has not been discussed previously.

"PQQ’s powerful free radical–scavenging capacity provides the mitochondria with superior antioxidant protection due to its high molecular stability and the role it plays in energy transfer directly within the mitochondria.

"Unlike other antioxidants, the exceptional molecular stability of PQQ allows it to carry out thousands of electron transfers without undergoing molecular breakdown.

"PQQ is especially effective in neutralizing superoxide and hydroxyl radicals, two prominent causes of mitochondrial dysfunction.

"According to a University of California at Davis study, “PQQ is 30 to 5,000 times more efficient in sustaining redox cycling (mitochondrial energy production) . . . than other common [antioxidant compounds], e.g. Ascorbic Acid (Vitamin C).”

http://en.wikipedia.org/wiki/Pyrroloquinoline_quinone

It sounds too good to be true, but I'm going to try some anyway.

This is the stunning part:

"In 2010, researchers at the University of California at Davis released a peer-reviewed publication showing that PQQ’s critical role in growth and development stems from its unique ability to activate cell signaling pathways directly involved in cellular energy metabolism, development, and function.

"Most significantly, the study demonstrated that PQQ not only protects mitochondria from oxidative stress—it promotes the spontaneous generation of new mitochondria within aging cells, a process known as mitochondrial biogenesis.

"The implications of this revelation for human health and longevity are significant because the only other known methods proven to stimulate mitochondiral biogenesis in aging humans are intense aerobic exercise, strict caloric restriction, and certain medications such as thiazolidinediones and the diabetes drug metformin."

This is very good news for me and others whose chronic fatigue has not allowed intense aerobic exercise.

There also appear to be other significant neuro benefits to PQQ.

mrsD 12-22-2011 09:54 AM

I agree it sounds very interesting. Let us know how you do.

I am in the middle of trying N-A-G... and a new histamine blocker (which just arrived, and waiting a bit to start). So I don't want to introduce a "new" thing at this time, which may confound the results of the NAG, etc. I have given the Daosin histamine blocker to Oreo twice--- a 1/3 capsule, and she seems comfortable so far. (she has that mast cell (histamine secreting tumor).

Let us know how you do. PQQ doesn't seem very expensive either!
I wonder why we don't hear more about it?

As far as statin toxicity goes... the mito issues may be a direct thing, or indirect. Since statins block our ability to normally make CoQ-10, and CoQ-10 is essential to mito functions, it may be this effect indirectly.

But since Big Pharma tends to release some of the negative studies on their patented products, after the patents expire, we may soon see some interesting (and horrifying) things.. As long as Pfizer pays people to ask for BRAND Lipitor, this will be delayed. This new ploy of theirs is unique in the industry. See the commercials on the Lipitor copay card? :rolleyes::rolleyes: I wonder if it will work?

hopeful 12-22-2011 12:49 PM

Quote:

Originally Posted by NeuroLogic (Post 834517)
I just heard about PQQ, which a search on this board indicated has not been discussed previously.

"PQQ’s powerful free radical–scavenging capacity provides the mitochondria with superior antioxidant protection due to its high molecular stability and the role it plays in energy transfer directly within the mitochondria.

"Unlike other antioxidants, the exceptional molecular stability of PQQ allows it to carry out thousands of electron transfers without undergoing molecular breakdown.

"PQQ is especially effective in neutralizing superoxide and hydroxyl radicals, two prominent causes of mitochondrial dysfunction.

"According to a University of California at Davis study, “PQQ is 30 to 5,000 times more efficient in sustaining redox cycling (mitochondrial energy production) . . . than other common [antioxidant compounds], e.g. Ascorbic Acid (Vitamin C).”

http://en.wikipedia.org/wiki/Pyrroloquinoline_quinone

It sounds too good to be true, but I'm going to try some anyway.

This is the stunning part:

"In 2010, researchers at the University of California at Davis released a peer-reviewed publication showing that PQQ’s critical role in growth and development stems from its unique ability to activate cell signaling pathways directly involved in cellular energy metabolism, development, and function.

"Most significantly, the study demonstrated that PQQ not only protects mitochondria from oxidative stress—it promotes the spontaneous generation of new mitochondria within aging cells, a process known as mitochondrial biogenesis.

"The implications of this revelation for human health and longevity are significant because the only other known methods proven to stimulate mitochondiral biogenesis in aging humans are intense aerobic exercise, strict caloric restriction, and certain medications such as thiazolidinediones and the diabetes drug metformin."

This is very good news for me and others whose chronic fatigue has not allowed intense aerobic exercise.

There also appear to be other significant neuro benefits to PQQ.

That is very interesting. Are you on any other medications? I am wondering about the contraindications. I think I would really like to give this a try. I am one of those with no energy. Thanks for the info!:)

mrsD 12-22-2011 01:01 PM

I don't think you'll find this PQQ on any drug checker.

