Key takeaways:
~ 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.
~ Cholesterol is essential and needed in your cells, in the right amounts.
~ Genetic variants can cause high cholesterol, and specific natural supplements or diet changes may work well, depending on your genes.
Members will see their genotype report below, plus additional solutions in the Lifehacks section. Join today.
Table of Contents
Cholesterol: Necessary in the right amounts
When you read about cholesterol and heart disease, it is easy to believe that cholesterol is something terrible that you don’t want in your body. But that is far from the whole picture! Cholesterol is essential for your health and well-being.
Cholesterol is a type of lipid (fat) created only by animals. It is an essential part of every cell and important for digesting foods and creating hormones.
A membrane composed mainly of phospholipids surrounds every cell in your body. Cholesterol molecules make up part of that cell membrane, stabilizing the membrane to help maintain its integrity. Cholesterol keeps the membrane firm enough to keep some very small water-soluble molecules out, yet not too rigid.
Cell membrane showing cholesterol molecules within the phospholipid bilayer. Wikimedia Commons.
In addition to being part of the structure of cells, cholesterol is also the precursor for bile acids, vitamin D, and steroid hormones.
Bile acids are essential for digesting fats in the diet
Vitamin D plays a significant role in calcium metabolism and bone health.
The steroid hormones include testosterone, estrogen, progesterone, cortisol, and aldosterone.
What is the right level of cholesterol?
Like most things in the body, optimal health is a matter of having neither too much nor too little cholesterol. The right amount is personal, and it depends on our genes, diet, age, and lifestyle.
Below is a chart showing that mortality is lowest in people with an LDL that is a little over 100. The chart shows a sharp increase in mortality with low cholesterol levels and with really high cholesterol levels. One reason for the high mortality rates with low cholesterol is that cholesterol helps protect against infectious diseases.[ref]
Chart from a study of over 500,000 adults in S. Korea, comparing LDL levels to mortality rates. PMC6832139
A large 10-year study out of Norway found the lowest mortality rates occurred in people with cholesterol levels between ~190 to 270 mg/dl (5 and 7 mmol/l).[ref]
The CDC and many other health organizations, though, have a narrower range of what they consider healthy.
These ranges vary in other countries, and the ‘normal’ level changes periodically. For example, according to a JAMA article, normal cholesterol ranged from 240 mg/dL in 1986 and up to 260 mg/dL in 1983.[ref]
Where does cholesterol come from?
There are two sources of cholesterol:
Cholesterol in foods
Cholesterol that your body makes
In addition to the cholesterol that your body makes, cholesterol from food (animal products) is absorbed in the intestines. Eating foods that contain cholesterol causes a temporary increase in serum cholesterol levels, with levels dropping to baseline in about seven hours.[ref]
Generally, eating cholesterol causes the body to produce less of it, and decreasing your cholesterol intake will trigger the body to make more of it. This doesn’t hold true for everyone, but this is the way that it usually works.
Most cholesterol in the body is synthesized in the liver, intestines, adrenals, and reproductive organs. It is a multi-step, complex process to make it.
The regulation of cholesterol synthesis occurs through several processes, with one of the main regulators being the SREBP protein, coded for by the SREBF1 and 2 genes. Other genes involved in your cholesterol levels include cholesterol transport and receptor genes.
How is cholesterol stored?
Cholesterol can be stored in fat droplets packaged with triglycerides and lipoprotein. Chylomicrons are created from dietary fats and contain apolipoproteins, triglycerides, and cholesterol. The backbone of chylomicrons is ApoB. Chylomicrons are taken up by the lymphatic system and then transferred to blood circulation. Once in circulation, chylomicrons incorporate into adipose (fat) or muscle tissue.[ref]
Chylomicron packing up triglycerides, cholesterol
Additionally, cholesterol can be made in the liver and packaged into LDL particles of different densities and sizes, such as VLDL (very low-density lipoprotein) particles. These circulating LDL particles can then bind to cells with an LDL receptor to be utilized by the cell.
How is cholesterol used?
Cholesterol levels are tightly regulated by cells.
LDL receptors control the uptake, and the cell then controls how many LDL-Rs are available via a couple of proteins, including PCSK9.
