HDL cholesterol is known as the ‘good’ cholesterol. A study in the late 1970s/early 80s known as the Framingham Study determined that higher levels of HDL cholesterol were protective against heart disease. This is one of those studies foundational to many cardiovascular health prevention ideas still around today.[ref] The general consensus seemed to be that HDL levels above 60 mg/dl are ‘good’ and decrease the risk of cardiovascular disease.
What does HDL do?
HDL stands for high-density lipoprotein. It is a transport vessel for cholesterol, triglycerides, and phospholipids built around an APOA1 protein. It usually is responsible for moving cholesterol and fats out of the cells. HDL cholesterol, then, is the cholesterol in the HDL particles.[ref]
However, a few recent studies show that you can have too much of a good thing, and HDL levels over 116 mg/dL for men or 135 mg/dL for women cause an increase in the risk of heart disease.[ref]
HDL cholesterol also plays a role in the immune system, with higher levels of HDL associated with better outcomes from parasites and bacterial infections.[ref]
HDL cholesterol levels are considered to be about half due to genes (with the rest due to diet, infection, etc.).[ref][ref]
HDL Cholesterol Genotype Report
Not a member? Join here. Membership lets you see your data right in each article and also gives you access to the member’s only information in the Lifehacks sections.
CETP gene:
The CETP gene codes for the cholesteryl ester transfer protein, which moves triglycerides or cholesterol between VLDL or LDL and HDL particles. It usually swaps a cholesterol ester from the HDL to an LDL particle in exchange for a triglyceride. Trials of drugs that inhibit CETP show an increase in HDL and a decrease in LDL cholesterol — but mostly with no positive impact on mortality from heart disease.[ref]
Check your genetic data for rs1800777 (23andMe v4, v5; AncestryDNA):
- A/A: lower HDL[ref] increased sepsis risk[ref]
- A/G: lower HDL, increased sepsis risk
- G/G: typical HDL
Members: Your genotype for rs1800777 is —.
Check your genetic data for rs5882 (23andMe v4, v5; AncestryDNA):
Members: Your genotype for rs5882 is —.
Note that while the majority of studies seem to show that the G allele of rs5882 correlates with higher HDL, not all studies show this. There may be differences depending on ancestry and gender.
Check your genetic data for rs708272 Taq1B (23andMe v4, v5; AncestryDNA):
- A/A: higher HDL cholesterol levels, lower risk of heart attack[ref][ref]
- A/G: slightly higher HDL cholesterol levels and lower risk of heart attack
- G/G: typical
Members: Your genotype for rs708272 is —.
Check your genetic data for rs3764261 (23andMe v4, v5):
- A/A: increased HDL cholesterol levels[ref]
- A/C: increased HDL cholesterol levels
- C/C: typical
Members: Your genotype for rs3764261 is —.
LIPC gene:
The LIPC gene codes for the hepatic lipase enzyme. This enzyme helps regulate intermediate, low, and high-density lipoprotein levels.[ref]
Check your genetic data for rs4775065 (23andMe v4 only):
- A/A: lower HDL[ref]
- A/G: typical HDL
- G/G: normal HDL
Members: Your genotype for rs4775065 is —.
Lifehacks:
If you want to raise your HDL levels, there are several dietary interventions you could try.
The rest of this article is for Genetic Lifehacks members only. Consider joining today to see the rest of this article.
Member Content:
An active subscription is required to access this content.
Join Here for full access to this article, genotype reports, and much more!
Already a member? Log in below.
Related Articles and Topics:
LDL Cholesterol Genes
Heart disease is the leading cause of death in the US and around the world, and high LDL-cholesterol levels have been linked in many studies to increased heart disease. Standard medical advice on ideal cholesterol levels and cardiovascular disease are often confusing, ever-changing, and sometimes downright contradictory.
The Genetics of High Triglycerides
Triglycerides are the main type of fat in your blood. Triglyceride is a general term for a type of lipid-containing three fatty acids (tri) bound to a glycerol. Most importantly, triglycerides are used by the body as energy and are stored in adipocytes (fat cells that compose adipose tissue).
Lipoprotein a: How to check your genetic data
High Lp(a) levels are a big risk factor for sudden heart attacks. Your Lp(a) levels are mainly controlled by your genetic variants. Check to see if you carry genetic variants that increase or decrease Lp(a).
What is YOUR risk of heart disease?
Coronary artery disease (CAD) is heritable. Understanding your genes and a ‘heart-healthy’ lifestyle can prevent heart attacks and death.
References:
Bustami, Jasmin, et al. “Cholesteryl Ester Transfer Protein (CETP) I405V Polymorphism and Cardiovascular Disease in Eastern European Caucasians – a Cross-Sectional Study.” BMC Geriatrics, vol. 16, July 2016, p. 144. PubMed Central, https://doi.org/10.1186/s12877-016-0318-y.
Colombo, Caroline Macoris, et al. “Short-Term Effects of Moderate Intensity Physical Activity in Patients with Metabolic Syndrome.” Einstein (Sao Paulo, Brazil), vol. 11, no. 3, Sept. 2013, pp. 324–30. PubMed, https://doi.org/10.1590/s1679-45082013000300011.
Di Raimondo, D., et al. “Metabolic and Anti-Inflammatory Effects of a Home-Based Programme of Aerobic Physical Exercise.” International Journal of Clinical Practice, vol. 67, no. 12, Dec. 2013, pp. 1247–53. PubMed, https://doi.org/10.1111/ijcp.12269.