It is not mainstream yet.

Here is a drug checker that is pretty good:
http://www.drugs.com/drug_interactions.html

The most serious interactions involve warfarin for any supplement, so anyone here on warfarin (Coumadin), should
discuss with your doctor.

hopeful 12-23-2011 11:35 AM

Thanks Mrs. D. I am not taking any anti-coagulants so I think I may try PQQ. Do you or Neurologic mention wher you can buy it? I am off for the holiday next week and may try this.Thansk!

mrsD 12-23-2011 11:46 AM

This Amazon entry has 3 choices...2 with free shipping. Net Rush has better customer satisfaction:

The 3rd is Amazon itself, with the 25 dollar free shipping.
These are the most reasonable IMO.

This one only has .75 shipping:
http://www.amazon.com/gp/product/B00...8JCVYNN03QPB33

I'd start at 10mg a day. There is really no dosage scale available for this yet.
As you can see from this food content chart, the food content ranges in micrograms. 10mg =10,000 micrograms

adelina 12-24-2011 12:58 PM

hopeful - I just wan't to be sure you let us know how the PQQ worked for you. If I don't keep this thread highlighted, with all the meds I am on I will forget which one I am trying to follow and not know which one is about what :p! I am really interested in the PQQ/CoQ10 supplements and would like to try them if/when life settles down...

melon 12-24-2011 09:35 PM

Quote:

Originally Posted by mrsD (Post 772636)
Glutathione does not work by mouth...it is destroyed in the stomach.

Supplements to encourage the body to make more are the way to go. n-acetyl cysteine is one--abbreviated as NAC. This is not expensive either.

The person on Dr. Cohen's website went to a holistic doctor and had IV infusions containing glutathione, and that way it improved his fluoroquinolone induced mito damage and his PN.

http://medicationsense.com/articles/...ity070508.html

Glutathione is made in the liver.

Here is a more complete article on it:
http://en.wikipedia.org/wiki/Glutathione

Interesting my pn symptoms started with a bang after being put on Amoxicillin and Metoclopramide .

What do you think of this Mrs D?

Merry Christmas to you and of course everyone else here .

m

mrsD 12-25-2011 11:35 AM

After some antibiotics... Candida can grow in the GI tract.
This releases toxins into your blood, mostly aldehydes.

Trying Benfotiamine is a good idea. Since thiamine it a cofactor in alcohol and aldehyde degradation.

NeuroLogic 12-28-2011 06:35 AM

I found an amazing article which supports most of what I've read on this board including your advice, Mrs.D, and could explain my skin temperature problems:

CFS - The Central Cause: Mitochondrial Failure

. . .

"The job of the heart is to maintain blood pressure. If the blood pressure falls, organs start to fail. If the heart is working inadequately as a pump then the only way blood pressure can be sustained is by shutting down blood supply to organs. Organs are shut down in terms of priority, i.e. the skin first. . . this creates further problems for the body in terms of toxic overload. . .

Effects on the Skin

"If you shut down the blood supply to the skin, this has two main effects. The first is that the skin is responsible for controlling the temperature of the body. This means that CFS patients become intolerant of heat.

"If the body gets too hot then it cannot lose heat through the skin (because it has no blood supply) and the core temperature increases.

"The only way the body can compensate for this is by switching off the thyroid gland (which is responsible for the level of metabolic activity in the body and hence heat generation) and so one gets a compensatory underactive thyroid. This alone worsens the problems of fatigue.

"The second problem is that if the micro-circulation in the skin is shut down, then the body cannot sweat. This is a major way through which toxins, particularly heavy metals, pesticides and volatile organic compounds are excreted. Therefore the CFS sufferer's body is much better at accumulating toxins, which of course further damage mitochondria."

http://www.drmyhill.co.uk/wiki/CFS_-...ndrial_Failure

That explains why I and other people with PN don't sweat properly. It may also hint at a possible cause of PN - the skin is the first target/most vulnerable to mito failure.

The entire article is well-written and it helped me a lot.

I hope I'm on the right track... I didn't want to assume hypothyroidism is my problem until my mitochondria has been tested. This is the second (or third) doctor I've found who says your thyroid could be alright, just partly inactive due to mito issues.

mrsD 12-28-2011 07:12 AM

I do think it is worth while to test mitochondria in patients with chronic low metabolic symptoms.

I am not sure about all the statements you are quoting, however.
Some forms of PN affect the autonomic nervous system itself and therefore sweating would be affected.

