za po 30 letu je fajn dodajati. prej pa niti ne.

Instead of using massive doses of Q10 to attempt to increase brain Q10 levels it may be more important to find ways to reduce brain levels of Q10. The neuroprotective effects of the popular statins may be because statins reduce Q10 levels. The benefits of a calorie restricted diet (ref) for HD mice may be due to less Q10.

Q10 is thought to cause oxidative damage. The blood brain barrier protects the brain from the effects of Q10 supplementation but there is no protection from the muscle damage found in HD patients.

Although this one study may not be definitive for humans it shifts the benefit/risk ratio for Q10 to unacceptable.

Under certain circumstances, Coenzyme Q10 (CoQ10) may become a pro-oxidant. These circumstances are conditions in which hypoxia or lack of oxygen occurs. In cases of shock, heart attack, stroke, or poor circulation, CoQ10 auto-oxidizes and unleashes massive amounts of various free radicals that damage delicate tissues and because CoQ10 is necessary for electron transport and ATP (chemical energy) production, cellular death may ensue.

The secret to long life, for worms at least, may be cutting back on a micronutrient called coenzyme Q, researchers report.

Worms deprived of the substance lived nearly 60% longer than worms on a normal diet, according to a report in the January 4th issue of the journal Science.

It is well known that animals that eat fewer calories live longer. Drs. Pamela L. Larsen and Catherine F. Clarke of the University of California, Los Angeles, set out to see whether the contents of an animal's diet might also affect its life span.

Working with a type of worm called C. elegans, the researchers eliminated coenzyme Q--a fatty substance found in cell membranes--from the animals' diet. This substance is involved in transporting electrons during the cellular respiration process.

Adult worms on the restricted diet lived an average of 59% longer than those fed a diet containing coenzyme Q, Larsen and Clarke report.

Larsen told Reuters Health that she and Clarke tested the ''Q-less'' diet on several different genetic varieties of C. elegans worms to understand the interaction between diet and genes. ``We found that all the mutants lived longer on a Q-less diet as adults,'' she said.

The researchers speculate that reduced consumption of coenzyme Q may extend the life span of worms by minimizing the damage caused by a cellular process called oxidation.

The results were surprising since coenzyme Q is an antioxidant, meaning it can counteract the effects of byproducts of the oxidation process, Larsen said. This may be true, but the substance also appears to be a ``pro-oxidant,'' according to the California researcher.

``Coenzyme Q may cause more oxidative damage than it prevents depending on how much is in the animal, where it is within the cell (and) the age and genetic make-up of the worm,'' she said.

But extending life span may not be as simple as removing the coenzyme from the diet.

``The amount of (coenzyme Q) that is most beneficial appears to be different for the larvae'' than for adult worms, Larsen said. ``Ones that consume it are better off than those that do not while they are growing up,'' she said.

The investigators found that worms fed a diet lacking the substance from birth were much more likely to develop reproductive defects than worms that started the diet towards the end of the larval stage of development.

Right now, how much coenzyme Q people need is uncertain, according to Larsen. ``We expect that the optimal amount of coenzyme Q will vary among individuals and may differ over the life cycle,'' she said.
There are several possible explanations for the link between longer life and a coenzyme Q-free diet in worms, including an effect on the communication between different parts of cells, according to Drs. Marc Tatar and David M. Rand of Brown University in Providence, Rhode Island.