When excess cholesterol is available, excretion through the liver into the feces occurs. This process is called reverse cholesterol transport. The ABCA1 protein is responsible for moving cholesterol back out of the cells.
See the genotype report section for more on how these gene impact your cholesterol levels.
Cholesterol and Heart Disease: Controversial?
According to the CDC, LDL, or ‘bad’ cholesterol, increases heart disease and stroke risk. They recommend eating “foods with plenty of fiber, such as oatmeal and beans, and healthy unsaturated fats, such as avocados, olive oil, and nuts.”[ref]
Essentially, LDL is linked to heart attacks because cholesterol is a component of plaques that can build up in the arteries. When the cells lining the blood vessels (endothelial cells) become inflamed, LDL particles are included in the layers of the arteries. When the LDL cholesterol becomes oxidized by reactive oxygen species, it increases inflammation in the vessel.[ref]
CC image showing plaque buildup in artery
It’s simplistic to say that LDL-c is “bad cholesterol”. Let’s dig into the research here because the truth isn’t always as black and white as health websites claim.
A 2010 meta-analysis of twenty-six large clinical trials using statins to reduce cholesterol found the following.[ref]
For every 39 mg/dL reduction in LDL cholesterol level:
all-cause mortality is 10% lower
mainly due to reduced heart attack deaths
no effect on strokes or cancer
Studies using genetic risk scores (looking at multiple genetic variants related to cholesterol) find that a lifetime of lower cholesterol levels is associated with lower overall mortality risk.[ref]
“Results of the current study indicate that a genetic predisposition to high LDL-C levels contributes to mortality throughout life, including in the oldest old, and a beneficial LDL genetic risk profile is associated with familial longevity.”
On the other hand, some researchers argue that there is no causality between high cholesterol and heart disease.[ref] Naturally, many of the research studies on statins, cholesterol levels, and heart disease are funded by pharmaceutical companies. And the endpoints and definitions of ‘high’ cholesterol make it hard to compare between studies. It makes it easy to create doubt about the link between really high cholesterol and heart disease.
Familial Hypercholesterolemia (FH)
A genetic mutation known as ‘familial hypercholesterolemia’ or FH causes really high cholesterol. Estimates show that 1 in 200 people have FH mutations, which increases the risk of heart disease by 20-fold. In adults, LDL-C levels are often over 190 mg/dL in people with FH mutations.[ref][ref]
While this is still an area of active research, so far, mutations have been identified in the PCSK9, APOB, LDLR, and LDLRAP1 genes.
Statins and Cholesterol-Lowering Medications
Statins, one type of cholesterol-lowering medicine, are among the most prescribed medications in the US and UK. In 2014 about 28% of Americans over age 40 were taking a statin.
A Cochrane study on atorvastatin found that LDL cholesterol decreased by 37 – 51%.[ref] However, this doesn’t answer the question of whether that is beneficial to health or prevents death.
The Number Needed to Treat website has an extensive review of studies on statins, including the significantly increased risk of diabetes and muscle pain. It is an interesting, well-crafted assessment of the risks and benefits that concludes that statins’ risks outweigh the benefits for most people. Everyone is unique. Talk with your doctor about your specific risks and benefits.
Studies on both high and low LDL cholesterol show a variety of different effects.
Low cholesterol links:
A March 2018 study found that lung cancer patients with low cholesterol were at a 61% higher risk of death.[ref]
Low LDL-C is associated with greater rates of sepsis in the elderly.[ref]
A study of over 100,000 people in Denmark found that having a lifeline lower LDL cholesterol level (1 mmol/L lower) reduced the risk of Alzheimer’s and dementia.[ref]
High cholesterol links:
A review in the JAMA found that each “additional 300 mg of dietary cholesterol consumed per day was significantly associated with a higher risk of incident” of cardiovascular disease.[ref]
A large review in the Lancet recently found that reducing LDL cholesterol reduces the risk of “major vascular events”.[ref]
A picture emerges that LDL levels that are neither lower than normal nor higher than normal are best for overall mortality rates.
Cholesterol Genotype Report:
Members: Log in to see your data below. Not a member? Join here.
