Carnitine Is Peaty? Study Shows Decreased Peroxidation

GorillaHead

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Or am i wrong here? I mean it not only reduced peroxidation in serum but in liver tissue as well. Tell me free radicals are much more abundant in serum perhaps? The mitochondria is safer?
 

Terma

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It can fix forms of fatty acid/amino overload and defective ketogenesis, has anti-oxidant effects and should help membranes - but only if carnitine isn't sufficient/high in the first place where it'll increase oxidative stress and become involved in pathology. Links in old posts.
 

Wilfrid

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It might have some interesting value in intestinal inflammation but never tried it myself.
 

Anders86

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I would guess you are low on T3, high on cortisol and free fatty acids with a temporary boost in dopamine. You are at the start of a "fast" with the parasympathetic nervous system working at its finest. Feeling sharp and solid, this is only temporary and should only be activated when in need. You are compromising important processes in your biology.
 
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jb116

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Carnitine will acutely increase energy using fatty acids and more importantly acutely upregulate PDH.
 

Dave Clark

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I thought the big boogaboo with carnitine was that it suppressed thyroid? And, this is probably for another thread, but what about carnosine, never was very clear as to whether it is Peaty or not?
 

GorillaHead

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Carnitine will acutely increase energy using fatty acids and more importantly acutely upregulate PDH.
Which is a good thing right. Especially the Pdh. I’ve been reading that it it also mediates aging to overconsumption of empty nutrients
 
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jb116

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Which is a good thing right. Especially the Pdh. I’ve been reading that it it also mediates aging to overconsumption of empty nutrients
Not necessarily, I mentioned the word acutely a couple of times for the very reason that for long term supplementing carnitine for example there are diminishing returns and counter productivity as it inhibits glucose oxidation while the carnitine build up in the mitochondria. I think in this sense it most certainly becomes anti thyroid. I think some carnitine from a good saturated fat diet is fine.
 

GorillaHead

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Not necessarily, I mentioned the word acutely a couple of times for the very reason that for long term supplementing carnitine for example there are diminishing returns and counter productivity as it inhibits glucose oxidation while the carnitine build up in the mitochondria. I think in this sense it most certainly becomes anti thyroid. I think some carnitine from a good saturated fat diet is fine.
Okay so not too much.
 

Lewis Acid

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Ray: Coconut oil is unusually rich in short and medium chain fatty acids. Shorter chain length allows fatty acids to be metabolized without use of the carnitine transport system. Mildronate, which I discussed in an article on adaptogens, protects cells against stress partly by opposing the action of carnitine, and comparative studies showed that added carnitine had the opposite effect, promoting the oxidation of unsaturated fats during stress, and increasing oxidative damage to cells. I suspect that a degree of saturation of the oxidative apparatus by short-chain fatty acids has a similar effect--that is, that these very soluble and mobile short-chain saturated fats have priority for oxidation, because they don't require carnitine transport into the mitochondrion, and that this will tend to inhibit oxidation of the unstable, peroxidizable unsaturated fatty acids.

So carnitine increases transportation and utilization of PUFA = double plus ungood.

Ray: Both adrenaline and ACTH mobilize fat from storage. Stress-mobilized fatty acids contribute to the increased lipid-peroxidation seen during stress, and they also tend to damage mitochondria. The large increase in the death rate from asthma in the last decade or two is now believed[*] to be the result of cardiovascular damage caused by the common use of inhalants containing catecholamines. Isoproteron01, a commonly used bronchodilator, causes mitochondrial damage, which can be prevented by blocking the carnitine-dependent oxidation of fatty acids. Since carnitine is required for the oxidation of long-chain fatty acids, its analog-betaines (which interfere with its transport of fatty acids into the mitochondria) protect against the damage that normally results from stress-induced (or catecholamine-induced) fatty acid oxidation. Since saturated fats protect against the cardiac necrosis produced by corn oil, I think it is probably lipid-peroxidation resulting from rapid oxidation of unsaturated fats which causes the heart damage in both catecholamine damage[ 3] and corn-oil toxicity. Vitamin E, coconut oil, and the carnitine antagonists (betaine derivatives) are adaptogens that protect respiration by directly decreasing lipid-peroxidation.
 

GorillaHead

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Ray: Coconut oil is unusually rich in short and medium chain fatty acids. Shorter chain length allows fatty acids to be metabolized without use of the carnitine transport system. Mildronate, which I discussed in an article on adaptogens, protects cells against stress partly by opposing the action of carnitine, and comparative studies showed that added carnitine had the opposite effect, promoting the oxidation of unsaturated fats during stress, and increasing oxidative damage to cells. I suspect that a degree of saturation of the oxidative apparatus by short-chain fatty acids has a similar effect--that is, that these very soluble and mobile short-chain saturated fats have priority for oxidation, because they don't require carnitine transport into the mitochondrion, and that this will tend to inhibit oxidation of the unstable, peroxidizable unsaturated fatty acids.

So carnitine increases transportation and utilization of PUFA = double plus ungood.

Ray: Both adrenaline and ACTH mobilize fat from storage. Stress-mobilized fatty acids contribute to the increased lipid-peroxidation seen during stress, and they also tend to damage mitochondria. The large increase in the death rate from asthma in the last decade or two is now believed[*] to be the result of cardiovascular damage caused by the common use of inhalants containing catecholamines. Isoproteron01, a commonly used bronchodilator, causes mitochondrial damage, which can be prevented by blocking the carnitine-dependent oxidation of fatty acids. Since carnitine is required for the oxidation of long-chain fatty acids, its analog-betaines (which interfere with its transport of fatty acids into the mitochondria) protect against the damage that normally results from stress-induced (or catecholamine-induced) fatty acid oxidation. Since saturated fats protect against the cardiac necrosis produced by corn oil, I think it is probably lipid-peroxidation resulting from rapid oxidation of unsaturated fats which causes the heart damage in both catecholamine damage[ 3] and corn-oil toxicity. Vitamin E, coconut oil, and the carnitine antagonists (betaine derivatives) are adaptogens that protect respiration by directly decreasing lipid-peroxidation.


What about the study i showed. It showed carnitine also reduced lipid per oxidation
 

GorillaHead

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Why do you guys think when carnitine is applied to the skin. Sebaceous glands secreting. I thought sebaceous gland activity was due to cortisol
 
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To saturate your tissues with Vitamin E by going for higher dosages up to 3000mg/d for a prolonged time is nice and necessary.The dominant Scavenger in membranes is the plain Alpha Form.


Member Hans has a nice Overview about some Angles on the Carnitine topic:

A Controversial View On Carnitine
 
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