So if I understand this correctly this mitoconhdrial booster is not natural to the human body and was found in Stardust? and is produced though a fermentation process.
If this feeds the mitochondria of human cells what about the mitochondria of bacteria and other pathogens..from what the article says that could be a possibility to consider.
hmmm.... as noted in this quote;
Because of their constant exposure to high levels of energy and oxygen, mitochondria are especially vulnerable to damage by oxidative stress.10 With time, they lose their ability to efficiently manage energy transfer through the flow of electrons.11-13 As they become increasingly inefficient, mitochondria accumulate structural and functional damage, which then leads to a vicious cycle of further inefficiency and damage.14-16 Oxidative mitochondrial decay is now recognized as a major contributor to aging.17
I will look at this some more when I have time but I seriously question the statement that oxyen is a cause of mitocondrial decay.. and it makes me think the author does not understand exactly what oxidation is.
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So if I understand this correctly this mitoconhdrial booster is not natural to the human body and was found in Stardust? and is produced though a fermentation process.
If this feeds the mitochondria of human cells what about the mitochondria of bacteria and other pathogens..from what the article says that could be a possibility to consider.
This aspect of bacteria and PQQ has indeed been well researched and documented.
hmmm.... as noted in this quote;
Because of their constant exposure to high levels of energy and oxygen, mitochondria are especially vulnerable to damage by oxidative stress.10 With time, they lose their ability to efficiently manage energy transfer through the flow of electrons.11-13 As they become increasingly inefficient, mitochondria accumulate structural and functional damage, which then leads to a vicious cycle of further inefficiency and damage.14-16 Oxidative mitochondrial decay is now recognized as a major contributor to aging.17
I will look at this some more when I have time but I seriously question the statement that oxyen is a cause of mitocondrial decay.. and it makes me think the author does not understand exactly what oxidation is.
Briefly, what the author is saying here is its not oxygen itself, but the chemical reaction in the mito in burning glucose and oxygen to produce energy,which in turn produces reactive oxygen species (ROS), which are transformed into 'nasties' such as superoxide and peroxynitrite, which damage the mito membrane and cause lower ATP and energy output from the mito. This is what eventually causes mito decay and cell death.
I have a friend in Canada who suffered with CFS and was housebound for over 20 years and it wasnt till she went on a low carb ketogenic diet and started taking 5,000iu of Vitamin D3 that she saw any improvement. She eats a large pork chop for breakfast, I dont think I could stick with that.
I have a friend in Canada who suffered with CFS and was housebound for over 20 years and it wasnt till she went on a low carb ketogenic diet and started taking 5,000iu of Vitamin D3 that she saw any improvement. She eats a large pork chop for breakfast, I dont think I could stick with that.
I have CFS and had to add large quantities of protein to my diet, and stay low carb. I had a piece of steak and a piece of chicken for dinner. Neverwas a huge meat person, now I have to be. Makes me feel good, though, so I can stick to it. Also 8,000 iu of D a day and sun exposure.
Well, you must be smart if you understood that. It was way over my head. I did skim it and read a few of the parts that had sentences that weren't full of all those funny letters.
I liked this chart because it lists nutrients and what they do:
Table 2 Metabolic and pharmacological agents used to treat mitochondrial disease
Ohhh, this must be where liverock got the info on the ketogenic diet:
In the absence of any other possible route forward doing everything possible to prevent further deterioration in mitochondrial function (making sure melatonin secretion and/or supplements protect the mitochondria) while using every possible strategy to encourage the production of new mitochondria (mitochondrial biogenesis) will help improve matters. So even if you don't understand how those supplements may be helping you can probably understand what they are trying to achieve.
I have CFS and had to add large quantities of protein to my diet, and stay low carb. I had a piece of steak and a piece of chicken for dinner. Neverwas a huge meat person, now I have to be. Makes me feel good, though, so I can stick to it. Also 8,000 iu of D a day and sun exposure.
But what's the connection to mitochondria?
Michael Eades gives a clear picture why antioxidants dont protect mitochondria and the role of saturated fats and low carbs in protecting mitos.(right after he has had a long rant about dodgy meta analysis studies).
Thanks, Ted, been trying to put some of the pieces together. It's like one of those 10,000 pieces puzzles that I certainly don't expect myself to put together if some great minds working on it can't. (The genetic aspect to this brought out a little in the paper was interesting, btw.) Taking or have taken a lot of things on that list, including PQQ which is not on the list. Most people with CFS can't exercise, including me. Not convinced it's only mitochondria involved with exercise or CFS but I just read this last week from Rich van Konynenburg about protein so I was interested in where liverock got that about ketogenic diet and microchondria:
Quote:
First, in my experience, most PWMEs/PWCs [patients with ME/CFS] report that they do better on a high-protein diet. I believe that the reason for this is that they are not able to burn carbs and fats for fuel as well as normal, because of a partial block of aconitase in the Krebs cycle, resulting from glutathione depletion. As a result, they burn amino acids from protein more than normal. Some amino acids can enter the Krebs cycle downstream of the partial blockade, and transaminase reactions can convert one amino acid to another, with the help of vitamin B6 as a cofactor, so that they can be fed to the Krebs cycle and burned for energy, to supply ATP.