Why is this section is now only for members? Here’s why…
Member Content:
An active subscription is required to access this content.
If you have high cholesterol and are trying to avoid going on a statin, here are some diet and supplement ideas to try. Of course, talk with your doctor if you have any medical questions.
Modifying Cholesterol with Diet
The old advice to give up eggs to lower your cholesterol is inaccurate[ref]. Similarly, choline from eggs or supplements does not raise cholesterol levels.[ref]
So what works to lower cholesterol? A whole-food diet and moderate exercise are usually beneficial for keeping cholesterol levels in check. Yep – standard advice to cut out fast food and hit the gym a few times per week. Cutting out processed food should decrease inflammation and lower cholesterol levels. Cleaning up the diet does work for most people and is an obvious route to try.[ref][ref]
A meta-analysis that combined the data from a bunch of studies found that fruit and vegetable intake of 3+ servings per day decreases triglyceride levels and improves total cholesterol. (Interestingly, the study found no extra benefit from consuming five or more servings of fruits and vegetables per day.)[ref]
How much does diet matter? Type 2 diabetics on a low-fat vegan diet (lots of fruits and vegetables) had a decrease in cholesterol levels of 13.5 mg/dL.[ref]
Ketogenic Diet and LDL:
A recent study of healthy, normal-weight women found that a low-carb, high-fat ketogenic diet for a month increases LDL cholesterol significantly (~70 mg/dL). The diet was high in saturated fats and low in fiber.[ref]
Keep in mind that individual results will likely vary – the range of increase was between 40 and 90 mg/dL for these study participants.
7 Natural supplements with solid research for lowering cholesterol
Member Content:
An active subscription is required to access this content.
Triglyceride Levels
High triglycerides are linked with an increased risk of cardiovascular disease. Both genetics and diet combine to elevate triglyceride levels. Learn how your genes interact with what you eat to lower your triglycerides.
Lipoprotein (a)
High Lp(a) levels are a big risk factor for sudden heart attacks. Your genetic variants mainly control your Lp(a) levels. Check to see if you carry genetic variants that increase or decrease Lp(a).
Top 10 Genes to Check in Your Genetic Raw Data
Wondering what is actually important in your genetic data? These 10 genes have important variants with a big impact on health. Check your genes (free article).
Adams, Stephen P., et al. “Atorvastatin for Lowering Lipids.” The Cochrane Database of Systematic Reviews, vol. 2015, no. 3, Mar. 2015. www.ncbi.nlm.nih.gov, https://doi.org/10.1002/14651858.CD008226.pub3.
Adorni, Maria Pia, et al. “Effect of a Novel Nutraceutical Combination on Serum Lipoprotein Functional Profile and Circulating PCSK9.” Therapeutics and Clinical Risk Management, vol. 13, 2017, pp. 1555–62. PubMed, https://doi.org/10.2147/TCRM.S144121.
Barnard, Neal D., et al. “A Low-Fat Vegan Diet and a Conventional Diabetes Diet in the Treatment of Type 2 Diabetes: A Randomized, Controlled, 74-Wk Clinical Trial.” The American Journal of Clinical Nutrition, vol. 89, no. 5, May 2009, pp. 1588S-1596S. PubMed, https://doi.org/10.3945/ajcn.2009.26736H.
Batuca, Joana R., et al. “Extended-Release Niacin Increases Anti-Apolipoprotein A-I Antibodies That Block the Antioxidant Effect of High-Density Lipoprotein-Cholesterol: The EXPLORE Clinical Trial.” British Journal of Clinical Pharmacology, vol. 83, no. 5, May 2017, pp. 1002–10. PubMed, https://doi.org/10.1111/bcp.13198.
Beheshti, Sabina, et al. “Relationship of Familial Hypercholesterolemia and High Low-Density Lipoprotein Cholesterol to Ischemic Stroke: Copenhagen General Population Study.” Circulation, vol. 138, no. 6, Aug. 2018, pp. 578–89. PubMed, https://doi.org/10.1161/CIRCULATIONAHA.118.033470.
Benito-Vicente, Asier, et al. “Familial Hypercholesterolemia: The Most Frequent Cholesterol Metabolism Disorder Caused Disease.” International Journal of Molecular Sciences, vol. 19, no. 11, Nov. 2018. www.ncbi.nlm.nih.gov, https://doi.org/10.3390/ijms19113426.
