Deciphering Your Genetic Destiny
Perhaps you saw the news articles in early September about how famed geneticist J. Craig Venter had deciphered and published his personal genetic code — in the process, as one writer noted, gaining "a new understanding of his genetic destiny."
I'm not sure that I want to know too much about what my genes might have in store for me (I'd rather not have a sneak preview, for example, of Alzheimer's disease). But here's one genetic component that I'd be interested in knowing about, and perhaps you would, too: APOA5.
If you have a particular variation of that gene, it could be much more important for you to watch your diet and lead a healthy lifestyle, compared with folks who don't have that gene variant. Researchers have found that people who have that particular gene variant tend to have higher levels of arterial plaque, which could be linked to greater risk of heart disease.
Here's the background: Scientists funded by the Agricultural Research Service (ARS) in Boston, Mass., set out to study the possibility of a link between that APOA5 variant and atherosclerosis, which is the 25-cent word for "hardening of the arteries."
The scientists took a closer look at results from an enormous human health study called the Framingham Offspring Study (FOS), begun in 1971 by the National Heart, Blood and Lung Institute, part of the National Institutes of Health.
The ARS-funded scientists found that among 2,273 participants of that study, those who had this particular variation of APOA5 had higher levels of arterial plaque, as measured by the thickness of the lining of their carotid arteries.
Now we've all heard that obesity boosts your risk of heart disease. But the bad news from the ARS-funded evaluation is that the detrimental impact of obesity was even greater among the 13 percent of FOS participants who had that particular variant of APOA5.
Among all the study participants who were obese, those with the gene variant had significantly more arterial plaque buildup than folks who didn't have that variant. And among all the APOA5 gene variant carriers in the study, those who were obese had significantly greater plaque buildup than those who weren't obese.
Even if the obese carriers of the APOA5 gene variant didn't smoke or have high fat and cholesterol, blood sugar or blood pressure levels — and even if they were younger than the non-obese carriers of that gene variant — they still had higher levels of arterial plaque!
There are a number of genetically controlled contributors to coronary artery disease risk, such as high levels of lipids (fats) in the blood — total cholesterol, "bad" cholesterol known as LDL, and triglycerides. But there are other risk factors, too: impaired glucose tolerance, diabetes, high blood pressure and abdominal obesity.
No one's ready to claim there's a definite link between having this particular gene variant and winding up with hardening of the arteries; the scientists say more studies are needed before we can make that type of connection. Still, the comparatively high levels of arterial plaque among the carriers of the APOA5 gene variant are consistent with the levels of plaque associated with symptoms of heart disease.
Your genetic makeup is a "gift" that you get from your mother and father. In my case, I'm equipped with the genes to crank out cholesterol like there was going to be a future shortage of it. And different genes or gene combinations respond differently to changes in diet, exercise and medication — as I learned, to my disappointment, when I started taking medication to control my cholesterol. My friends on the same medication saw an 80-point drop in their LDL "bad" cholesterol after four months, whereas my "bad" number went down a mere 8 points! (Thankfully, I did get a bigger improvement after taking the medicine for another four months.)
Still, as researchers learn more about important genetic clues such as that variation of the APOA5 gene, our doctors' recommendations for lifestyle and diet changes may become more customized than ever before — and more understandable, once we can see the interaction between our genes and the impact of our day-to-day choices.
"Everybody's
Science" is written by Sandy Miller Hays, Director of Information for
the Agricultural Research Service, the chief scientific research agency
of the U.S. Department of Agriculture. Hays is a native of Fort Smith,
Ark. From the late 1970s until early 1988, Hays was a reporter, editor
and columnist at the Arkansas Democrat (now the Arkansas Democrat-Gazette),
a Little Rock-based daily newspaper. She joined the ARS Information
Staff in 1988, and became Director of Information in April 1998.
