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Genetic Biotechnology

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Even as the 2008 Olympics in Beijing are gaining momentum, the subject of doping is making its way into the coverage. That is to be expected. The prevalence of doping among athletes in professional, college and high school sports is well documented. And up till now, doping has always involved muscle-enhancing drugs such as steroids and recombinant growth factors.

Growth factors such as Human Growth Hormone, or HGH, and other new age drugs result from recombinant DNA technologies of the mid-1980s that a decade later led to drugs approved for human use to treat growth deficiencies.

In theory, these same growth-promoting drugs could be introduced into humans using gene therapy. However, gene therapy has been notoriously difficult to control, and once you introduce the gene, how do you take it back after its effect is no longer needed? After all, modern athletes who wish to cheat the system to achieve their athletic goals may wish to return to a normal life after athletic ambitions have been satisfied. With gene therapy there may be no way to reverse the unending effects of alien muscle-enhancing genes.

However, a new genetic solution is emerging that may solve the problem of uncontrollable long-term effects and offer a new, easier way to cheat the system.

In a 2004 Scientific American article titled, “Gene Doping,” H. Lee Sweeney describes the “Belgian Blue Bull” as the bovine version of the Incredible Hulk. The Belgian Blue Bull is a freak of nature because an inherited genetic mutation in the breed deactivates both copies of the gene that encodes myostatin, a protein that inhibits muscle growth so the organism can maintain a balance between muscles and skeleton. The absence of this protein not only allows unchecked muscle growth, it also inhibits fat deposition. As a result, this bull is incredible lean muscle bulk-a bigger, stronger, and, yes, faster bull.

In a recent paper in Trends in Genetics titled “Sprinting without myostatin: a genetic determinant of athletic prowess,” author Se-Jin Lee of Johns Hopkins University describes the occurrence of this myostatin mutation in mice, sheep and bully whippet racing dogs. In whippets, mutations in both copies of the myostatin gene lead to a dog with twice as much muscle mass. A mutation of only one copy of the myostatin gene results in about a 25 percent increase in muscle bulk with increased athleticism.

Among humans, a 2004 article in the New England Journal of Medicine reported on a child whose mutation affected both gene copies, meaning the child has no myostatin. The child’s mother, who was an accomplished sprinter, has one mutated copy of her myostatin gene. The child appeared extraordinarily muscular at birth and was noted to be unusually strong at seven months. At age 4 the child was monitored for cardiac function, but no cardiomyopathy was found.

Beyond naturally occurring mutations, the last five years have seen a new approach known as RNA interference to intentionally silence genes to treat diseases. The effectiveness of what is known as siRNA has been established for silencing genes , such as a gene in the liver of primates that causes high blood cholesterol.

Development of this technology has brought about rapid growth, creating a billion-dollar industry in just five years. In addition, large pharmaceutical companies such as Merck, GlaxoSmithKline, Novartis, Pfizer, and Hoffmann-La Roche are buying up or partnering with the smaller, innovative companies including Alnylam and Sirna Therapeutics, which own the patent rights to the siRNA technology.

It would take only a few weeks to design and synthesize an RNA interfering drug that could silence the gene that encodes myostatin, which is active only in muscle. Gene silencing of myostatin to produce a better athlete could, in theory, be accomplished by injecting siRNA into the area targeted for muscle building.

Indeed, researchers at Sirna Therapeutics have already produced siRNA’s that shut down myostatin expression, and Sirna has filed a U.S. patent application (US 20050124566) on the use of these compounds to increase muscle mass for increased strength, athleticism, bodybuilding, or cosmetic applications.

Targeting other genes has demonstrated lasting inhibitory effects of three to four weeks with a single siRNA injection. Since this is not classic gene therapy, this approach to muscle building can be reversed, avoiding problems associated with the life-long physiologic consequences of non-reversible myostatin deficiency.

A number of other human genes have also been mentioned as possible targets for gene doping in athletes. However, those muscle-enhancing genes would have to be introduced into the athlete with no guarantee of the lasting outcome. It seems more likely that siRNA will find its way to athletes who wish to cheat and the enablers who wish to exploit athletes to make money.

There may be no way to test for the type of genetic manipulation. Nevertheless, the US and International Olympic Committees should advocate for national laws to be enacted by all participating nations to make genetic manipulation of athletic traits unlawful. The ethical dilemma here is should athletes be denied the ability to acquire athletic traits that have been naturally acquired by others?

Biotech Websites

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A keynote slide show while talking to a class about cutting-edge RNA interference.

Genetic Testing Center

Want to Live an Extra 10 Years?

