Acetyl-L-carnitine

Improve your memory!!!

Other names for Acetyl L-Carnitine: acetylcarnitine, l acetylcarnitine, levacecarnine and ST -200. After many years of research, the properties of a nutrient are increasingly recognized as being so powerful that it can increase cell energy and prevent neuronal cell death in the long term (Manfridi, 1992). In small amounts, acetyl-L-carnitine is present in milk and is found in many tissues of the body. It can be used to help treat depression (Gecele 1991; Nasca 1989), cognitive disorders, Alzheimer's disease and possibly AIDS. It is a neuroprotective factor that helps inhibit neuronal degeneration such as in polyneuropathy or retinopathy in diabetes or sciatica. It is also a nutrient for the nerves that helps prevent ischemic damage (caused by lack of blood flow) such as occurs during reperfusion after infarcts (so-called reperfusion injury), which leads to strokes (Rosenthal 1992). Even better, it also appears to have a wide range of applications for improving memory and other cognitive functions (such as concentration), prolonging life and having anti-ageing effects. Acetyl L-carnitine appears to be in a league of its own when it comes to nootropic and anti-ageing effects. Since Acetyl L Carnitine has so many benefits in so many different tissues and parts of the body, it makes sense to look at them chapter by chapter. But first, let's look at how acetyl L-carnitine gets into the body in the first place.

ACETYL-L-CARNITINE is an ester of the amino acid L-carnitine, which in turn can be synthesized by the body from the building blocks lysine and methionine. ACETYL-L- CARNITINE itself is formed by a transferase enzyme in the human liver, kidneys and brain. In terms of biological effects, ACETYL-L-CARNITINE increases the uptake of acetyl-CoA into the mitochondria - the "power plants" of the cell - as part of fatty acid oxidation. In addition, the production of acetylcholine is stimulated and the synthesis of proteins and cell membrane building blocks is supported. Due to these basal biochemical effects, L-carnitine and its ester act as fuels for the supply of energy in the cells. A deficiency of these important substances can therefore be noticeable in all cells of the body, although particularly stressed tissues (muscles, myocardium, brain etc.) have a higher requirement and are therefore in principle more susceptible to disruption. ACETYL-L-CARNITINE is found naturally in the brain in particular, but also in other tissues. The substance is also available as a dietary supplement. Although there should be no actual deficiency states of ACETYL-L-CARNITINE in the actual sense, as the ester is synthesized by the body itself, the levels of ACETYL-L-CARNITINE in the tissue decrease with increasing age. According to medical studies, the amino acid can be successfully used to treat dementia (e.g. Alzheimer's disease), age-related depression, HIV infections, diabetic neuropathy, cerebral circulatory disorders and alcohol-induced cognitive deficits.

Absorption in the intestine

When you swallow a tablet of acetyl-L-carnitine, usually between 250mg to 2g, it first dissolves in the stomach and is transported to the small intestine, where it easily passes through the lipophilic membranes of the intestinal wall. During this process, part of the molecule releases its acetate part. ALC is more easily absorbed than L-carnitine due to its acetyl part. This makes it significantly different from L-carnitine (also in terms of effectiveness). Intestinal absorption does not appear to be age-dependent (Maccari 1990). After absorption in the small intestine, it reaches the liver with the portal vein blood flow.

Liver passage

While the onward transport of L-carnitine from the liver into the bloodstream and thus other parts of the body decreases with age, acetyl-L-carnitine has been shown to increase transport activity in older rats to such an extent that they resemble young rats in this respect. This property is important because carnitine is needed to transport long-chain fatty acids into the mitochondria for combustion.

Without sufficient carnitine, cells cannot utilize fat. Although the liver and kidneys can produce carnitine from other molecules, other tissues that need fatty acids for energy production, such as the heart muscle, are dependent on the carnitine that the liver releases into the bloodstream due to a lack of self-synthesis. Recent research even suggests that the most important role of acetyl-L-carnitine is to enrich the energy metabolism of the mitochondria. By acting as an energy carrier, acetyl-L-carnitine controls the availability of acetyl-coenzyme A, which facilitates energy transfer across mitochondrial membranes (Calvani 1991). Acetly-coenzyme A is a substrate of acetylcholintransferase, whose activity is significantly reduced in people suffering from Alzheimer's disease. As we shall see, this is the background to the possible use of ALC in age-related cholinergic deficits. In a study of shock patients, ALC helped to reduce the effects of oxygen deprivation. In these patients with septic, cardiogenic or traumatic shock, intravenous ALC improved blood oxygen levels and normalized blood pressure and other vital signs during the course of sepsis and heart failure (Gasparetto 1991). Another study of elderly patients found that ALC improved memory and other mental functions in the rehabilitation phase after acute stroke (Arrigo 1990). ALC improved recovery, mood and concentration in patients suffering from hemiplegia. It also increased blood flow to the legs in peripheral arterial occlusive disease (PAD) (Bagliani 1985).

