| Parkinson's Disease: New Coenzyme Q10 Research | |
Results of the first
placebo-controlled, multicenter clinical trial of the compound coenzyme Q10
suggest that it can slow disease progression in patients with early-stage
Parkinson's disease (PD). While the results must be confirmed in larger studies,
they provide hope that this compound may ultimately provide a new way of
treating PD.
The phase II study, led by Clifford Shults, M.D., of the University of
California, San Diego (UCSD) School of Medicine, looked at a total of 80 PD
patients at 10 centers across the country to determine if coenzyme Q10 is safe
and if it can slow the rate of functional decline. The study was funded by the
National Institute of Neurological Disorders and Stroke (NINDS) and appears in
the October 15, 2002, issue of the 'Archives of Neurology'. (1)
"This trial suggested that coenzyme Q10 can slow the rate of deterioration
in Parkinson's disease," says Dr. Shults. "However, before the
compound is used widely, the results need to be confirmed in larger groups of
patients."
PD is a chronic, progressive neurological disease that affects about 500,000
people in the United States. It results from the loss of brain cells that
produce the neurotransmitter dopamine and causes tremor, stiffness of the limbs
and trunk, impaired balance and coordination, and slowing of movements. Patients
also sometimes develop other symptoms, including difficulty swallowing,
disturbed sleep, and emotional problems. PD usually affects people over
the age of 50, but it can affect younger people as well. While levodopa and
other drugs can ease the symptoms of PD, none of the current treatments has been
shown to slow the course of the disease.
The investigators believe coenzyme Q10 works by improving the function of
mitochondria, the "powerhouses" that produce energy in cells. Coenzyme
Q10 is an important link in the chain of chemical reactions that produces this
energy. It also is a potent antioxidant -- a chemical that "mops up"
potentially harmful chemicals generated during normal metabolism. Previous
studies carried out by Dr. Shults, Richard Haas, M.D., of UCSD and Flint Beal,
M.D., of Cornell University have shown that coenzyme Q10 levels in mitochondria
from PD patients are reduced and that mitochondrial function in these patients
is impaired.
Animal studies have shown
that coenzyme Q10 can protect the area of the brain that is damaged in PD.
Dr. Shults and colleagues also conducted a pilot study with PD patients which
showed that consumption of up to 800 mg/day of coenzyme Q10 was well-tolerated
and significantly increased the level of coenzyme Q10 in the blood.
All of the patients who took part in the new study had the three primary
features of PD -- tremor, stiffness, and slowed movements -- and had been
diagnosed with the disease within 5 years of the time they were enrolled. After
an initial screening and baseline blood tests, the patients were randomly
divided into four groups. Three of the groups received coenzyme Q10 at three
different doses (300 mg/day, 600 mg/day, and 1,200 mg/day), along with vitamin
E, while a fourth group received a matching placebo that contained vitamin E
alone. Each participant received a clinical evaluation 1 month later and every 4
months for a total of 16 months or until the investigator determined that the
patient needed treatment with levodopa. None of the participants or the study
investigators knew which treatment each patient had received until the study
ended.
The investigators found that
most side effects of coenzyme Q10 were mild, and none of the patients required a
reduction of their dose. The percentage of people receiving coenzyme Q10 who
reported side effects was not significantly different from that of the placebo
group. During the study period, the group that received the largest dose of
coenzyme Q10 (1,200 mg/day) had 44 percent less decline in mental function,
motor (movement) function, and ability to carry out activities of daily living,
such as feeding or dressing themselves. The greatest effect was on activities of
daily living. The groups that received 300 mg/day and 600 mg/day developed slightly less disability than the placebo group, but the effects were less than those in the group that received the highest dosage of coenzyme Q10. The groups that received coenzyme Q10 also had
significant increases in the level of coenzyme Q10 in their blood and a
significant increase in energy-producing reactions within their mitochondria.
The results of this study suggest that doses of coenzyme Q10 as high as 1,200
mg/day are safe and may be more effective than lower doses, says Dr. Shults. The
findings are consistent with those of a recently published study of patients
with early Huntington's disease -- another degenerative neurological disorder --
that showed slightly less functional decline in groups that received 600 mg/day
of coenzyme Q10.
Dr. Shults and his colleagues strongly caution patients against taking coenzyme
Q10 until a larger, definitive trial can be conducted. Because coenzyme Q10 is
classified as a dietary supplement, it is not regulated by the U.S. Food and
Drug Administration. The versions of the supplement sold in stores may differ,
they may not contain potentially beneficial amounts of the compound, and taking
coenzyme Q10 over a number of years may be costly, says Dr. Shults. In addition,
the current study included only a small number of patients, and the findings may not extend to people in later stages of PD or to those who are at risk but have not been diagnosed with
the disorder, he notes. Finally, if many people begin taking coenzyme Q10
because of these early results, it might make it impossible for investigators to
find enough patients to carry out definitive studies of the compound's
effectiveness and the proper dosages, since patients must not be taking any
treatments in order to be considered for enrollment in a definitive trial.
The investigators are now planning a larger clinical trial that will examine the
effects of 1,200 mg/day of coenzyme Q10, and possibly a higher dose as well, in
a larger number of patients.
Source: National Institute of Neurological Disorders and Stroke (NINDS)
The NINDS is a component of the National Institutes of Health in Bethesda, Maryland, and is the nation's primary supporter of biomedical research on the brain and nervous system.
1. Shults CW, Oakes D, Kieburtz K, Beal F, Haas R, Plumb S, Juncos JL, Nutt J, Shoulson I, Carter J, Kompoliti K, Perlmutter JS, Reich S, Stern M, Watts RL, Kurlan R, Molho E, Harrison M, Lew M, and the Parkinson Study Group. "Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline." 'Archives of Neurology', October 2002, Vol. 59, No. 10, pp. 1541-1550.
