48-Year-Old, Life-long Athlete Suffers Near Fatal Heart Attack
With Normal Cholesterol Profile
June 2009
Arnold Johnson of Mead, Washington, a 48-year-old, health-conscious athlete, was given a clean bill of health by his doctors after standard cholesterol testing showed a completely normal profile and no heart disease risk. Two months later, despite this news and his lifelong pattern of physical activity and diet restriction, he suffered a near fatal heart attack.
Following his fortunate resuscitation and recovery, Arnold was diagnosed with coronary artery blockages and recommended for bypass surgery. Understandably angry and confused about this turn of events, he traveled to the Mayo Clinic for some answers.
Testing by the Mayo Clinic again revealed a normal cholesterol profile (LDL, HDL, triglycerides) except for one particular cholesterol reading on a test that is not routinely performed by mainstream medical practitioners when screening for heart disease risk factors -- his Lipoprotein(a) score was over 350 (normal range should be 0-20).
Arnold's Lp(a) score is significant because of studies suggesting a clear association between Lp(a) and an increased risk of heart disease. In the year 2000, study findings published in Circulation, the Journal of the American Heart Association, showed that elevated levels of the little-known cholesterol lipoprotein (a) (Lp(a)) increase heart attack risk by 70%, though the announcement seemed to have little impact on the public and mainstream medicine. See LIPOPROTEIN UPS HEART ATTACK RISK.
The Mayo Clinic told Arnold that there was nothing they could do to lower his Lp(a) except to try a cholesterol-lowering statin drug, even though statins had never been shown to lower Lp(a) cholesterol, and Arnold agreed to take the drug.
Lipoprotein (a) (Lp(a)) is an LDL cholesterol particle that is attached to a special protein called apo(a). In large part, a person's level of Lp(a) in the blood is genetically inherited. Elevated levels of Lp(a) (higher than 20 mg/dl to 30 mg/dl) in the blood are linked to a greater likelihood of atherosclerosis and heart attacks in both men and women. The risk is even more significant if the Lp(a) cholesterol elevation is accompanied by high LDL/HDL ratios. Unfortunately, there is no international standard for determining Lp(a) cholesterol levels and specifically measuring and treating elevated Lp(a) cholesterol levels are not widely performed in this country.
Interestingly, athletes tend to have higher levels of Lipoprotein(a), as borne out in Arnold's case.
"Previous studies have reported that exercise tends to lower LDL-C. Because of the structural homology between Lp(a) and LDL particles, one might therefore expect that the atherogenic Lp(a) particle would be influenced by physical activity in a similar way. However, published results are inconsistent. Hellsten et al. [11] found that Lp(a) may significantly decrease in well trained individuals, where, a study investigating a long term effect of exercise in sedentary individuals demonstrated that Lp(a) levels rose almost twofold over a period of 9 months [12]. Hubinger reported higher Lp(a) serum concentration in adult long distance runners compared to non-athletic controls. [13]. A similar trend was observed in our study. Athletes presented with significantly higher Lp(a) levels compared with controls. Moreover, median Lp(a) concentration of Lp(a) in endurance athletes could be due to greater physical demands which cause muscular or systemic stress reaction. This condition may be associated with raised Lp(a) values, as Lp(a) has been shown to share characteristics of inflammatory parameters. . . . Possible Lp(a) concentration variations observed during years of physical activity could be attributed to the direct effect of exercise." Children and Exercise XIX: promoting health and wellbeing, Chapter Lipids and lipoprotein(a) as atherosclerosis factors in young athletes."
Athletes also suffer from lysine deficiency because of their frequent, rigorous exercise. Together with vitamin C and another amino acid proline, the amino acid lysine contributes to the stimulation of new collagen production, but without it, collagen synthesis is reduced. Collagen is essential to the maintenance of the structure of all cells in the body, including in the blood vessels and arteries.
Therefore, lysine depletion in athletes, lifelong vitamin C deficiency at the levels Pauling recommended for optimal collagen production (3,000 mg or greater per day), and the higher levels of Lp(a) cholesterol typically seen in athletes would all work toward the onset of early cardiovascular disease and the rapid accumulation of plaques in athletes who would otherwise think themselves healthy and free of disease.
Because we at Tower had never seen a documented case like this and because Arnold's story could help to save the lives of many athletes like him, we now include his testimonial.