Genga, Kelly Roveran, et al. “CETP Genetic Variant Rs1800777 (Allele A) Is Associated with Abnormally Low HDL-C Levels and Increased Risk of AKI during Sepsis.” Scientific Reports, vol. 8, no. 1, Nov. 2018, p. 16764. www.nature.com, https://doi.org/10.1038/s41598-018-35261-2.
Gordon, T., et al. “High Density Lipoprotein as a Protective Factor against Coronary Heart Disease. The Framingham Study.” The American Journal of Medicine, vol. 62, no. 5, May 1977, pp. 707–14. PubMed, https://doi.org/10.1016/0002-9343(77)90874-9.
Guo, Shu-Xia, et al. “Associations of Cholesteryl Ester Transfer Protein TaqIB Polymorphism with the Composite Ischemic Cardiovascular Disease Risk and HDL-C Concentrations: A Meta-Analysis.” International Journal of Environmental Research and Public Health, vol. 13, no. 9, Sept. 2016, p. E882. PubMed, https://doi.org/10.3390/ijerph13090882.
Kajani, Sarina, et al. “Unravelling HDL—Looking beyond the Cholesterol Surface to the Quality Within.” International Journal of Molecular Sciences, vol. 19, no. 7, July 2018, p. 1971. PubMed Central, https://doi.org/10.3390/ijms19071971.
Mackay, Dylan S., et al. “Cholesterol Ester Transfer Protein Polymorphism Rs5882 Is Associated with Triglyceride-Lowering in Response to Plant Sterol Consumption.” Applied Physiology, Nutrition, and Metabolism = Physiologie Appliquee, Nutrition Et Metabolisme, vol. 40, no. 8, Aug. 2015, pp. 846–49. PubMed, https://doi.org/10.1139/apnm-2015-0039.
Madsen, Christian M., et al. “Extreme High High-Density Lipoprotein Cholesterol Is Paradoxically Associated with High Mortality in Men and Women: Two Prospective Cohort Studies.” European Heart Journal, vol. 38, no. 32, Aug. 2017, pp. 2478–86. PubMed, https://doi.org/10.1093/eurheartj/ehx163.
Marrugat, Jaume, et al. “Effects of Differing Phenolic Content in Dietary Olive Oils on Lipids and LDL Oxidation–a Randomized Controlled Trial.” European Journal of Nutrition, vol. 43, no. 3, June 2004, pp. 140–47. PubMed, https://doi.org/10.1007/s00394-004-0452-8.
Nyberg, Sofia, et al. “Effects of Exercise with or without Blueberries in the Diet on Cardio-Metabolic Risk Factors: An Exploratory Pilot Study in Healthy Subjects.” Upsala Journal of Medical Sciences, vol. 118, no. 4, Nov. 2013, pp. 247–55. PubMed Central, https://doi.org/10.3109/03009734.2013.825348.
Okumura, Kenji, et al. “Differential Effect of Two Common Polymorphisms in the Cholesteryl Ester Transfer Protein Gene on Low-Density Lipoprotein Particle Size.” Atherosclerosis, vol. 161, no. 2, Apr. 2002, pp. 425–31. PubMed, https://doi.org/10.1016/s0021-9150(01)00653-0.
Peloso, Gina M., et al. “Common Genetic Variation in Multiple Metabolic Pathways Influences Susceptibility to Low HDL-Cholesterol and Coronary Heart Disease.” Journal of Lipid Research, vol. 51, no. 12, Dec. 2010, pp. 3524–32. PubMed Central, https://doi.org/10.1194/jlr.P008268.
Pirillo, Angela, et al. “HDL in Infectious Diseases and Sepsis.” Handbook of Experimental Pharmacology, vol. 224, 2015, pp. 483–508. PubMed, https://doi.org/10.1007/978-3-319-09665-0_15.
Tay, Jeannie, et al. “Comparison of Low- and High-Carbohydrate Diets for Type 2 Diabetes Management: A Randomized Trial.” The American Journal of Clinical Nutrition, vol. 102, no. 4, Oct. 2015, pp. 780–90. PubMed, https://doi.org/10.3945/ajcn.115.112581.
Tsai, Michael Y., et al. “Cholesteryl Ester Transfer Protein Genetic Polymorphisms, HDL Cholesterol, and Subclinical Cardiovascular Disease in the Multi-Ethnic Study of Atherosclerosis.” Atherosclerosis, vol. 200, no. 2, Oct. 2008, pp. 359–67. PubMed, https://doi.org/10.1016/j.atherosclerosis.2007.12.038.
Weaver-Goss, Suzanne. “Olive Oil Health Benefits | Organic Olive Oil | Olive Oil Nutrition.” Gimme the Good Stuff, 23 Mar. 2018, https://gimmethegoodstuff.org/safe-product-guides/healthy-olive-oil-guide/.
Weissglas-Volkov, Daphna, and Päivi Pajukanta. “Genetic Causes of High and Low Serum HDL-Cholesterol.” Journal of Lipid Research, vol. 51, no. 8, Aug. 2010, pp. 2032–57. PubMed Central, https://doi.org/10.1194/jlr.R004739.
Willer, Cristen J., et al. “Newly Identified Loci That Influence Lipid Concentrations and Risk of Coronary Artery Disease.” Nature Genetics, vol. 40, no. 2, Feb. 2008, pp. 161–69. PubMed Central, https://doi.org/10.1038/ng.76.
Zhu, Yanna, et al. “Anthocyanin Supplementation Improves HDL-Associated Paraoxonase 1 Activity and Enhances Cholesterol Efflux Capacity in Subjects with Hypercholesterolemia.” The Journal of Clinical Endocrinology and Metabolism, vol. 99, no. 2, Feb. 2014, pp. 561–69. PubMed, https://doi.org/10.1210/jc.2013-2845.
..