A Controversial View On Carnitine

[Jon2547]

Back many years ago when I lived under the false notion that most supplements were pretty much benign and posed no risk to health, I got onto the acetyl-l-carnitine. It boosted my mitochondria but it came with some side effects that I did not connect the dots on right away.
It is very over stimulating and should not be used for very long. In fact, I would just say skip this one altogether.

 

[Rafael Lao Wai]

I believe the reason why some studies show that elderly as well as obese and diabetic people have lower levels of carnitine is because all these situations( aging, diabetes, excessive fat production) harm the ability of the cells to burn glucose. This has been proven in a study comparing young cells vs old cells. Of course, if the cell can't burn that much sugar anymore, then it will have to burn fat. The fat that we eat and that we have in our adipose tissue is mostly long- chain fat, which requires carnitine to be burned. So this means that these people who have lower carnitine levels aren't in poor health necessarily due to having less carnitne, but because they have metabolic problems, which inhibit glucose oxidation and increase fat oxidation. Improving their glucose oxidation could bring their carnitine levels to normal levels without supplementation, since just supplementing it would be simply treating the symptom. It would help in the short term, but the impaired glucose oxidation, which is what needs to be tackled, would be bad long- term.

 

[Aries]

Back many years ago when I lived under the false notion that most supplements were pretty much benign and posed no risk to health, I got onto the acetyl-l-carnitine. It boosted my mitochondria but it came with some side effects that I did not connect the dots on right away.
It is very over stimulating and should not be used for very long. In fact, I would just say skip this one altogether.

What were the side effects?

 

[grithin]

Carnitine: a controversial view and why it can actually be bad for you » MenElite

The FADH2 is taking up all the free space in complex II. The electrons from complex I has to run past complex II, but it’s all jammed up with the electron from FADH2. Where do the electrons go? Out of the electron transport chain. This is called reverse electron flow and this leads to an increased generation of ROS. Leaked electrons react with oxygen to create superoxide. Superoxide is a highly reactive free radical.

To help clarify what seems to be ubiquitous misunderstandings of ETC:
- the complexes are not attached to each other. It is a conceptual chain, linking {pre-complex III}, {complex III}, {complex IV}, but it is a physical grid. I'm not even certain the Complexes necessarily appear in uniform proportions to each other.
- Complex I is not linked to Complex II. They both separately produce QH2 which is processed at Complex III.
- FADH2 doesn't take up space in complex II, it is part of complex II.

The problem with carnitine still exists, however. Excessive production of QH2, particularly consequent to ETFO contribution while Complex I and Complex II are also running, leads to reverse electron transport and ROS.

Complex II and ETFO are particularly disposed to cause QH2 overproduction. I won't mention why, I don't know if science has figured it out and I wouldn't want to advance science in the current climate (imagine helping a bunch of {monopolist medical professionals} and {boomers who sold out the following generations})

But, I imagine ramping up complex III activity (somehow) would {alleviate the issue of excessive QH2 from whatever source, and would prevent most of the problematic mitochondrial ROS}.

 

[Jon2547]

What were the side effects?

The side effects for me seemed to be distressed sleep and slight nerve pain. I may have some type of problem with the myelin surrounding my nerves and this was aggravating the situation.

 

[Hans]

To help clarify what seems to be ubiquitous misunderstandings of ETC:
- the complexes are not attached to each other. It is a conceptual chain, linking {pre-complex III}, {complex III}, {complex IV}, but it is a physical grid. I'm not even certain the Complexes necessarily appear in uniform proportions to each other.
- Complex I is not linked to Complex II. They both separately produce QH2 which is processed at Complex III.
- FADH2 doesn't take up space in complex II, it is part of complex II.

The problem with carnitine still exists, however. Excessive production of QH2, particularly consequent to ETFO contribution while Complex I and Complex II are also running, leads to reverse electron transport and ROS.

Complex II and ETFO are particularly disposed to cause QH2 overproduction. I won't mention why, I don't know if science has figured it out and I wouldn't want to advance science in the current climate (imagine helping a bunch of {monopolist medical professionals} and {boomers who sold out the following generations})

But, I imagine ramping up complex III activity (somehow) would {alleviate the issue of excessive QH2 from whatever source, and would prevent most of the problematic mitochondrial ROS}.

Yes agreed with everything. Supercomplexes are also created linking complex I and III and also II and III as well as others. So yes, the electrons from complex I don't flow through complex II to complex III. And excess fat oxidation creates too much QH2 and combined with those from complex I overwhelm complex III as you alluded to.
Complex III can be upregulated (or assisted) with vitamins K2 and methylene blue.

 

[grithin]

Yes agreed with everything. Supercomplexes are also created linking complex I and III and also II and III as well as others. So yes, the electrons from complex I don't flow through complex II to complex III. And excess fat oxidation creates too much QH2 and combined with those from complex I overwhelm complex III as you alluded to.
Complex III can be upregulated (or assisted) with vitamins K2 and methylene blue.

I'll look into K2, but the situation of MB is not straightforward. I've added a post to explain:

Methylene Blue Mitochondria ETC

A bit ago, when I read the studies about MB and ETC, the model I came up with was: In thinking about it now, there's another possible model/application of MB: In perhaps over 5 years of testing with MB, I've found: - 15mg high concentration dose (just below the burning threshold) on back...

raypeatforum.com

 

[TheBeastPanda]

Yes, I'd rather eat a bunch of meat for carnitine as well as the precursors and then focus on restoring PDH activity.

Precursors from what foods?

So you recommend not to supplement carnitine and just get it from animal products (ie meat)?

 

[Hans]

Precursors from what foods?

So you recommend not to supplement carnitine and just get it from animal products (ie meat)?

Do you want to supplement carnitine for androgen receptors? I personally would just eat a bunch of fatty red meat for testosterone instead of taking a supp. You'll get all the precursors as well as cofactors for testosterone production (and AR production) from food. Most people who eat a bunch of fatty red meat report feeling and looking more androgenic. For the people I work with, it increases T a lot on their test results as well.