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Habitual coffee intake and plasma lipid profile: Evidence from UK Biobank
1Australian Centre for Precision Health, Unit of Clinical and Health Sciences, University of South Australia, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia.
Insights
Heavy coffee consumption is linked to higher levels of LDL cholesterol, ApoB, and total cholesterol. This may increase cardiovascular disease risk, especially for individuals with existing high LDL cholesterol.
Area of Science:
- Cardiovascular Science
- Nutritional Epidemiology
- Genetics
Background:
- Long-term heavy coffee consumption may negatively impact cardiovascular disease (CVD) risk.
- Hyperlipidemia is a known contributor to CVD risk.
Purpose of the Study:
- Investigate the association between habitual coffee intake and plasma lipid profiles.
- Examine the causal relationship between coffee consumption and lipid levels using Mendelian randomization.
Main Methods:
- Utilized data from 362,571 UK Biobank participants.
- Analyzed self-reported coffee intake and plasma lipid profiles (LDL-C, HDL-C, total-C, triglycerides, ApoA1, ApoB).
- Employed Mendelian randomization (MR) analysis with genetically instrumented coffee intake.
Main Results:
- Observed a dose-dependent positive association between coffee intake and plasma LDL-C, ApoB, and total-C.
- Individuals drinking >6 cups/day showed the highest lipid levels.
- MR analysis indicated higher coffee intake causally linked to increased LDL-C, ApoB, and total-C concentrations.
Conclusions:
- Long-term heavy coffee consumption is associated with an unfavorable lipid profile.
- This may elevate CVD risk, particularly in individuals with elevated LDL cholesterol.
- Findings hold potential clinical relevance for managing hyperlipidemia.
Background & Aims:
There is evidence that long-term heavy coffee consumption may adversely affect individuals' cardiovascular disease (CVD) risk. As hyperlipidemia is a well-established contributor to CVD risk, we investigated the association between habitual coffee intake and plasma lipid profile.
Methods:
We used data from up to 362,571 UK Biobank participants to examine phenotypic associations between self-reported coffee intake and plasma lipid profiles, including low-density-lipoproteins cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (total-C), triglycerides, and apolipoproteins A1 and B (ApoA1 and ApoB). Mendelian randomization (MR) analysis using genetically instrumented coffee intake was used to interrogate the causal nature of coffee-lipid associations.
Results:
We observed a positive dose-dependent association between self-reported coffee intake and plasma concentration of LDL-C, ApoB and total-C, with the highest lipid levels seen among participants reported drinking >6 cups/day (Plinear trend≤ 3.24E-55 for all). Consistently, in MR analyses using genetically instrumented coffee intake one cup higher coffee intake was associated with a 0.07 mmol/L (95% CI 0.03 to 0.12), 0.02 g/L (95% CI 0.01 to 0.03), and 0.09 mmol/L (95% CI 0.04 to 0.14) increase in plasma concentration of LDL-C, ApoB, and total-C, respectively.
Conclusions:
Our phenotypic and genetic analyses suggest that long-term heavy coffee consumption may lead to unfavourable lipid profile, which could potentially increase individuals' risk for CVD. These findings may have clinical relevance for people with elevated LDL cholesterol.
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