Abstract
Changes occur in lipid and lipoprotein concentrations with age that increase the risk of developing atherosclerotic disease. In children and young adults (less than 20 years of age), the plasma total cholesterol concentration decreases between the ages of 10 and 20 years. After age 20, the plasma total cholesterol concentration increases progressively, and in men reaches a plateau between the ages of 50 and 60 years, whereas in women, it reaches a peak between 60 and 70 years of age. The low-density lipoprotein cholesterol concentration increases progressively in men and women after age 20, but more rapidly in men, accounting for most of the overall gender difference in total cholesterol. The rate at which the low-density lipoprotein cholesterol concentration increases in women begins to accelerate between 40 and 50 years of age, and the concentration exceeds that in men by 55 to 60 years. High-density lipoprotein cholesterol concentrations decrease in males during puberty and early adulthood, and thereafter remain lower than those in women at all comparable ages. The high-density lipoprotein cholesterol concentrations remain constant in women throughout their lifetime. Beyond 30 years of age, women taking estrogen preparations have higher high-density lipoprotein cholesterol concentrations than women who are not taking estrogens. The triglyceride concentration increases progressively in men, reaching peak values between 40 and 50 years of age, and then declining slightly thereafter. In women, the triglyceride concentration increases throughout their lifetime, but is always higher in those using estrogens. Whether these changes in lipoprotein concentrations merely accompany the increasing prevalence of atherosclerotic vascular disease that occurs with age, or contribute to it, is unknown at this time.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 54-60 |
| Number of pages | 7 |
| Journal | The American journal of medicine |
| Volume | 82 |
| Issue number | 1 SUPPL. 2 |
| DOIs | |
| State | Published - Jan 26 1987 |
| Externally published | Yes |
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Cite this
Cholesterol metabolism and aging. / Kreisberg, Robert A.; Karakas, Siddika E.
In: The American journal of medicine, Vol. 82, No. 1 SUPPL. 2, 26.01.1987, p. 54-60.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cholesterol metabolism and aging
AU - Kreisberg, Robert A.
AU - Karakas, Siddika E
PY - 1987/1/26
Y1 - 1987/1/26
N2 - Changes occur in lipid and lipoprotein concentrations with age that increase the risk of developing atherosclerotic disease. In children and young adults (less than 20 years of age), the plasma total cholesterol concentration decreases between the ages of 10 and 20 years. After age 20, the plasma total cholesterol concentration increases progressively, and in men reaches a plateau between the ages of 50 and 60 years, whereas in women, it reaches a peak between 60 and 70 years of age. The low-density lipoprotein cholesterol concentration increases progressively in men and women after age 20, but more rapidly in men, accounting for most of the overall gender difference in total cholesterol. The rate at which the low-density lipoprotein cholesterol concentration increases in women begins to accelerate between 40 and 50 years of age, and the concentration exceeds that in men by 55 to 60 years. High-density lipoprotein cholesterol concentrations decrease in males during puberty and early adulthood, and thereafter remain lower than those in women at all comparable ages. The high-density lipoprotein cholesterol concentrations remain constant in women throughout their lifetime. Beyond 30 years of age, women taking estrogen preparations have higher high-density lipoprotein cholesterol concentrations than women who are not taking estrogens. The triglyceride concentration increases progressively in men, reaching peak values between 40 and 50 years of age, and then declining slightly thereafter. In women, the triglyceride concentration increases throughout their lifetime, but is always higher in those using estrogens. Whether these changes in lipoprotein concentrations merely accompany the increasing prevalence of atherosclerotic vascular disease that occurs with age, or contribute to it, is unknown at this time.
AB - Changes occur in lipid and lipoprotein concentrations with age that increase the risk of developing atherosclerotic disease. In children and young adults (less than 20 years of age), the plasma total cholesterol concentration decreases between the ages of 10 and 20 years. After age 20, the plasma total cholesterol concentration increases progressively, and in men reaches a plateau between the ages of 50 and 60 years, whereas in women, it reaches a peak between 60 and 70 years of age. The low-density lipoprotein cholesterol concentration increases progressively in men and women after age 20, but more rapidly in men, accounting for most of the overall gender difference in total cholesterol. The rate at which the low-density lipoprotein cholesterol concentration increases in women begins to accelerate between 40 and 50 years of age, and the concentration exceeds that in men by 55 to 60 years. High-density lipoprotein cholesterol concentrations decrease in males during puberty and early adulthood, and thereafter remain lower than those in women at all comparable ages. The high-density lipoprotein cholesterol concentrations remain constant in women throughout their lifetime. Beyond 30 years of age, women taking estrogen preparations have higher high-density lipoprotein cholesterol concentrations than women who are not taking estrogens. The triglyceride concentration increases progressively in men, reaching peak values between 40 and 50 years of age, and then declining slightly thereafter. In women, the triglyceride concentration increases throughout their lifetime, but is always higher in those using estrogens. Whether these changes in lipoprotein concentrations merely accompany the increasing prevalence of atherosclerotic vascular disease that occurs with age, or contribute to it, is unknown at this time.
UR - http://www.scopus.com/inward/record.url?scp=0023665488&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023665488&partnerID=8YFLogxK
U2 - 10.1016/0002-9343(87)90272-5
DO - 10.1016/0002-9343(87)90272-5
M3 - Article
C2 - 3544833
AN - SCOPUS:0023665488
VL - 82
SP - 54
EP - 60
JO - American Journal of Medicine
JF - American Journal of Medicine
SN - 0002-9343
IS - 1 SUPPL. 2
ER -