Like many other researchers in his field, biochemist Carl Breckenridge says that Canadians have mostly themselves to blame for their relatively high rates of heart disease. Breckenridge, 50, who is head of the department of biochemistry at Dalhousie University in Halifax, says that most people can reduce the risk of heart attack or stroke by quitting smoking, eating fewer fatty substances and exercising regularly. But unlike many of his colleagues, Breckenridge also says that governments with limited budgets should target prevention campaigns at individuals who have inherited characteristics that put them at a high risk of developing heart problems, rather than the population as a whole. Breckenridge reached that conclusion after 20 years of research, during which he has zeroed in on what he and many other scientists suspect is one of the main genetically inherited causes of heart disease: a tiny particle that is present in high concentrations in the blood of one in five Canadians.
The substance is known as lipoprotein (a)—Lp(a) for short. Declared Breckenridge: “The issue is the interaction of genetics and lifestyle.”
In focusing on the characteristics that people inherit from their parents, Breckenridge and a small but growing number of Canadian scientists and doctors are on the leading edge of one of the dominant trends in heart research in North America and Europe.
By the early 1970s, most researchers agreed that high levels of cholesterol in the blood dramatically increase the risk of suffering a heart attack or a stroke. Cholesterol is a waxy, oily substance that the body manufactures itself, but which is also absorbed from food, particularly eggs and meat. The body needs cholesterol to manufacture hormones and construct new cells. But when cholesterol deposits accumulate along the walls of arteries, they can restrict the flow of blood to the heart, increasing the risk of a heart attack.
Dangerous: Breckenridge and other scientists contend that Lp(a), which was first identified by a Swedish physician in 1963, is an efficient, and poten-
Experts say that research into Lp(a) may eventually help to explain why some people who have low levels of cholesterol in their blood suffer heart attacks or strokes, while others who have high levels of cholesterol do
tially deadly, transporter of cholesterol in the blood. Normal amounts of Lp(a) cause relatively harmless buildups of cholesterol in the arteries. But in people who have excessive amounts, Lp(a) can result in dangerous cholesterol concentrations. not. Said Dr. Robert Hegele, 35, a staff physician at St. Michael’s Hospital in Toronto: “In many ways we are trying to answer the old question of why Winston Churchill could eat, drink and smoke until he was 90 while Arthur Ashe, the tennis player, had a heart attack when he was 36.”
Breckenridge, who was bom in Peterborough, Ont., and earned a PhD in biochemistry at the University of Toronto, first became interested in Lp(a) during the early 1970s as an assistant professor of biochemistry at U of T. At the time, Breckenridge was studying the way in which fats travel through the human bloodstream. While examining blood samples taken from patients identified by their doctors as prime candidates for heart disease, he noticed that many of them contained high concentrations of Lp(a). By comparing measurements of Lp(a) concentrations from the blood of more than 50 sets of identical twins and finding that they were the same in all cases, Breckenridge confirmed that elevated levels of Lp(a) could be inherited, and not just the product of individual lifestyles.
Although he knew that high levels of Lp(a) are an inherited trait, genetic science at the time was not as advanced as it is today, and Breckenridge did not try to identify the gene responsible for producing Lp(a). But in 1987, a team of scientists working for the giant San Francisco-based biomedical company Genentech Inc. identified the gene responsible for the production and levels of concentration of Lp(a) in the body. Hegele, who was studying at the University of Utah at Salt Lake City at the time, collaborated with the Genentech team that found the gene. Hegele said that Genentech scientists were interested in Lp(a) because they were trying to develop new drugs to thin human blood and break down blood clots.
Risk: Breckenridge, who currently is studying Lp(a) levels in patients who have normal cholesterol levels but suffered heart attacks at a relatively young age, says that it should be possible eventually to screen young adults to determine what level of Lp(a) concentrations they have. Once identified, high-risk patients could be counselled on how to minimize dangerous buildups of cholesterol.
Still, other experts say that such a narrowly focused strategy might send the wrong signals and result in more heart attacks among lower-risk segments of the population. Dr. John Hoey, a professor of epidemiology at McGill University in Montreal, for one, contends that governments should encourage all Canadians to lower their cholesterol levels and lead healthier
lives. Said Hoey: “You really are better to target the large group in the middle, rather than just the small number of people at the extreme.” But for the moment, at least, the debate is a purely theoretical one. At present, few health-care professionals are equipped to carry out the complicated Lp(a) screening procedures which, at some future time, could turn into a valuable weapon in the war against heart disease.
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