UC Santa Barbara chemist goes nano with CoQ10

If Bruce Lipshutz has his way, you may soon be buying bottles of water brimming with the life-sustaining coenzyme CoQ10 at your local Costco.

Lipshutz, a professor of chemistry at UC Santa Barbara, is the principal author of an upcoming review, "Transition Metal Catalyzed Cross-Couplings Going Green: in Water at Room Temperature," which will be published in Aldrichimica Acta in September. In it, Lipshutz and post-doctoral researcher Subir Ghorai discuss how recent advances in chemistry can be used to solubilize otherwise naturally insoluble compounds like CoQ10 into water.

Never heard of CoQ10? Lipshutz says you're not alone. "If you don't know anything about it," Lipshutz said during a recent interview, "that's not surprising to me. Much of the public hasn't heard of it." But he's on a mission to correct what he views as a major oversight. "In a sense, I'm just a messenger. People need to not only know about CoQ10, they need to take it."

Like vitamin C, CoQ10 is a compound that's vital to our survival. It's a coenzyme that our cells synthesize, albeit in 21 steps, and it's in every cell. This contrasts with a vitamin, such as vitamin C, which is not made by the body. Both CoQ10 and vitamin C are "compounds of evolution," Lipshutz said. "Everybody accepts the importance of vitamin C. The reason the public does not fully appreciate it is that there's no Linus Pauling for CoQ10. There is no champion."

Pauling, a Nobel Prize-winning scientist, was also an advocate for greater consumption of vitamin C. "CoQ is not really in that category of public awareness yet," Lipshutz said.

Don’t know for sure but heard it’s good in large dosage for Parkinsons.

http://www.ninds.nih.gov/news_and_events/press_releases/pressrelease_parkinsons_coenzymeq10_101402.htm

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 a larger study, 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 a larger group of patients.”

Statin Snag

By Nathan Seppa
July 23rd, 2008

Size Gene variant places some people at risk of side effect from statins

Cholesterol-reducing drugs called statins do their job with remarkable efficiency, but in rare individuals they can cause a painful muscle side effect called myopathy. Researchers report in an upcoming issue of the New England Journal of Medicine the discovery of a gene variant that places people at risk of this complication.

The gene, called SLCO1B1, encodes a protein that shuttles compounds from the blood stream into the liver for processing. This cargo includes statins.

Properly deposited, these drugs then go on to decrease the levels of LDL, the bad cholesterol.

But people with the variant form of the gene make a version of this protein that transports statins poorly, leaving an excess amount in the blood stream, says study coauthor Rory Collins, a physician and epidemiologist at the University of Oxford in England.

From there the story gets rather mysterious. “It’s still not clear how statins cause myopathy,” he says. But left to linger in the blood, statins seem to have that effect. “The mechanism is unknown.”

Collins and his colleagues suspected that statins were involved because a trial had shown that people getting high doses of a statin were 10 times as likely to develop the side effect as people receiving a low dose, Collins says. But since not everyone gets myopathy on high-dose statins, the scientists guessed that a gene — or a rogue form of one — might explain some of the risk.

Blood samples were collected from 192 of the trial volunteers between 1998 and 2001. Half the volunteers had myopathy, half did not. The statin used in the trial was simvastatin, marketed as Zocor. The scientists screened thousands of genes in these blood samples, and the one that stood out was SLCO1B1.

Genes often come in a variety of forms, resulting in the assemblage of slightly different proteins. The researchers found that among people taking high-dose simvastatin, those who carried one particular variant of the SLCO1B1 gene had four times the risk of myopathy compared with people carrying other forms of SLCO1B1. If a person carried two copies of this variant — one inherited from each parent — the risk shot up 17-fold, the researchers report.

“We’ve always suspected there are genetic differences,” says endocrinologist Robert Hegele of the University of Western Ontario in London, Ontario “It’s great that they did this study.”

Hegele estimates that roughly five to 10 percent of patients on statins report some muscle aches and pains at some point.

Collins and his team calculated that 18 percent of people with two copies of the gene variant who take a high does of statins would develop myopathy, while three percent of people who harbor only one copy and take the high drug dose would get myopathy.

Severe myopathy can damage muscles and even the kidneys. The researchers calculated that nearly two-thirds of the cases of myopathy in patients taking high-dose statins are attributable to the variant.

Doctors might avoid giving statins to people who have two copies of the variant and prescribe only low-dose statins for people carrying one copy, reasons physician Yusuke Nakamura of the University of Tokyo, writing in the same NEJM issue.

As an alternative, doctors might use the anti-cholesterol drug ezetimibe, sold as Zetia, which lowers LDL via a mechanism different from that employed by statins, Hegele says. Statins reduce cholesterol production in the liver, whereas Zetia inhibits cholesterol absorption in the intestines.

While doctors’ offices aren’t equipped to test for the gene, Collins says, the actual lab test for the variant is inexpensive. “The technology is straightforward. It would cost less than a dollar in a standard genetics lab,” he says.

The number of people in the United States taking statins nearly doubled from 2000 to 2005, rising from 15.8 million to 29.7 million, according to the Medical Expenditure Panel Survey conducted by the federal government.

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