Support of the heart

In the heart muscle, ALC has been shown to reverse the age-related breakdown of phosphate carriers in rats. These phasphate transport molecules are fundamentally important for membrane function and thus for energy transfer (Paradies 1992). Other studies have shown that ALC can prevent oxygen deficiency in the heart muscle (Paulson 1984).

Lungs and immune system

In a double-blind placebo study of tuberculosis patients, ALC was shown to prevent the decrease in antibacterial lymphocyte activity or even increase this activity (Jirillo 1991). Other immune system boosting effects were the prevention of the decline in macrophage production and increased levels of thyroid stimulating hormone (TSH) (De Simone 1989). Some preliminary studies have indicated that ALC acts by stimulating the production of certain cytokines. ALC increased T-cell activity in TB patients after 30 days of use, while this activity decreased in patients receiving placebo.

This shows that ALC also appears to be a powerful immunomodulator in tuberculosis patients, perhaps also in other mycobacterial infections.

Physical performance

Another benefit of ALC was found in pre-exercised animals. The authors conclude that ALC statistically clearly increased maximum running speed and endurance after 10 days of use, whereas DL-carnitine did not. The effect in terms of improving running speed was directly proportional to its anti-oxidative activity (Seifulla 1993).

Acetyl-carnitine DNA defects

In peripheral blood lymphocytes, carnitine treatment was observed to accelerate the repair of DNA damage caused by oxygen radicals and alkylating agents (Boerrigter METI Carcinogenesis 1993).

Central nervous system

The brain is surrounded by a network of fine capillaries, known as the blood-brain barrier, which prevents many substances from entering the brain. Fortunately, this does not apply to ALC, which passes through this barrier relatively unhindered and enters the brain. The beneficial effects of ALC are more evident in the brain than almost anywhere else. Increased ALC levels in the brain cause the formation of nerve growth factor receptors (NGFR). A recent study showed that ALC also prevents the decline of these receptors, especially in the hippocampus and the basal frontal brain, parts of the brain that are very important for memory, intelligence and personality. Data suggest that ALC rescues aging neurons from destruction by improving responsiveness to nootropic (nerve-nourishing) factors in the brain (Taglialatela 1991). Some of the beneficial influences of ALC in the brain are: increased alertness, improved learning and memory, decreased forgetfulness, improved mental ability and long-term memory. Also mood enhancement and improved concentration. ALC can also slow down natural cell death in the hippocampus.

Alzheimer's disease

By increasing energy conversion in brain mitochondria (Petruzzella 1992) and controlling the availability of acetyl coenzyme A, ALC contributes to the reversal and prevention of age-related processes in the brain and neurodegeneration. Conclusions from a review of several controlled clinical trials suggest that ALC may also favorably influence the course of Alzheimer's disease. Alzheimer's patients have significantly reduced carnitine acetyl transferase activity in most parts of the brain and brain capillaries. ALC can increase this activity in Alzheimer's disease (Kalaria 1992). With regard to dementia (senile dementia), ALC was shown to be more affective than piracetam (Sinforiani 1990). It also reduced depression. Studies in humans have shown that ALC can favorably affect some clinical manifestations of Alzheimer's-like dementia, especially those affecting short-term memory. In a double-blind study that ran for one year, ALC showed a clear reduction in signs of deterioration compared to placebo in Alzheimer's patients (Pettegrew 1995). The authors of this publication emphasize that this is the first evidence of a substance (ALC) that is also effective in the real clinic and has a beneficial effect on both neurochemical factors and clinical manifestations.

Lipofuscin

ALC can probably halt some of the long-term effects of brain ageing. For example, it counteracts the solidification of cholesterol through lipid peroxidation, which is thought to increase with age and dementia (Arienti 1992). It reduces some of the age-typical changes in the shape of fat pigments, a type of cell degradation that indicates cell decay and certain diseases. Lipofuscin, which has long been associated with aging and declining mental vigor, can be reduced by ALC in the cytoplasm of neurons of the pyramidal system. ALC also has anti-oxidant activity and has been shown to neutralize the superoxide anion, a very destructive radical, at all concentrations, thus preventing lipoperoxidation and lipofuscin formation (Geremia 1988). Perhaps also interesting in this context is that it supports acetylcholine metabolism, which additionally reduces lipofuscin formation. There is also growing evidence that ALC may be very useful in the prevention of neuropathy in diabetics, including the prevention of damage to the sciatic nerve, spinal cord and facial nerves.