Let us know what the results are, in any event.
And your research is very helpful here...please do keep that coming. In medical systems, often factoids are scattered about and may not be understood properly. " The B12 on an empty stomach" is an example. Research with drugs in microgram amounts/doses showed poor or no absorption when food was present in the GI tract.(thyroid hormone and digoxin) This is a huge issue with the microgram amounts of B12 we need to absorb orally. But this evidence so far is not connected to B12 information (except for me) it appears!

melon 12-29-2011 01:59 PM

Quote:

Originally Posted by mrsD (Post 835908)
I do think it is worth while to test mitochondria in patients with chronic low metabolic symptoms.

I am not sure about all the statements you are quoting, however.
Some forms of PN affect the autonomic nervous system itself and therefore sweating would be affected.

Let us know what the results are, in any event.
And your research is very helpful here...please do keep that coming. In medical systems, often factoids are scattered about and may not be understood properly. " The B12 on an empty stomach" is an example. Research with drugs in microgram amounts/doses showed poor or no absorption when food was present in the GI tract.(thyroid hormone and digoxin) This is a huge issue with the microgram amounts of B12 we need to absorb orally. But this evidence so far is not connected to B12 information (except for me) it appears!

I wonder how many other supplements only work following the same protocol ? esp without someone in the know ( like you ) to spot them

m

NeuroLogic 12-30-2011 12:14 AM

The thing I don't get is why so many doctors and socalled experts focus on the thyroid, adrenal glands, etc., and get all caught up in that, but don't take it back a step to the mitochondria. They assume a specific part of the endocrine system is dysfunctional.

I'm looking up mitochondria in my chronic fatigue books and references are few and far between.

I also don't get why Dr. Teitelbaum, one of the experts on chronic fatigue, who seems to get the importance of mitochondria, wants people to get on thyroid meds, and then wean them off the meds once their mitochondria are working right.

I think Dr. Sarah Myhill is a genius.

I'm starting some testing on possible synergy between Mg and CoQ10 absorbed at the same time. A significant amount of Mg with CoQ10 seems to make the CoQ10 much more effective. Both of course play major roles with ATP. The tests are transdermal Mg (4-6 tblsz:30 mins)+ oral CoQ10 (100mg).

I've been having difficulty finding local testing for ATP/mitochondria.

Dr. Myhill does ATP profiles:

"The first part of the test is called "ATP profiles" and has been developed by Dr John McLaren-Howard at Biolab in London. It measures the rate at which ATP is recycled in cells and because production of ATP is highly dependent on magnesium status so the first part of the test studies this aspect. The second part of the test measures the efficiency with which ATP is made from ADP. If this is abnormal, then this could be as a result of magnesium deficiency, and/or low levels of Co-enzyme Q10, and/or low levels of vitamin B3 (NAD) and/or low levels of acetyl L-carnitine. The third possibility is that the protein which transports ATP and ADP across mitochondrial membrane is impaired and this is also measured."

I'd love to know if my mito membranes are shot. One of the reasons I'm keen on taurine is its membrane powers. Taurine is a powerful cell membrane stabilizer.

mrsD 12-30-2011 01:59 AM

Choline and DHA (essential fatty acid) are also membrane stabilizers.

The mitochondria have always been mysterious. That is changing now I believe with improved techniques in biochemistry. But there are very few doctors who even treat mito disorders (which are mostly genetic at this time). The vaguer concepts of acquired mito damage is still very new in medicine.

Dr. Bruce Ames, PhD. has spent his life on the biochemistry of the body and has long believed that mitochondria hold the answer to aging and many ills.

His Juvenon site has some of that information:
http://juvenon.com/juvenoncapshome.h...FQQCQAod2AJynw

NeuroLogic 12-30-2011 10:18 AM

I think I wrote in a previous post that up to 30% of the cell's energy is used for the Mg-Ca pump. Dr. Myhill says it's higher:

Quote:

I actually now believe that a low red cell magnesium is a symptom of mitochondrial failure. It is the
job of mitochondria to produce ATP for cell metabolism and about 40% of all mitochondrial output
goes into maintaining calcium/magnesium and sodium/potassium ion pumps. I suspect that when
mitochondria fail, these pumps malfunction and therefore calcium leaks into cells and magnesium
leaks out of cells. This, of course, compounds the underlying mitochondrial failure because calcium
is toxic to mitochondria and magnesium necessary for normal mitochondrial function. This is just
one of the many vicious cycles we see in patients with fatigue syndromes.

http://drmyhill.co.uk/drmyhill/image...fs_book_27.pdf (p. 40).
If Ca is indeed "toxic to mitochondria," I wonder how many people who've bought into the Calcium hype are suffering mito problems because of it.

Myhill is the first doctor I've come across who advocates Mg injections when it's not a cardiac emergency. But she explains the reason well. She's been helping CFS patients for 20 years and seen over 4,500 of them. She even advocates self-injections of Mg, which is interesting.

mrsD 12-30-2011 11:37 AM

I decided to look this up...