—. “Familial Hypercholesterolemia: The Most Frequent Cholesterol Metabolism Disorder Caused Disease.” International Journal of Molecular Sciences, vol. 19, no. 11, Nov. 2018. www.ncbi.nlm.nih.gov, https://doi.org/10.3390/ijms19113426.
Benn, Marianne, Børge G Nordestgaard, et al. “Low LDL Cholesterol, PCSK9 and HMGCR Genetic Variation, and Risk of Alzheimer’s Disease and Parkinson’s Disease: Mendelian Randomisation Study.” The BMJ, vol. 357, Apr. 2017, p. j1648. PubMed Central, https://doi.org/10.1136/bmj.j1648.
Benn, Marianne, Børge G. Nordestgaard, et al. “PCSK9R46L, Low-Density Lipoprotein Cholesterol Levels, and Risk of Ischemic Heart Disease: 3 Independent Studies and Meta-Analyses.” Journal of the American College of Cardiology, vol. 55, no. 25, June 2010, pp. 2833–42. ScienceDirect, https://doi.org/10.1016/j.jacc.2010.02.044.
Calandra, Sebastiano, et al. “Mechanisms and Genetic Determinants Regulating Sterol Absorption, Circulating LDL Levels, and Sterol Elimination: Implications for Classification and Disease Risk.” Journal of Lipid Research, vol. 52, no. 11, Nov. 2011, pp. 1885–926. DOI.org (Crossref), https://doi.org/10.1194/jlr.R017855.
—. “Mechanisms and Genetic Determinants Regulating Sterol Absorption, Circulating LDL Levels, and Sterol Elimination: Implications for Classification and Disease Risk.” Journal of Lipid Research, vol. 52, no. 11, Nov. 2011, pp. 1885–926. DOI.org (Crossref), https://doi.org/10.1194/jlr.R017855.
Cao, Shijie, et al. “Berberrubine and Its Analog, Hydroxypropyl-Berberrubine, Regulate LDLR and PCSK9 Expression via the ERK Signal Pathway to Exert Cholesterol-Lowering Effects in Human Hepatoma HepG2 Cells.” Journal of Cellular Biochemistry, Oct. 2018. PubMed, https://doi.org/10.1002/jcb.27102.
CDC. “Cholesterol Myths and Facts | Cdc.Gov.” Centers for Disease Control and Prevention, 26 Jan. 2021, https://www.cdc.gov/cholesterol/myths_facts.htm.
—. “How and When to Have Your Cholesterol Checked | Cdc.Gov.” Centers for Disease Control and Prevention, 15 Apr. 2021, https://www.cdc.gov/cholesterol/checked.htm.
Chen, Suet N., et al. “A Common PCSK9 Haplotype, Encompassing the E670G Coding Single Nucleotide Polymorphism, Is a Novel Genetic Marker for Plasma Low-Density Lipoprotein Cholesterol Levels and Severity of Coronary Atherosclerosis.” Journal of the American College of Cardiology, vol. 45, no. 10, May 2005, pp. 1611–19. PubMed, https://doi.org/10.1016/j.jacc.2005.01.051.
Chen, Yeda, et al. “Association Between Apolipoprotein B XbaI Polymorphism and Coronary Heart Disease in Han Chinese Population: A Meta-Analysis.” Genetic Testing and Molecular Biomarkers, vol. 20, no. 6, June 2016, pp. 304–11. PubMed, https://doi.org/10.1089/gtmb.2015.0126.
Chikowore, Tinashe, et al. “C679X Loss-of-Function PCSK9 Variant Lowers Fasting Glucose Levels in a Black South African Population: A Longitudinal Study.” Diabetes Research and Clinical Practice, vol. 144, Oct. 2018, pp. 279–85. PubMed, https://doi.org/10.1016/j.diabres.2018.09.012.
Cohen, Jonathan, et al. “Low LDL Cholesterol in Individuals of African Descent Resulting from Frequent Nonsense Mutations in PCSK9.” Nature Genetics, vol. 37, no. 2, Feb. 2005, pp. 161–65. PubMed, https://doi.org/10.1038/ng1509.
