Article ; Online: Non-genetic influences on lipoprotein(a) concentrations.
2022 Volume 349, Page(s) 53–62
Abstract: An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by ... ...
Abstract | An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by genetic factors, emphasizing a potential role for non-genetic factors. In this review, we provide an overview of current evidence on non-genetic factors influencing Lp(a) levels with a particular focus on diet, physical activity, hormones and certain pathological conditions. Findings from randomized controlled clinical trials show that diets lower in saturated fats modestly influence Lp(a) levels and often in the opposing direction to LDL cholesterol. Results from studies on physical activity/exercise have been inconsistent, ranging from no to minimal or moderate change in Lp(a) levels, potentially modulated by age and the type, intensity, and duration of exercise modality. Hormone replacement therapy (HRT) in postmenopausal women lowers Lp(a) levels with oral being more effective than transdermal estradiol; the type of HRT, dose of estrogen and addition of progestogen do not modify the Lp(a)-lowering effect of HRT. Kidney diseases result in marked elevations in Lp(a) levels, albeit dependent on disease stages, dialysis modalities and apolipoprotein(a) phenotypes. In contrast, Lp(a) levels are reduced in liver diseases in parallel with the disease progression, although population studies have yielded conflicting results on the associations between Lp(a) levels and non-alcoholic fatty liver disease. Overall, current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels. |
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MeSH term(s) | Cardiovascular Diseases/blood ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/therapy ; Cholesterol, LDL ; Estradiol ; Estrogen Replacement Therapy ; Estrogens ; Exercise ; Female ; Humans ; Lipoprotein(a)/adverse effects ; Lipoprotein(a)/blood ; Lipoprotein(a)/genetics ; Risk Factors |
Chemical Substances | Cholesterol, LDL ; Estrogens ; Lipoprotein(a) ; Estradiol (4TI98Z838E) |
Language | English |
Publishing date | 2022-05-21 |
Publishing country | Ireland |
Document type | Journal Article ; Review |
ZDB-ID | 80061-2 |
ISSN | 1879-1484 ; 0021-9150 |
ISSN (online) | 1879-1484 |
ISSN | 0021-9150 |
DOI | 10.1016/j.atherosclerosis.2022.04.006 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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