Mechanism of RNA silencing; a cool video clip based on the animation from “Nature”. Video material: Nature Magazine; music mix and sound effects by boulderdash. Music: Skylight (Overseer)

Genetic Testing Center

Want to Live an Extra 10 Years?

Serious Visual Side Effects Found With New AMD Treatment

A study in the August 2008 New England Journal of Medicine (NEJM) suggested that Dry AMD–a form of Age-related Macular Degeneration (AMD) found in eight to nine million Americans–may be associated with a gene in our body. The study also found that in individuals with this genetic variation, a currently practiced modern treatment for AMD may lead to serious adverse consequences, including blindness.

Researcher Kang Zhang and co-workers from the Shiley Eye Center at the University of California, San Diego, found that a key protein that alerts our immune system to the presence of viral infections–called Toll-like Receptor 3 (TLR3)–was linked with dry AMD. Zhang and co-workers also noted that if individuals with a genetic variant of TLR3 are treated with a modern treatment for AMD–called RNA interference (RNAi)–they could be at risk for serious adverse effects, including blindness. RNAi is a modern modality of treatment that is used to silence the genes related to various disease conditions.

The study links the occurrence of dry AMD with a genetic variation of TLR3, which indicates that some persons with this particular genetic variation will be more prone to develop dry AMD. Given that gene test is emerging as a new trend in personal health, genetic linkage of dry AMD may help people know–through gene tests–whether they’ve propensity for the disease. And this in turn may help them adopt proper preventive measures to stay away from the disease. The second component of the study has raised the question of safety in adopting modern treatments for AMD. It has cited the evidence that a new treatment approach for AMD–RNAi–may lead to serious adverse consequences, including blindness. This finding has reinforced the position of nutritional treatment in AMD, because treatment of AMD with nutritional supplements is safe and substantially effective.

Elderly People Remain in the Dark About Age-Related Macular Degeneration

Research released this month by the Toronto-based AMD Alliance International (AMDAI) showed that AMD ranked lowest among a list of conditions that are likely to affect the aging population, when participants in that study were asked how much they know about those conditions.

This study suggested that people lack knowledge and concern regarding AMD, and it is preventing them from taking critical steps to halt or slow the progression of the disease. According to the study, amid those who had a high propensity for loss of vision due to AMD, only 56 percent of the participants met an eye specialist once a year and more. That apart, when the participants were asked about their knowledge about conditions that are likely to affect the aging populations, AMD ranked lowest in the list.

The AMDAI spoke for the necessity of increased understanding about AMD. In the web document related to the study, the chair of the organization David Herman says, “This study clearly indicates that there is a low level of concern about AMD and many people aren’t seeking adequate eye care until the disease has reached more of an advanced stage.” As antioxidants help keep the eyes healthy (for example, by cutting the risk and slowing the progress of AMD)–regular intake of antioxidant-rich nutritional supplements may be of some practical help for people who avoid visit an eye doctor at regular intervals.

More Support for Biochemistry of Antioxidants in the Treatment of AMD

The Journal of Biological Chemistry (JBC), has reconfirmed that antioxidants substantially help combat AMD in a study published on September 9, 2008.

The study showed two damaging processes in retina that play an important role in the development of AMD. Conducted by researchers from Brigham Young University (BYU) and Cornell University, the research also found that antioxidants fight against AMD by significantly disrupting the link between those two processes (in retina) and extending the lifetime of the irreplaceable photoreceptors and other cells in retina. “The implication is that people at risk of macular degeneration could help prevent the disease by consuming antioxidants,” says, in a news release, Heidi Vollmer-Snarr, co-author of the study and a chemist at the BYU.

The authors explained the role that antioxidants play in tackling AMD. In the study, the researchers looked at a compound called A2E (which is a byproduct of natural cellular activity) and damage to mitochondria (the power plants present inside the cells). The researchers found that when oxidative stress is created on A2E, by light exposure, it disrupts the energy production in mitochondria. It results a shortage of energy inside the cells which in turn hampers the daily cleaning and maintenance of photoreceptors and other type of retinal cells. “The result is more A2E buildup, and the cycle of destruction hastens the death of these vital visual cells, which are not replaced when they die,” says a BYU news release associated with the study, adding, “The experiments performed with visual cells from rats, cows and humans showed that antioxidants could completely counter the damage.” Regarding the role of antioxidants in AMD, research in past suggested that antioxidants found in nutritional supplements (for example, Lutein, Zeaxanthin, Vitamin E and beta-carotene) work as scavengers for free radicals and protect the retina against damages caused by oxidative stress.

Genetic Assessment

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