Experts suggest that pharmacogenomics and personalized medicine may soon change the practice of community pharmacy.
This year marks the tenth anniversary of what may be the most significant achievement of Western science. In 2001, the Human Genome Project successfully sequenced 90% of the 3 billion pairs of the human genome. Since then, genomics and molecular biology have advanced personalized medicine from a conceptual ideal to a fast-growing reality. The word pharmacogenomics - how well a drug therapy works depending upon individual variations in genomic responses - is now an everyday term and has its own shortcut acronym, PGx.s
Tracy S. Hunter, RPh, PhD, professor and assistant dean of pharmacy at Wingate University Pharmacy School near Charlotte, N.C., suggests that pharmacogenomics and personalized medicine may soon change the practice of community pharmacy.
"Pharmacogenomics is a tool that pharmacists can use to optimize drug outcomes for patients. This is also an opportunity for pharmacists to provide an expanded educational link with patients, physicians, and payors," she said, adding, "We learn something new every day about genomic variance and how these impairments affect drug metabolism."
Personalizing this therapy does not depend upon new drugs but upon an organic substance known as bioactive folate, which is found in the leafy green garden vegetables. Folate, it turns out, is the key agent that silences or activates certain genes involved in methylation.
"What we've done is to look more directly at this metabolism, the gene, and its variants that are contributing to worsening symptoms and failed treatments in people with this disease," Roffman said.
A focus on folate
According to Hunter, "Folate is essential for humans and is a critical factor in proper methylation metabolism. Unfortunately, because it is found in leafy green vegetables and very unstable, most of us don't get enough of the bioactive form, L-methylfolate. Genes, medications, disease conditions, or unhealthy life style choices like excessive alcohol and smoking also lower folate levels. Individuals who have a specific genetic variant in their folate metabolism, who also have symptoms of depression or schizophrenia plus low folate, will exhibit worsened symptoms."
While folate derived from folic acid or broccoli is a 'pro-drug' for L-methylfolate once digested, Hunter said, folic acid is an oxidized synthetic not found in nature. She recommends caution with high-dose use. People who are exhibiting symptoms of or are being treated for schizophrenia and also depression cannot substitute folic acid for dietary folate, Hunters said. "In high doses it can leak unmetabolized into circulation."
Once that happens, "this foreign substance blocks folate receptors on the blood-brain barrier, thwarting any active folate that you might have from doing its job and preventing neurotransmitter synthesis, including dopamine production."
Through his research with brain imaging of schizophrenic patients who have a specific genetic variance, or polymorphism, Roffman observed the effects of genetic differences on parts of the brain. "We know for sure that the dopamine life cycle relies on methylation," he said, and more important, "the effect of the genetics is very dependent on folate levels in the blood."