Heart disease is the number one cause of death in the world and the leading cause of death in the United States, killing over 800,000 Americans a year, or 1 in 3 deaths in the U.S. (1). Is high cholesterol to blame?

Another 1 in 3 Americans have high cholesterol and/or high cholesterol (2, 3), conditions most often associated as risk factors for heart disease.

However, the claim that “high cholesterol” causes heart disease is actually a myth. Get the facts…

High Cholesterol 101

doctor explaining to patient about high cholesterol

“High cholesterol” has long been touted as a sign of heart disease, but did you know that over 80% of heart attack patients do not have high cholesterol?!

Nevertheless, if you go to your doctor and your cholesterol falls out of “normal range”, there’s a good chance you’ll have a talk about diet, exercise and possibly statin drugs or baby aspirin.

“High Cholesterol” According to Blood Work

According to U.S. guidelines in 2018, “High Cholesterol” markers meet the following criteria:

• Total Cholesterol
• Ideal: Below 200 mg/dL
• Borderline High: Above 200 mg/dL
• High: Above 240 mg/dL

• LDL (low density lipoprotein):
• Ideal: Below 100 mg/dL (for high risk patients), Below 130 mg/dL (for non-risk patients)
• Borderline High: 130-160 mg/dL
• High: Above 160-190 mg/dL

• HDL (high density lipoprotein):
• Ideal: Above 50-60 mg/dL
• High Risk: Below 40 mg/dL (men); Below 50 mg/dL (women)
• High: Above 240 mg/dL

• Triglycerides:
• Ideal: Below 150 mg/dL
• Borderline High: Above 150 mg/dL
• High: Above mg/dL

In medicine, a diagnosis of true or “pure” hypercholesterolemia (high cholesterol) equals:

High total cholesterol
High LDL levels
Normal triglycerides
Normal HDL levels

Pure hypercholesterolemia is also called “Familia hypercholesterolemia” because it is passed down to a person by their parents because of a genetic mutation on chromosome 19, and affects only 1 in 500 people (4).

Most People Have Dyslipidemia or “Inflammation” (NOT True “High Cholesterol”)
Dyslipidemia, on the other hand, (i.e. “pseudo high cholesterol” or “inflammation”) is much more common, affecting more than 1 in 2 people (4).

Dyslipidemia typically presents on lab work as:
• High Triglycerides
• Low HDL
• Normal or high total cholesterol
• Normal or high LDL cholesterol
• It is even possible to have normal and even low total cholesterol and high LDL particle number.

Dyslipidemia (“pseudo high cholesterol”) is most common type of “high cholesterol.’

What Is Inflammatory High Cholesterol (Dyslipidemia)

The driving explanations behind high cholesterol, along with heart disease, is most often connected to dietary and lifestyle factors. In fact, only about 3 percent of contemporary hunter-gatherers had heart disease risk markers (like high cholesterol and high blood pressure) compared to the industrialized world (5, 6). Common triggers cited for causing high cholesterol and heart disease in our modern day world include:

• Insulin resistance
• Metabolic dysfunction
• Standard American Diet (low protein or conventional protein, high-grain, low vegetable, low fat, industrial seed oils)
• Sugar, artificial sweeteners and food additives
• High coffee or alcohol consumption
• Sedentary lifestyle
• Low water intake (dehydration)
• Poor quality sleep or lack of sleep
• Excessive screen exposure
• Excessive sitting
• Inflammation and stress

The “cure”for the epidemic? The American Heart Association and USDA has long preached the following guidelines:

woman saying no to food with high cholesterol

• Avoid red meat and high cholesterol foods (like eggs, bacon and butter)
• Avoid saturated fat
• Take it easy on the salt
• Move more
• Eat heart healthy whole grains, fruits and vegetables—potentially even consider a vegan or vegetarian diet
• Eat less overall

However, despite knowing what we’ve known for the past 40-50 years, the rates of heart disease, and associated conditions (“high cholesterol” and (hypertension) continue to climb. Given this evidence, the bigger question then is why?

If cutting cholesterol and saturated fat, FitBit calorie tracking, and statin drugs are not “curing” these epidemics, what does? The answer is not what we’ve been made to believe.

6 Reasons Why High Cholesterol is Not as Bad as You Think

Fact 1: “Eating cholesterol and saturated fat is bad for you” is a MYTH.

Studies show that approximately 3 in 4 people’s cholesterol levels are not affected at all by the cholesterol they eat (7). The remaining 25 percent do experience an increase in cholesterol, however both their LDL and HDL levels raise, therefore not affecting their LDL-to-HDL ratio nor clinically relevant. In fact, even the U.S. Dietary Guideline removed their restrictions on intake of dietary cholesterol in 2015, no longer cautioning against the intake of dietary cholesterol. Similarly, research on saturated fat consumption and its link to heart disease is weak. Several meta-analyses confirm the saturated fat scare is bogus (8-10), suggesting that saturated fats may even have important health effects.

Fact 2: Heart attack patients do not have high cholesterol

You heard that right. More than 70% of heart attack victims do not have high cholesterol markers deemed “unhealthy” by current U.S. guidelines (11). Many of them even have low cholesterol.