Perhaps you saw the news articles in early September about how famed geneticist J. Craig Venter had deciphered and published his personal genetic code — in the process, as one writer noted, gaining "a new understanding of his genetic destiny."
I'm not sure that I want to know too much about what my genes might have in store for me (I'd rather not have a sneak preview, for example, of Alzheimer's disease). But here's one genetic component that I'd be interested in knowing about, and perhaps you would, too: APOA5.
If you have a particular variation of that gene, it could be much more important for you to watch your diet and lead a healthy lifestyle, compared with folks who don't have that gene variant. Researchers have found that people who have that particular gene variant tend to have higher levels of arterial plaque, which could be linked to greater risk of heart disease.
Molecular biologist Chao Qiang Lai (left) and geneticist Jose Ordovas use a DNA sequence system to identify which individuals carry a specific mutation associated with high triglycerides or obesity. (Photo by Stephen Ausmus)
The scientists took a closer look at results from an enormous human health study called the Framingham Offspring Study (FOS), begun in 1971 by the National Heart, Blood and Lung Institute, part of the National Institutes of Health.
The ARS-funded scientists found that among 2,273 participants of that study, those who had this particular variation of APOA5 had higher levels of arterial plaque, as measured by the thickness of the lining of their carotid arteries.
Now we've all heard that obesity boosts your risk of heart disease. But the bad news from the ARS-funded evaluation is that the detrimental impact of obesity was even greater among the 13 percent of FOS participants who had that particular variant of APOA5.
Among all the study participants who were obese, those with the gene variant had significantly more arterial plaque buildup than folks who didn't have that variant. And among all the APOA5 gene variant carriers in the study, those who were obese had significantly greater plaque buildup than those who weren't obese.
Even if the obese carriers of the APOA5 gene variant didn't smoke or have high fat and cholesterol, blood sugar or blood pressure levels — and even if they were younger than the non-obese carriers of that gene variant — they still had higher levels of arterial plaque!
There are a number of genetically controlled contributors to coronary artery disease risk, such as high levels of lipids (fats) in the blood — total cholesterol, "bad" cholesterol known as LDL, and triglycerides. But there are other risk factors, too: impaired glucose tolerance, diabetes, high blood pressure and abdominal obesity.
No one's ready to claim there's a definite link between having this particular gene variant and winding up with hardening of the arteries; the scientists say more studies are needed before we can make that type of connection. Still, the comparatively high levels of arterial plaque among the carriers of the APOA5 gene variant are consistent with the levels of plaque associated with symptoms of heart disease.
Your genetic makeup is a "gift" that you get from your mother and father. In my case, I'm equipped with the genes to crank out cholesterol like there was going to be a future shortage of it. And different genes or gene combinations respond differently to changes in diet, exercise and medication — as I learned, to my disappointment, when I started taking medication to control my cholesterol. My friends on the same medication saw an 80-point drop in their LDL "bad" cholesterol after four months, whereas my "bad" number went down a mere 8 points! (Thankfully, I did get a bigger improvement after taking the medicine for another four months.)
Still, as researchers learn more about important genetic clues such as that variation of the APOA5 gene, our doctors' recommendations for lifestyle and diet changes may become more customized than ever before — and more understandable, once we can see the interaction between our genes and the impact of our day-to-day choices.
The Agricultural Research Service is the chief in-house scientific
research agency of the U.S. Department of Agriculture. You can read
more about ARS discoveries at http://www.ars.usda.gov/news/.
About the author
"Everybody's
Science" is written by Sandy Miller Hays, Director of Information for
the Agricultural Research Service, the chief scientific research agency
of the U.S. Department of Agriculture. Hays is a native of Fort Smith,
Ark. From the late 1970s until early 1988, Hays was a reporter, editor
and columnist at the Arkansas Democrat (now the Arkansas Democrat-Gazette),
a Little Rock-based daily newspaper. She joined the ARS Information
Staff in 1988, and became Director of Information in April 1998.