Journal
ATHEROSCLEROSIS
Volume 349, Issue -, Pages 53-62Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2022.04.006
Keywords
Lp(a) plasma level; Diet; Saturated fat; Physical activity; Hormones; Kidney disease; Liver disease
Funding
- National Heart, Lung, And Blood Institute of the National Institutes of Health [R01HL157535]
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An elevated level of lipoprotein(a) is a genetically regulated risk factor for cardiovascular disease, but non-genetic factors may also influence its levels. Diet, physical activity, hormones, and certain pathological conditions can all impact lipoprotein(a) levels.
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 nonalcoholic 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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