—. “Low LDL Cholesterol in Individuals of African Descent Resulting from Frequent Nonsense Mutations in PCSK9.” Nature Genetics, vol. 37, no. 2, Feb. 2005, pp. 161–65. PubMed, https://doi.org/10.1038/ng1509.
—. “Low LDL Cholesterol in Individuals of African Descent Resulting from Frequent Nonsense Mutations in PCSK9.” Nature Genetics, vol. 37, no. 2, Feb. 2005, pp. 161–65. PubMed, https://doi.org/10.1038/ng1509.
Collaboration, Cholesterol Treatment Trialists’ (CTT). “Efficacy and Safety of More Intensive Lowering of LDL Cholesterol: A Meta-Analysis of Data from 170 000 Participants in 26 Randomised Trials.” Lancet, vol. 376, no. 9753, Nov. 2010, p. 1670. www.ncbi.nlm.nih.gov, https://doi.org/10.1016/S0140-6736(10)61350-5.
Dubois, C., et al. “Effects of Increasing Amounts of Dietary Cholesterol on Postprandial Lipemia and Lipoproteins in Human Subjects.” Journal of Lipid Research, vol. 35, no. 11, Nov. 1994, pp. 1993–2007.
Fahed, Akl C., et al. “Variable Expressivity and Co-Occurrence of LDLR and LDLRAP1 Mutations in Familial Hypercholesterolemia: Failure of the Dominant and Recessive Dichotomy.” Molecular Genetics & Genomic Medicine, vol. 4, no. 3, May 2016, pp. 283–91. PubMed, https://doi.org/10.1002/mgg3.203.
—. “Variable Expressivity and Co-Occurrence of LDLR and LDLRAP1 Mutations in Familial Hypercholesterolemia: Failure of the Dominant and Recessive Dichotomy.” Molecular Genetics & Genomic Medicine, vol. 4, no. 3, May 2016, pp. 283–91. PubMed, https://doi.org/10.1002/mgg3.203.
“Familial Hypercholesterolemia.” NORD (National Organization for Rare Disorders), https://rarediseases.org/rare-diseases/familial-hypercholesterolemia/. Accessed 26 Oct. 2021.
Fouladseresht, Hamed, et al. “Association of ABCA1 Haplotypes with Coronary Artery Disease.” Laboratory Medicine, vol. 51, no. 2, Mar. 2020, pp. 157–68. PubMed, https://doi.org/10.1093/labmed/lmz031.
Group, Graham Walker and The NNT. “Statins for Heart Disease Prevention (Without Prior Heart Disease).” TheNNT, http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/. Accessed 26 Oct. 2021.
Guirgis, Faheem W., et al. “Cholesterol Levels and Long-Term Rates of Community-Acquired Sepsis.” Critical Care, vol. 20, 2016. www.ncbi.nlm.nih.gov, https://doi.org/10.1186/s13054-016-1579-8.
Haghighatdoost, Fahimeh, and Mitra Hariri. “Effect of Resveratrol on Lipid Profile: An Updated Systematic Review and Meta-Analysis on Randomized Clinical Trials.” Pharmacological Research, vol. 129, Mar. 2018, pp. 141–50. PubMed, https://doi.org/10.1016/j.phrs.2017.12.033.
—. “Effect of Resveratrol on Lipid Profile: An Updated Systematic Review and Meta-Analysis on Randomized Clinical Trials.” Pharmacological Research, vol. 129, Mar. 2018, pp. 141–50. PubMed, https://doi.org/10.1016/j.phrs.2017.12.033.
Hayat, Mahtaab, et al. “Genetic Associations between Serum Low LDL-Cholesterol Levels and Variants in LDLR, APOB, PCSK9 and LDLRAP1 in African Populations.” PLoS ONE, vol. 15, no. 2, 2020. www.ncbi.nlm.nih.gov, https://doi.org/10.1371/journal.pone.0229098.
Hubacek, J. A., et al. “Polygenic Hypercholesterolemia: Examples of GWAS Results and Their Replication in the Czech-Slavonic Population.” Physiological Research, vol. 66, no. Suppl 1, Apr. 2017, pp. S101–11. PubMed, https://doi.org/10.33549/physiolres.933580.
