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Supplement Repairs Cell Damage

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Tuesday, 26 Jan 2016 04:01 PM Current | Bio | Archive

Carnitine is another compound that is attracting great interest, especially for heart and brain protection. There are two major forms of carnitine compounds — acetyl-L-carnitine and L-carnitine.

Other metabolic compounds can be added to L-carnitine to boost its energy-producing effects and absorption. These include a proprionyl-L-carnitine, L-carnitine tartrate and L-carnitine fumarate. I prefer the first and last of these.

Mitochondria are the microscopic “factories” within all cells that play a critical role in keeping cells supplied with energy. But they do a lot more than that.

For instance, mitochondria also regulate the concentration of calcium within cells, which is essential, as too much calcium can trigger reactions that can make cells get sick and die.

Mitochondria also play a major role in metabolism of fatty acids, which supply energy and have a number of other special functions in cells.

L-carnitine aids in the metabolism of long-chained fats in the mitochondria. One of the major effects of aging is the decreased efficiency (decay) in the function of mitochondria within all cells, but especially in brain cells and heart cells.

The rate and extent of decay varies considerably between individuals. Those with the most rapid and extensive mitochondrial decay have the poorest health. They become infirm and are more likely to develop a neurodegenerative or cardiovascular disease.

Many studies have been done on this decaying process in mitochondria. The studies have shown extensive damage to the various structures of the mitochondria, along with damage to enzymes and DNA.

As the mitochondria produce less energy, several things happen:

• They begin to produce very high levels of free radicals

• They cause brain cells (microglia and astrocytes) to release toxic levels of glutamate (progressive excitotoxicity)

• Calcium begins to accumulate in the cell’s cytoplasm

• The cell membranes stiffen, causing receptors to become less responsive

This mitochondrial decay process is greatly magnified and accelerated in disorders such as Alzheimer’s disease and heart failure. The decline in cell function occurs in all types of cells throughout the body.

A recent study found that acetyl-L-carnitine combined with R-lipoic acid could repair damaged mitochondria and restore cellular energy levels to that of younger cells.

Incredibly, the researchers also found that this combination also helped the mitochondria of young animals work more efficiently, which indicates that starting to take these compounds early in life would be even more beneficial.

In a meta-analysis of 21 double-blind studies in which acetyl-L-carnitine was used to treat mild cognitive impairment and mild Alzheimer’s disease, researchers found a modest but significant improvement in brain function.

Supplying the combination of compounds repaired many types of damage seen on electron microscopy of mitochondria in the hippocampus of aged animals.

Impairments that were healed included mitochondrial swelling, damage to its membranes, and formation of lipofuscin, a brownish pigment left over from the breakdown of damaged membrane lipids.

Mitochondrial damage is an early event in a number of degenerative diseases, such as heart failure, kidney failure, Parkinson’s, Alzheimer’s, ALS, and overall aging of the body.

Repairing this damage and making the mitochondria more efficient dramatically improves energy levels and organ function, thus warding off many diseases.

One interesting study found that feeding both young and old rats acetyl-L-carnitine significantly increased their overall energy levels and activity.

Other studies have shown that both L-carnitine and acetyl-L-carnitine can improve immune function, which also reduces the likelihood of many degenerative diseases associated with aging.
 

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Dr-Blaylock
Carnitine is another compound that is attracting great interest, especially for heart and brain protection.
carnitine, aging, mitochondria, Alzheimers
564
2016-01-26
Tuesday, 26 Jan 2016 04:01 PM
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