Life in the Genomic Era

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Editor’s Note: Dr. Eugenia Wang is a Distinguished Chair Professor in the Department of Biochemistry and Molecular Biology at the University of Louisville. She received the 2013 Alltech Medal of Excellence for her pioneering work in using high-throughput technologies to explore the molecular signatures of Alzheimer’s disease, other dementias and heart disease. This honor is awarded each year during Alltech’s International Symposium.

With the recent news headlines of Angelina Jolie’s pre-emptive double mastectomy and her inherited BRCA1 gene, people are becoming more curious about the role science plays in preventive healthcare and personalized medicine. While Ms. Jolie can afford the $4,000 genetic test and reconstructive surgery today, recent research suggests that the average Joe and Jane should have access to advanced, inexpensive healthcare diagnostics by 2020.

Human and animal science researchers are now exploring beyond the genes defined by our DNA and are increasing their focus on RNA, specifically the world of microRNAs. Regardless of our genetic makeup, these newly discovered, tiny pieces of RNA dictate how and when specific genes function throughout an animal’s or human’s lifespan. We now know there are at least 2,000 microRNAs, and that they can be influenced by environment and nutrition. For example, an individual’s battle with obesity is now estimated to be won or lost by the age of two, based on his or her environment and nutrition at the start of life. In response to stress, microRNAs direct specific cells to either survive or die, and specific genes to come into play.

For example, one monozygotic (identical) twin may develop diabetes, cancer or arthritis, while the genetically identical co-twin remains relatively healthy. Epigenetic tags are more prone to change over time than genetic DNA, so even though twins may start out with very similar epigenomes, they can diverge over time. 

Since the 1970s, the aging population of the United States (among other countries) has expanded remarkably. According to the U.S. Census Bureau, between 2010 and 2050, the United States is projected to experience rapid growth in its older population. In 2050, the number of Americans aged 65 and older is projected to be 88.5 million, more than double the same age group of 40.3 million in 2010.

This creates a predictable tsunami in elder care, both here and abroad. Through the globalization of environment and e-commerce, we will see a storm of increased health perils across all age groups, such as dementia, cancer, diabetes, hypertension, life stress and childhood obesity.

An increasing number of us will survive to old age; but what sort of health will we enjoy along the way? Various biological systems undergo degradation at different rates and ages, and a good deal of this aging process seems to be controlled not only directly by our genes, but also specifically by certain microRNAs. As a result of any combination of factors, these microRNAs may become dysfunctional years or decades before we manifest identifiable symptoms of a recognized disease.

By the time we reach mid- to late life, these precursors for disease may already be in place, so the sooner we can recognize them, the better the likelihood of being able to slow down or reduce the risks of the disease process. For example, the definitive diagnosis of Alzheimer’s disease is based upon finding characteristic late “tombstone” hallmarks, amyloid plaques and tangles, in the brain upon autopsy. At present there is no inexpensive, blood-based diagnostic to predict the development of the disease process that ultimately results in these pernicious brain structures before they show up. Nor are there any drugs to prevent the disease, which creates a costly healthcare problem. In 2013, Alzheimer’s is estimated to cost the U.S. healthcare system more than $200 billion to treat some five million victims.

But there is a light at the end of this tunnel, due to recent research into slowing down the lifetime accumulation of oxidative stress that can derail the delicate balance of molecular control by microRNAs, functioning as molecular ‘dimmer switches’ in aging and age-dependent diseases. We investigate the genetic and epigenetic mechanisms that may cause predisposition to an increasing number of diseases, using microarray technology, proteomic profiling and several other high-throughput enabling platforms, to study the factors controlling how people respond to environmental exposures and the molecular mechanisms of wound healing, including response to microgravity and radiation.

It’s not witchcraft. We are beginning to understand, for instance, the role a Mediterranean diet (French bread, dark chocolate, fish, nuts, low red meat, red wine and extra virgin olive oil) can play in modifying the rate of aging. Dietary polyphenols, DHA, Omega 3, etc. can help us regain healthy nutritional/epigenomic profiles; and plasma microRNA biomarkers can provide positive monitoring of the reduction of disease processes.

How can this technology help fight diseases of aging? Imagine diagnostic tests that enable family physicians to simply take a drop of blood from a finger prick and determine whether the patient is progressing towards (or is predisposed to) a potentially fatal disease. By 2020, we hope to have at our disposal: smart phone dial-ins to track nutritional biomarkers of disease risk reduction management; nutriceutical/small drug healthcare; and nutritional intervention of microRNA profiles to overcome genetic errors such as the BRCA mutation that predisposes Ms. Jolie to the risk of cancer.

In the healthcare business of 2020, I hope average Americans will have e-access to $2 nutritional genomic markers to reduce individuals’ risks of cancer, heart attacks and Alzheimer’s disease. In the meantime, we should take care of our health from the very beginning. After all, we are the keepers of our own preventive health care.


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