Hussain, Yasin, et al. “G-Protein Estrogen Receptor as a Regulator of Low-Density Lipoprotein Cholesterol Metabolism: Cellular and Population Genetic Studies.” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 35, no. 1, Jan. 2015, pp. 213–21. PubMed, https://doi.org/10.1161/ATVBAHA.114.304326.
Kent, Shia T., et al. “PCSK9 Loss-of-Function Variants, Low-Density Lipoprotein Cholesterol, and Risk of Coronary Heart Disease and Stroke: Data From 9 Studies of Blacks and Whites.” Circulation. Cardiovascular Genetics, vol. 10, no. 4, Aug. 2017, p. e001632. PubMed, https://doi.org/10.1161/CIRCGENETICS.116.001632.
Khera, Amit V., et al. “Diagnostic Yield and Clinical Utility of Sequencing Familial Hypercholesterolemia Genes in Patients With Severe Hypercholesterolemia.” Journal of the American College of Cardiology, vol. 67, no. 22, June 2016, pp. 2578–89. PubMed, https://doi.org/10.1016/j.jacc.2016.03.520.
Khoury, D. El, et al. “Beta Glucan: Health Benefits in Obesity and Metabolic Syndrome.” Journal of Nutrition and Metabolism, vol. 2012, 2012. www.ncbi.nlm.nih.gov, https://doi.org/10.1155/2012/851362.
Kwon, H. J., et al. “Molecular Basis for LDL Receptor Recognition by PCSK9.” Proceedings of the National Academy of Sciences, vol. 105, no. 6, Feb. 2008, pp. 1820–25. DOI.org (Crossref), https://doi.org/10.1073/pnas.0712064105.
Malekmohammad, Khojasteh, et al. “Antioxidants and Atherosclerosis: Mechanistic Aspects.” Biomolecules, vol. 9, no. 8, Aug. 2019. www.ncbi.nlm.nih.gov, https://doi.org/10.3390/biom9080301.
Mbikay, Majambu, et al. “Mice Fed a High-Cholesterol Diet Supplemented with Quercetin-3-Glucoside Show Attenuated Hyperlipidemia and Hyperinsulinemia Associated with Differential Regulation of PCSK9 and LDLR in Their Liver and Pancreas.” Molecular Nutrition & Food Research, vol. 62, no. 9, May 2018, p. e1700729. PubMed, https://doi.org/10.1002/mnfr.201700729.
Moazzen, Hossein, and Mohammad Alizadeh. “Effects of Pomegranate Juice on Cardiovascular Risk Factors in Patients with Metabolic Syndrome: A Double-Blinded, Randomized Crossover Controlled Trial.” Plant Foods for Human Nutrition (Dordrecht, Netherlands), vol. 72, no. 2, June 2017, pp. 126–33. PubMed, https://doi.org/10.1007/s11130-017-0605-6.
Niu, Caiqin, et al. “Associations of the APOB Rs693 and Rs17240441 Polymorphisms with Plasma APOB and Lipid Levels: A Meta-Analysis.” Lipids in Health and Disease, vol. 16, no. 1, Sept. 2017, p. 166. BioMed Central, https://doi.org/10.1186/s12944-017-0558-7.
NM_000384.2(APOB):C.10580G>A (p.Arg3527Gln) AND Familial Hypercholesterolemia – ClinVar – NCBI. https://www.ncbi.nlm.nih.gov/clinvar/RCV000019479.30/. Accessed 26 Oct. 2021.
Petursson, Halfdan, et al. “Is the Use of Cholesterol in Mortality Risk Algorithms in Clinical Guidelines Valid? Ten Years Prospective Data from the Norwegian HUNT 2 Study.” Journal of Evaluation in Clinical Practice, vol. 18, no. 1, Feb. 2012, pp. 159–68. PubMed, https://doi.org/10.1111/j.1365-2753.2011.01767.x.
Postmus, Iris, Joris Deelen, et al. “LDL Cholesterol Still a Problem in Old Age? A Mendelian Randomization Study.” International Journal of Epidemiology, vol. 44, no. 2, Apr. 2015, pp. 604–12. PubMed, https://doi.org/10.1093/ije/dyv031.
