少時不努力，老大徒傷悲，20歲就要開始注意飲食
3000多人，自18-20歲起，看20年
中間測lipid level
year 15及20時做CT 測calcium score
和LDL <70 的人相比
calcium score異常的機率
LDL 70-90 1.5 X
LDL 100-130 2.4X
LDL 160- 5.6X
幹，我的LDL......
今天早上的crestor忘了吃
但小時候吃statin，就可以降calcium score嗎????
等我吃20年再說吧
August 3, 2010 (San Francisco, California) — A new prospective cohort study suggests younger people will pay for high cholesterol in the present with coronary calcium in the future, according to results of a study published in the August 3, 2010 issue of the Annals of Internal Medicine [1].
In the latest study from the ongoing Coronary Artery Risk Development in Young Adults (CARDIA) trial, Dr Mark Pletcher (University of California, San Francisco) and colleagues measured LDL cholesterol, HDL cholesterol, triglycerides, and coronary calcium in 3258 subjects age 18 to 20 in 1985 and 1986. They estimated time-averaged cumulative exposures to lipids between age 20 and 35 with repeated serum lipid measurements over 20 years and then related these data to coronary calcium scores acquired with computed tomography at years 15 and 20.
Nonoptimal levels of LDL cholesterol (>100 mg/dL), HDL cholesterol (<60 mg/dL), or triglycerides >150 mg/dL were found in 87% of young adults in the study. Coronary calcium prevalence 20 years later was 8% in participants who maintained optimal LDL levels <70 mg/dL and 44% in participants with LDL-cholesterol levels of >160 mg/dL (p<0.001). The same association was found in all races and genders.
The odds of finding coronary calcium increased as LDL increased. For example, compared with people with LDL levels less than 70 mg/dL, the odds ratio for coronary calcium later in life for patients with 70 to 99 mg/dL in their early adulthood was 1.5. For people with LDL of 100 to 129 mg/dL, the odds ratio was 2.4, and for people with LDL of 160 mg/dL or greater, the odds ratio was 5.6.
The results show that nonoptimal LDL-cholesterol levels during young adulthood are linked to coronary calcification down the road and that accounting for later-life lipid exposure does not explain the association of young adult LDL-cholesterol levels with later calcification. After the authors adjusted their analysis for "the potentially obscuring influences" of subjects' medication and clinically abnormal levels of other lipids, they observed an inverse association with HDL-cholesterol levels but no association with triglyceride levels.
Pletcher et al acknowledge that coronary calcium is a "subclinical end point," because the cohort is still too young to have enough MIs or deaths to study the connection between early lipid levels and those clinical outcomes. However, they point out that coronary calcium has been shown to be a strong independent predictor of CHD events and that the absence of coronary calcium is a strongly protective factor.
The authors recall previous studies that have found associations between lipid levels and atherosclerosis in children and young adults, demonstrated by autopsy, carotid intima–media thickness, and coronary calcium. But this CARDIA analysis is the first with adequate sample size, repeated measurements of the three major lipids, and sufficient follow-up to isolate the link between lipid levels during young adulthood with atherosclerosis during middle age while controlling for confounders, they claim.
"Our results suggest that atherosclerotic changes begin during young adulthood as a result of commonly observed nonoptimal lipid levels, that these changes persist into middle age, and that maintaining optimal levels of lipids--particularly LDL cholesterol--throughout young adulthood could provide substantial benefits in terms of lifetime coronary heart disease prevention," Pletcher et al conclude. "These findings reinforce the importance of a heart-healthy diet, exercise, and maintenance of normal weight beginning in young adulthood."
"What we show here is that it matters what your cholesterol level is during young adulthood, and you should be thinking about it and trying to optimize it during young adulthood so that you have less built-up atherosclerosis later in life, and that will stand you in good stead for reducing your heart-attack risk later in life," Pletcher told heartwire. "We're not directly testing the hypothesis that modifying cholesterol with diet and exercise during young adulthood makes a difference later in life. But there's so much evidence that cholesterol really is a cause of heart disease that we think that it's reasonable that the same thing is going on here--that it's a treatable cause of disease that can be avoided."
He cautioned that the study does not address whether medication to lower cholesterol early in life will be beneficial, but Pletcher says these data support the AHA recommendation to begin cholesterol tests as early as 20. "I'm a general believer in the tenet that if you want to have an effect on some parameter, you have to measure it and watch it. It provides motivation."
https://docs.google.com/fileview?id=0B278nGJMQBk7YTJjZWQzNzktOGRhZC00M2QxLWFkNmUtM2RiN2M2ZDFiNjQ2&hl=zh_TW
中間測lipid level
year 15及20時做CT 測calcium score
和LDL <70 的人相比
calcium score異常的機率
LDL 70-90 1.5 X
LDL 100-130 2.4X
LDL 160- 5.6X
幹，我的LDL......