Here is one article so far:

Quote:

Performing your original search, calcium function in mitochondria, in PubMed will retrieve 12219 records.

FEBS Lett. 2004 Jun 1;567(1):96-102.
Calcium and mitochondria.
Gunter TE, Yule DI, Gunter KK, Eliseev RA, Salter JD.
Source

Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, 575 Elmwood Avenue, Rochester, NY 14642, USA. thomas_gunter@urmc.rochester.edu
Abstract

The literature suggests that the physiological functions for which mitochondria sequester Ca(2+) are (1). to stimulate and control the rate of oxidative phosphorylation, (2). to induce the mitochondrial permeability transition (MPT) and perhaps apoptotic cell death, and (3). to modify the shape of cytosolic Ca(2+) pulses or transients. There is strong evidence that intramitochondrial Ca(2+) controls both the rate of ATP production by oxidative phosphorylation and induction of the MPT. Since the results of these processes are so divergent, the signals inducing them must not be ambiguous. Furthermore, as pointed out by Balaban [J. Mol. Cell. Cardiol. 34 (2002 ) 11259-11271], for any repetitive physiological process dependent on intramitochondrial free Ca(2+) concentration ([Ca(2+)](m)), a kind of intramitochondrial homeostasis must exist so that Ca(2+) influx during the pulse is matched by Ca(2+) efflux during the period between pulses to avoid either Ca(2+) buildup or depletion. In addition, mitochondrial Ca(2+) transport modifies both spatial and temporal aspects of cytosolic Ca(2+) signaling. Here, we look at the amounts of Ca(2+) necessary to mediate the functions of mitochondrial Ca(2+) transport and at the mechanisms of transport themselves in order to set up a hypothesis about how the mechanisms carry out their roles. The emphasis here is on isolated mitochondria and on general mitochondrial properties in order to focus on how mitochondria alone may function to fulfill their physiological roles even though the interactions of mitochondria with other organelles, particularly with endoplasmic and sarcoplasmic reticulum [Sci. STKE re1 (2004) 1-9], may also influence this story.

PMID:
15165900
[PubMed - indexed for MEDLINE]
This link goes into detail about calcium in the mitochondria:
http://en.wikipedia.org/wiki/Mitochondrion
It is really complicated!

This article explains what happens in cold exposed rats, who are magnesium deficient... We don't know if it applies to humans though from this paper alone:
http://www.mgwater.com/dur08.shtml

This link is also a very good overview about magnesium:
http://en.wikipedia.org/wiki/Magnesium_in_biology

This is turning into a great discussion!;)

adelina 12-30-2011 01:04 PM

Quote:

Originally Posted by mrsD (Post 836534)
This is turning into a great discussion!;)

I'll 2nd that! It's been a great education!

NeuroLogic 12-31-2011 08:31 AM

Quote:

Originally Posted by mrsD (Post 479813)
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. . . . what is coming out of the new research is that ANTIBIOTICS and other drugs (like statins), can damage mitochondria.

I was reading part of The Magnesium Miracle yesterday to see what Dr. Dean has to say about mitochondria, and spotted a section on statins relevant to this thread:

MAGNESIUM ACTS LIKE A NATURAL STATIN

"Magnesium acts by the same mechanisms as statin drugs to lower cholesterol.

. . .

"Magnesium is necessary for the activity of an enzyme that lowers LDL, the "bad" cholesterol; it also lowers triglycerides and raises the "good" cholesterol, HDL."

Page 90

Trust the medical elite to come up with a damaging way to control something that nature can do without damage! :icon_rolleyes:

I was wondering how drug companies can fail to provide adequate warnings. Sure enough, the company making Lipitor has been sued:

"Among the new plaintiffs is a professional airline pilot from Virginia, who claims that permanent muscle and nerve damage he suffered from Lipitor have made it impossible for him to continue flying — ironically, he began taking the drug to maintain satisfactory cholesterol levels to pass his employment physical...

"Also filing suit is . . . a resident of Port Jervis, NY. . . since starting Lipitor in 1999, she has suffered a series of irreversible health problems that she and her family assert were caused by Pfizer’s drug Lipitor. Among the damages she alleges were triggered by Lipitor are peripheral nervous system damage (peripheral neuropathy). . .

mrsD 12-31-2011 08:44 AM

I've never seen that comment before. Is there a footnote to
the paper he got that from? I'd like to confirm his statement, and then put it up on my magnesium thread.

Oh, I see it here:
http://books.google.ca/books?id=aqMP...statin&f=false

I have not had experience with my magnesium lowering my cholesterol. However it does help my HDLs and triglycerides, but not the LDLs at all.

I know I'd probably be dead without my magnesium! It lowers my blood pressure really well.


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