The highlights from a study published in the Proceedings of the National Academy of Sciences (1998; 95):

When coenzyme Q10 was administered to middle-age and old rats, the level of coQ10 increased by 10% to 40% in the cerebral cortex region of the brain. This increase was sufficient to restore levels of coQ10 to those seen in young animals.

After only two months of coQ10 supplementation, mitochondrial energy expenditure in the brain increased by 29% compared to the group not getting coQ10. The human equivalent dose of coQ10 to achieve these results was 100-200 mg a day.

When a neurotoxin was administered, coQ10 helped protect against damage to the striatal region of the brain where dopamine is produced.

When coQ10 was administered to rats genetically bred to develop ALS (Lou Gehrig's disease), a significant increase in survival time was observed.

The conclusion by the scientists was:

CoQ10 can exert neuroprotective effects that might be useful in the treatment of neurodegenerative diseases.

This study showed that short-term supplementation with moderate amounts of coQ10 produced profound antiaging effects in the brain.

Previous studies have shown that coQ10 may protect the brain via several mechanisms including reduction in free radical generation and protection against glutamate-inducted excitotoxicity. This study documented that orally supplemented coQ10 specifically enhanced metabolic energy levels of brain cells. While this effect in the brain has been previously postulated, the new study provides hard-core
evidence.

Based on the types of brain cell injury that coQ10 protected against, the scientists suggested that it may be useful in the prevention or treatment of Huntington's disease and Lou Gehrig's disease (amyotrophic lateral sclerosis). It was noted that while vitamin E delays the onset of Lou Gehrig's disease in mice, it does not increase survival time. CoQ10 was suggested as a more effective treatment strategy for neurodegenerative disease than vitamin E because survival time was increased in mice treated with coQ10.

CoQ10 might be effective in the prevention and treatment of Parkinson's disease. (Reference: Annals of Neurology (1997 August). A study showed that the brain cells of Parkinson's patients have a specific impairment that causes the disruption of healthy mitochondrial function. It is known that "mitochondrial disorder" causes cells in the substantia nigra region of the brain to malfunction and die, thus creating a shortage of dopamine.

An interesting finding was that coQ10 levels in Parkinson's patients were 35% lower than age-matched controls. This deficit of coQ10 caused a significant reduction in the activity of enzyme complexes that are critical to the mitochondrial function of the brain cells affected by Parkinson's disease.

The ramifications of this study are significant. Parkinson's disease is becoming more prevalent as the human lifespan is increased. The new study confirms previous studies that Parkinson's disease may be related to coQ10 deficiency. The conclusion of the scientists was:

"The causes of Parkinson's disease are unknown. Evidence suggests that mitochondrial dysfunction and oxygen free radicals may be involved in its pathogenesis. The dual function of coQ10 as a constituent of the mitochondrial electron transport chain and a potent antioxidant suggest that it has the potential to slow the progression of Parkinson's disease." (see Parkinson's protocol for more information.)

CoQ10 levels decrease with aging. Depletion is caused by reduced synthesis of coQ10 in the body along with increased oxidation of coQ10 in the mitochondria. A coQ10 deficit results in the inactivation of enzymes needed for mitochondrial energy production, whereas supplementation with coQ10 preserves mitochondrial function.

Aged humans have only 50% of the coQ10 compared to young adults, thus making coQ10 one of the most important nutrients for people to supplement.

CoQ10 for Cancer

Coenzyme Q10 was used for cancer treatment and impressive results were reported (Lockwood K., et al., 1995; Lockwood K., et al. 1994; Folkers, K., et al. 1993).

Mechanism of action: The mechanism of the anticancer property of coenzyme Q10 is currently not well understood. It may be due to its immune system modulating activity and free radical quenching capability.

Evidence of Cancer-preventive effects: Use of coenzyme Q10 in treating cancer patients was reported several times by Folkers, M.D and his collaborators, (Lockwood K., et al., 1995; Lockwood K., et al. 1994; Folkers, K., et al. 1993). In these reports, patients with various cancers were treated with coenzyme Q10 in a dosage ranging from 90-390 mg daily. Some patients, considered terminal with metastases, were reported cured and others showed improvement. The blood levels of coenzyme Q10 was found low in 199 Swedish and American cancer patients (Lockwood K., et al., 1995). CoQ10 also enhances the effectiveness of chemotherapy and reduces toxic side effects.

Conclusion: Based on the evidence available, it seems reasonable to postulate that supplementation with coenzyme Q10 may have protective and therapeutic effects against cancer.

References:
Folkers K., et al. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q10. Proc. Nat. Acad. Sci., 62:901-904, 1985.
Lockwood K., Moesgaard S., Yamamoto T., Folkers, K. Progress on therapy of breast cancer with vitamin Q10 and regression of metastases, Biochem. Biophys. Res. Comm., 212:172-177, 1995.
Lockwood K., Moesgaard S., Folkers, K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10, Biochem. Biophys. Res. Comm., 199:1504-1508, 1994.

Folkers, K., et al. Survival of cancer patients on therapy with coenzyme Q10, Biochem. Biophys. Res. Comm., 192:241-242, 1993.

COQ10 -ST 100 mg. 60 Capsules