"Alcohol consumption during pregnancy is a significant public health problem and may result in a wide range of adverse outcomes for the child," said Dr Dipak Sarkar, who recently received a USD 3.5 million (Rs 164 million) MERIT (Method to Extend Research in Time) award from the National Institutes of Health to continue research on the damaging effects of alcohol on the nervous systems of the unborn.
The NIH recognises researchers who have demonstrated superior competence and outstanding productivity with the highly selective award, which provides long-term support in research area of special importance or promise.
"Many Fetal Alcohol Syndrome patients have problems coping with stress; they have learning disabilities, infections, and increased susceptibility to diseases," Sarkar said.
The research focuses on the alcohol abuse of the mother only, which affects the child even in the womb, he added.
Sarkar, an alumnus of Calcutta, Oxford, Yale and Michigan State universities, is a professor in the Department of Animal Science at the School of Environmental and Biological Sciences, director of the Endocrine Research Program, and a faculty member of the Center for Alcohol Studies at Rutgers University in New Jersey.
He has five grants that support the work of 16 research assistants, including post-doctoral students, graduate students, undergraduates, and a senior scientist, who collaborate on his research projects. The MERIT award will extend NIH support for another 10 years for one of Sarkar's research grants, now in its 13th year.
His interest in alcohol research began in 1990 when he observed the neuron-killing effect of a small dose of alcohol while working on neuronal development.
The problem in the child arises, he explained, due to the alcohol-induced destruction of neurons in the part of the brain known as the hypothalamus. These beta-endorphin neurons produce the endorphin hormone and are particularly vulnerable during the early development of the fetus. His research has shown that a seemingly irreversible reduction in the number and function of beta-endorphin neurons results in a permanent impairment of stress and immune system functions throughout life. While the body often displays the ability to recover from damage or disease, this does not seem to come into play with the loss of beta-endorphin neurons.
He noted that preliminary data on the reduced function of beta-endorphin neurons points toward epigenetic changes -- changes in the biochemistry that inhibit the genes responsible for these particular neurons -- as a causal factor. The genes themselves become abnormal and, while they may be producing some cells, the cells do not produce endorphin.
"One thing we cannot reverse is the death of these cells, but maybe we can reverse those epigenetic alterations that are ultimately responsible for their demise," Sarkar said.
His current research is aimed at discovering the molecular mechanism involved in alcohol's toxic action on beta-endorphin neurons. A clear understanding of the underlying mechanism could offer a starting point from which to develop medicines for fetal alcohol patients in the future. Currently none is available.
Beta-endorphin neurons are also known as opioids because, like opium-based narcotics, their hormone products have the ability to reduce pain and increase a sense of wellbeing. Their loss would have an opposite effect, reducing the ability to manage stress. A reduction in the number of these neurons can lessen the immune response and decrease the body's ability to fight infection and disease. The opioid system is also involved in metabolism. Sarkar noted that researchers are finding substantial evidence that an altered opioid system is involved in the metabolic changes leading to diabetes as well as obesity.
Image: Dr Dipak Sarkar
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