Life extension

Apart from its ability to support nerve metabolism, ALC can also be considered for its life-prolonging effect. One study showed that ALC significantly reduced mortality in rats. It should be noted that comparable studies in humans are of course not available. We would all like to see such studies to substantiate the use of acetyl-L-carnitine to prolong life in humans as well. However, practical and ethical problems in the "design" of such studies are of course immense. Such a study would also have to be carried out over at least 5 years and would be very expensive. For various reasons, there will never be such a study. Everyone must therefore decide for themselves whether they consider the available study results to be valid enough to take a dietary supplement such as acetyl-L-carnitine with the intention of prolonging life and/or because of its memory and concentration-enhancing properties. Its positive effects on signs of ageing in the brain are relatively well established. It has even been proven that it can partially reverse the above-mentioned age-related deposition of pigments in the brain. In view of the significance of brain degeneration in terms of the need for care, but also in terms of cohabitation, e.g. in marriage, such prevention of dementia symptoms makes a lot of sense.

Acetyl-carnitine influence on hormones

One of the most interesting fields of research deals with questions of receptor sensitivities in the regulatory circuits between the hypothalamus-pituitary gland and the peripheral glands. Without making things completely incomprehensible: One of the reasons why cortisol levels often rise to fatal levels as we age is because the adrenal cortex, where cortisol is produced, is increasingly stimulated to produce it by the pituitary gland. This in turn is due to the fact that inhibitory influences from other parts of the brain on the pituitary gland diminish in the course of normal ageing, mainly because cortisol receptors there die off, so that it is practically feigned that there is too little cortisol "on the way". Here too, ALC has been shown to be able to normalize elevated cortisol levels in laboratory animals. Interestingly, another substance that is often administered to improve memory, piracetam, could not keep up in this respect. The melatonin levels of rats treated with ALC increased significantly. Melatonin, which is produced by the pineal gland during deep sleep and is one of the main regeneration hormones (alongside growth hormone) and a highly potent antioxidant, is unfortunately produced less and less by the ageing, increasingly calcifying pineal gland. So if ALC reverses this, then this is a major sensation and possibly a better method of halting ageing than taking melatonin directly.

Diabetes

The disturbances in the carnitine metabolism of diabetics are generally known. The result is a deterioration in the supply of fatty acids to cells for the purpose of combustion (energy production) and thus a chronic lack of energy in cells, which has a very negative effect on the heart muscle, for example, but also on the eye retina and peripheral nerves. ALC can prevent these changes or, if not too advanced, reverse them. The potency problems of diabetics are often due to reduced excitability of peripheral sensory nerves. This is an effect of peripheral diabetic neuropathy. Acetyl-L-carnitine has been shown to significantly improve this neurogenic impotence with a daily dose of 1500mg acetyl-L-carnitine.

Influences on mood and moodiness

ALC increases cholinergic and serotonergic activity by improving nerve excitability to these two neurotransmitters (acetylcholine and serotonin). This facilitates both the excitatory and inhibitory effects of serotonin. Serotonin is considered to be the brain's "good mood/satisfaction" molecule and is related to melatonin. Antidepressants attempt to inhibit the breakdown of serotonin in order to lift the mood (so-called serotonin reuptake inhibitors). This is often successful, but is associated with side effects. The administration of ALC is probably a much more intelligent way of normalizing the serotonin metabolism, because here the metabolism of serotonin is not manipulated, but the receptor sensitivity is upregulated. It is therefore to be expected that ALC will primarily help older people with chronic depression who suffer from the general desensitization of receptors that is typical of old age.

Optimal dosage

The amounts commonly used in humans range from 1000 to 2000 mg daily, taken in two equal portions. However, it will generally be more beneficial to take 4 times 500mg rather than 2 times 1000mg in order to maintain plasma levels more consistently.

Safety and side effects

Acetyl-L-Carnitine is probably safe and harmless for most adults. It may cause some side effects including stomach upset, nausea, vomiting and restlessness. It may also cause a fishy odor from urine, breath and sweat.

Precautions and warnings

Pregnancy and lactation: Not enough is known about the safety of Acetyl-L-Carnitine during pregnancy and lactation. For this reason, pregnant and breastfeeding women should avoid Acetyl-L-Carnitine to be on the safe side.

Hypothyroidism: There are concerns that acetyl-L-carnitine may interfere with thyroid hormone production. For this reason, you should not use Acetyl-L-Carnitine if you suffer from hypothyroidism.

Seizures: There have been reports of an increase in the number of seizures in people with a history of seizures who had used L-Carnitine orally or intravenously. As L-carnitine is closely related to acetyl-L-carnitine, there are concerns that this may also be the case with acetyl-L-carnitine. For this reason, you should not use Acetyl-L-Carnitine if you have ever had seizures.

Interactions

Acetyl-L-Carnitine should not be taken in combination with the following medications:

Acenocoumarol

Acenocoumarol is used to slow down blood clotting. Acetyl-L-Carnitine could increase the effectiveness of acenocoumarol. By increasing the effectiveness of acenocoumarol, acetyl-L-carnitine could slow down blood clotting too much. It is possible that the acenocoumarol dosage may need to be changed when taking acetyl-L-carnitine.

Care should be taken when combining Acetyl-L-Carnitine with the following medications.

References

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