Postmus, Iris, Stella Trompet, et al. “PCSK9 SNP Rs11591147 Is Associated with Low Cholesterol Levels but Not with Cognitive Performance or Noncardiovascular Clinical Events in an Elderly Population.” Journal of Lipid Research, vol. 54, no. 2, Feb. 2013, pp. 561–66. PubMed Central, https://doi.org/10.1194/jlr.M033969.
Qiu, Chengfeng, et al. “What Is the Impact of PCSK9 Rs505151 and Rs11591147 Polymorphisms on Serum Lipids Level and Cardiovascular Risk: A Meta-Analysis.” Lipids in Health and Disease, vol. 16, no. 1, June 2017, p. 111. PubMed, https://doi.org/10.1186/s12944-017-0506-6.
Ravnskov, Uffe, et al. “LDL-C Does Not Cause Cardiovascular Disease: A Comprehensive Review of the Current Literature.” Expert Review of Clinical Pharmacology, vol. 11, no. 10, Oct. 2018, pp. 959–70. PubMed, https://doi.org/10.1080/17512433.2018.1519391.
Schucker, B., et al. “Change in Cholesterol Awareness and Action. Results from National Physician and Public Surveys.” Archives of Internal Medicine, vol. 151, no. 4, Apr. 1991, pp. 666–73.
Slimani, Afef, et al. “Effect of E670G Polymorphism in PCSK9 Gene on the Risk and Severity of Coronary Heart Disease and Ischemic Stroke in a Tunisian Cohort.” Journal of Molecular Neuroscience: MN, vol. 53, no. 2, June 2014, pp. 150–57. PubMed, https://doi.org/10.1007/s12031-014-0238-2.
SREBF1 Sterol Regulatory Element Binding Transcription Factor 1 [Homo Sapiens (Human)] – Gene – NCBI. https://www.ncbi.nlm.nih.gov/gene/6720. Accessed 26 Oct. 2021.
“Statins – Prices and Information.” GoodRx, https://www.goodrx.com/statins. Accessed 26 Oct. 2021.
VCV000002873.2 – ClinVar – NCBI. https://www.ncbi.nlm.nih.gov/clinvar/variation/2873/. Accessed 26 Oct. 2021.
Wang, Nelson, et al. “Intensive LDL Cholesterol-Lowering Treatment beyond Current Recommendations for the Prevention of Major Vascular Events: A Systematic Review and Meta-Analysis of Randomised Trials Including 327 037 Participants.” The Lancet. Diabetes & Endocrinology, vol. 8, no. 1, Jan. 2020, pp. 36–49. PubMed, https://doi.org/10.1016/S2213-8587(19)30388-2.
Wang, Yanan, et al. “Barley β-Glucan Reduces Blood Cholesterol Levels via Interrupting Bile Acid Metabolism.” The British Journal of Nutrition, vol. 118, no. 10, Nov. 2017, pp. 822–29. PubMed, https://doi.org/10.1017/S0007114517002835.
Xu, Lin, et al. “Egg Consumption and the Risk of Cardiovascular Disease and All-Cause Mortality: Guangzhou Biobank Cohort Study and Meta-Analyses.” European Journal of Nutrition, vol. 58, no. 2, Mar. 2019, pp. 785–96. PubMed, https://doi.org/10.1007/s00394-018-1692-3.
Zhang, Gu, et al. “Low Serum Levels of Pre-Surgical Total Cholesterol Are Associated with Unfavorable Overall Survival in Patients with Operable Non-Small Cell Lung Cancer.” Clinical Laboratory, vol. 64, no. 3, Mar. 2018, pp. 321–27. PubMed, https://doi.org/10.7754/Clin.Lab.2017.170823.
Zhong, Victor W., et al. “Associations of Dietary Cholesterol or Egg Consumption With Incident Cardiovascular Disease and Mortality.” JAMA, vol. 321, no. 11, Mar. 2019, pp. 1081–95. PubMed, https://doi.org/10.1001/jama.2019.1572.
About the Author: Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and also an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.