今天早上的crestor忘了吃
但小時候吃statin，就可以降calcium score嗎????
等我吃20年再說吧
August 3, 2010 (San Francisco, California) — A new prospective cohort study suggests younger people will pay for high cholesterol in the present with coronary calcium in the future, according to results of a study published in the August 3, 2010 issue of the Annals of Internal Medicine [1].
In the latest study from the ongoing Coronary Artery Risk Development in Young Adults (CARDIA) trial, Dr Mark Pletcher (University of California, San Francisco) and colleagues measured LDL cholesterol, HDL cholesterol, triglycerides, and coronary calcium in 3258 subjects age 18 to 20 in 1985 and 1986. They estimated time-averaged cumulative exposures to lipids between age 20 and 35 with repeated serum lipid measurements over 20 years and then related these data to coronary calcium scores acquired with computed tomography at years 15 and 20.
Nonoptimal levels of LDL cholesterol (>100 mg/dL), HDL cholesterol (<60 mg/dL), or triglycerides >150 mg/dL were found in 87% of young adults in the study. Coronary calcium prevalence 20 years later was 8% in participants who maintained optimal LDL levels <70 mg/dL and 44% in participants with LDL-cholesterol levels of >160 mg/dL (p<0.001). The same association was found in all races and genders.
The odds of finding coronary calcium increased as LDL increased. For example, compared with people with LDL levels less than 70 mg/dL, the odds ratio for coronary calcium later in life for patients with 70 to 99 mg/dL in their early adulthood was 1.5. For people with LDL of 100 to 129 mg/dL, the odds ratio was 2.4, and for people with LDL of 160 mg/dL or greater, the odds ratio was 5.6.
The results show that nonoptimal LDL-cholesterol levels during young adulthood are linked to coronary calcification down the road and that accounting for later-life lipid exposure does not explain the association of young adult LDL-cholesterol levels with later calcification. After the authors adjusted their analysis for "the potentially obscuring influences" of subjects' medication and clinically abnormal levels of other lipids, they observed an inverse association with HDL-cholesterol levels but no association with triglyceride levels.
Pletcher et al acknowledge that coronary calcium is a "subclinical end point," because the cohort is still too young to have enough MIs or deaths to study the connection between early lipid levels and those clinical outcomes. However, they point out that coronary calcium has been shown to be a strong independent predictor of CHD events and that the absence of coronary calcium is a strongly protective factor.
The authors recall previous studies that have found associations between lipid levels and atherosclerosis in children and young adults, demonstrated by autopsy, carotid intima–media thickness, and coronary calcium. But this CARDIA analysis is the first with adequate sample size, repeated measurements of the three major lipids, and sufficient follow-up to isolate the link between lipid levels during young adulthood with atherosclerosis during middle age while controlling for confounders, they claim.
"Our results suggest that atherosclerotic changes begin during young adulthood as a result of commonly observed nonoptimal lipid levels, that these changes persist into middle age, and that maintaining optimal levels of lipids--particularly LDL cholesterol--throughout young adulthood could provide substantial benefits in terms of lifetime coronary heart disease prevention," Pletcher et al conclude. "These findings reinforce the importance of a heart-healthy diet, exercise, and maintenance of normal weight beginning in young adulthood."
"What we show here is that it matters what your cholesterol level is during young adulthood, and you should be thinking about it and trying to optimize it during young adulthood so that you have less built-up atherosclerosis later in life, and that will stand you in good stead for reducing your heart-attack risk later in life," Pletcher told heartwire. "We're not directly testing the hypothesis that modifying cholesterol with diet and exercise during young adulthood makes a difference later in life. But there's so much evidence that cholesterol really is a cause of heart disease that we think that it's reasonable that the same thing is going on here--that it's a treatable cause of disease that can be avoided."
He cautioned that the study does not address whether medication to lower cholesterol early in life will be beneficial, but Pletcher says these data support the AHA recommendation to begin cholesterol tests as early as 20. "I'm a general believer in the tenet that if you want to have an effect on some parameter, you have to measure it and watch it. It provides motivation."
https://docs.google.com/fileview?id=0B278nGJMQBk7YTJjZWQzNzktOGRhZC00M2QxLWFkNmUtM2RiN2M2ZDFiNjQ2&hl=zh_TW
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