I think the 'ME is psychological' mantra is worse in the U.K., put forward by some doctor over there, can't remember his name, he's sort of despised by PWMEs, but it's here as well. Originally the response when doctor's couldn't find anything and so it was assumed it was 'all in the head', now that they know it's not some think it's a deliberate ploy to distract from something they're hiding. I don't know, but I think for some at least, it may be damage in the physiological, rather than psychological, response to stress and issues.
Anyway, I'm sure you're all sick of me with my 'I have CFS' on so many threads, but maybe it will help someone that's reading.
Michael Eades gives a clear picture why antioxidants dont protect mitochondria and the role of saturated fats and low carbs in protecting mitos.(right after he has had a long rant about dodgy meta analysis studies).
Thanks for this! I sometimes feel it's so complicated (wow, when something goes wrong with the body you see how incredibly complicated it is and how little is known, all these pieces put forth by good minds doing their thing, we need someone to connect them all) I should just forget it and do nothing, but I feel better with the antioxidants and supplements. I respect Dr. Cheney who comes out with statements regarding things that seem to help but then they make things worse, phew. Being fatigued may be a way for the body to make you rest and prevent further damage, who knows?
Quote:
So, if free radicals cause this damage, why can�t we stop it with antioxidants? We do. But not the antioxidants that we take in supplement form�those don�t make their way into the interior of the mitochondria where the damage takes place. Nature has endowed us with our own antioxidant system located within the mitochondria where, so to speak, the rubber meets the road in terms of free radical damage. The antioxidants produced require sulfur, which comes from the sulfur-containing amino acids, i.e. methionine. There are certain substances contained in particular foods that stimulate the enzymatic machinery that increases the production of these intramitochondrial antioxidants. Sulforaphane, for instance, a substance found in broccoli sprouts greatly stimulates a particular enzymatic pathway within the mitochondria, resulting in an increased production of antioxidants where they need to be. Sulforaphane has been shown to prevent cancer, vascular damage, and a host of other disorders thought to result from excess free radical damage.
Our defense against free radicals, then, really comes in two forms. First, the production of antioxidants within the mitochondria, and, second, by making the fats in the mitochondrial membrane less prone to damage. How can we do that? By making them more saturated.
Saturated fats aren�t prone to free radical attack�only unsaturated fats can be damaged by free radicals. Fats that have double carbon-carbon bonds, i.e. unsaturated fats, are the only fats susceptible to free radical damage. If the fats in the mitochondrial membrane are more saturated, then the membrane is less prone to free radical damage.
Quote:
Why would the body be designed for ketones to stimulate CMA? Simple. Ketosis is one of the signs of long term starvation. Ketones are produced throughout the day and are perfectly normal, but sustained ketosis takes place during starvation and sends a message that the body needs to conserve both glucose and protein. The body begins to conserve glucose by signaling to many of the organs and tissues to start using ketones for energy instead of glucose. The body conserves protein by decreasing its use of glucose because in the absence of dietary carbohydrate (as in starvation) the body makes glucose out of protein. Conserving glucose by switching to ketones allows the body can preserve its protein stores. The other thing the body can do is to make sure that the protein it does break down to use for glucose formation comes from non-essential sources. What more non-essential source can we have than useless junk proteins floating around in the cells?
The ketones themselves stimulate the process of CMA to salvage all the junk protein to be used for glucose conversion. Ain�t nature great?
Michael Eades gives a clear picture why antioxidants dont protect mitochondria and the role of saturated fats and low carbs in protecting mitos.(right after he has had a long rant about dodgy meta analysis studies).
Why would the body be designed for ketones to stimulate CMA? Simple. Ketosis is one of the signs of long term starvation. Ketones are produced throughout the day and are perfectly normal, but sustained ketosis takes place during starvation and sends a message that the body needs to conserve both glucose and protein. The body begins to conserve glucose by signaling to many of the organs and tissues to start using ketones for energy instead of glucose. The body conserves protein by decreasing its use of glucose because in the absence of dietary carbohydrate (as in starvation) the body makes glucose out of protein. Conserving glucose by switching to ketones allows the body can preserve its protein stores. The other thing the body can do is to make sure that the protein it does break down to use for glucose formation comes from non-essential sources. What more non-essential source can we have than useless junk proteins floating around in the cells?
The ketones themselves stimulate the process of CMA to salvage all the junk protein to be used for glucose conversion. Ain’t nature great?
So when I did the Atkins diet, a ketone producing diet, I lost fat and gained muscle.. my weight did not drop for a while for as fat went the heavier muscle appeared and I was working out very moderately.. and I test stripped positive for ketones through out it all almost every day... I would not say I was starving as I built muscle and did not feel nor look like i was starving.. I do not think ketones always reflects a starvation diet. I think ketones are part of the bodies process for redistribution and perhaps reflect a more NORMAL metabolic process than they are given credit for.
Most of the studies done on melatonin appear to be using rats and very high doses up to 80mg/kg. Has there been any studies on humans showing what is an effective dose for mitochondrial dysfunction?
Reversing Brain Cell Death With New Mitochondria
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