Fact 3: We’ve been focusing on the wrong cholesterol blood markers (LDL is not bad for you)

When people talk about cholesterol, they often use the terms LDL and HDL. Both are lipoproteins (compounds made of fat and protein) that are responsible for carrying cholesterol throughout the body in the blood.
• LDL is low-density lipoprotein, often called “bad” cholesterol.
• HDL is high-density lipoprotein, or “good” cholesterol.

LDL is called the “bad” cholesterol because it’s believed that too much of it can lead to hardening of the arteries.HDL, on the other hand, is called the “good cholesterol” because it is believed to aid in the removal of LDL from the arteries and carries the bad cholesterol back to the liver, where LDL is then broken down and eliminated from the body. However, while the LDL-HDL theory SOUNDS good, NEITHER of these markers are as important as two cholesterol markers that are NOT tested on average cholesterol panels: lipoprotein (a) or “Lp(a)” and LDL-P. Your Lp(a) or lipoprotein numbers shows the measure of the TOTAL AMOUNT of lipoprotein particles (i.e. LDL and HDL) in your body. Current research overwhelmingly reveals that your Total lipoprotein levels—specifically the LDL particle number (LDL-P)—are more strongly associated with heart disease, “clogged arteries” and whether or not you’re genetically at risk for such conditions instead of the standard HDL and LDL levels.(12-17).

Fact 4: Stains do not reverse heart disease

Statins are the “go to” drug of choice with 1 in 4 adults above age 40 on these “cholesterol lowering” medications nationwide. In fact, it is perhaps not coincidence that, in 2004, when the statin Lipitor went viral in the pharmaceutical market , that same year the FDA changed the “healthy” lab ranges for high total cholesterol markers from 250 mg/dL or below, to 200 mg/dL or below; and “healthy” LDL ranges from 130 to 100 mg/dL or below—making more of a case for more Americans to need these life saving medications. (18) By 2005, Lipitor had generated a total profit of $12 billion alone in sales. For years, we’ve been told by the pharmaceutical industry that lowering cholesterol via statin drugs prevents heart disease, but can statins really cure or reverse coronary heart disease? The answer is a clear “no.”

The risks of heart attacks and death have been seemingly reduced, but not eliminated, nor statistically “significant” —making researchers question whether or not statins for “high cholesterol” are really worthwhile. For example, in the widely pub-licized Scandinavian Simvastatin Survival Study, 4,444 participants took the statin drug (Zocor®) or a placebo (19, 20). Heart attacks and death decreased from 28% in the placebo group to 19% in the statin group. In other words: for every 100 people who took a statin drug (Zocor®), 9 heart attacks were prevented, however 19 heart attacks still occurred. The researchers concluded that the statin group had only a 30% less likely chance of getting a heart attack at best. Similar trials (21-23) have yielded similar unimpressive results for high-cholesterol patients in particular (especially considering that MOST heart attack patients do not have high cholesterol in the first place).

Certainly statins lower cholesterol markers on paper, but the side effects may far outweigh the benefits as well. Statin therapy for high cholesterol is just one piece of a bigger picture. Heart disease has many other risk factors, and there are many other ways to reduce risk and identify people at risk.Using statins to “lower cholesterol” may not be beneficial unless the individually is clearly genetically at risk for heart disease and all other lifestyle and inflammatory causes of heart disease and high cholesterol have been addressed first.

Fact 5: Certain gut bacteria that Influence the risk for hardened of the arteries

Beyond lifestyle factors, the reason certain lifestyle factors are bigger triggers for some than others when it comes to heart disease may come down to their gut bacteria. Researchers in one study (24) found that people with one group of (healthier) gut bacteria had a lower risk of developing hardened arteries than people with a different set of (unhealthy) gut bacteria, Ruminococcus, connected to more genes that also caused inflammation. Bacteria in the healthy people on the other hand had genes that protected them from inflammation by soaking up dangerous chemicals. The final report concluded that genes and lifestyle aren’t the only things important in figuring out our risk of disease.

Fact 6: High cholesterol and high triglycerides may really be a sign of high inflammation (in the liver and gut)

Cholesterol is produced and metabolized in the liver. Given that 1 in 4 people have a non-alcoholic fatty liver, and another 1 in 3 have high cholesterol markers, the connection may be strongly related. A study (25) on the association between gut microbes and blood lipid levels in 893 people from Netherlands identified 34 different types of bacteria that contributed to differences in body fat and blood lipids such as triglycerides and cholesterol. Gut bacteria contributed to 4.6 percent of the difference in body fat, six percent in triglycerides and four percent in HDL (“less inflammation”).

The High Cholesterol Gut Connection

Most “high cholesterol” markers on blood work (1 in 2 people) are signs of inflammation in the body— often connected to an unhealthy gut.

References

  1. CDC. 2018. Heart Disease Facts & Statistics. https://www.cdc.gov/heartdisease/facts.htm
  2. CDC. 2018. High Blood Pressure. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_bloodpressure.htm
  3. CDC. 2018. High Cholesterol Facts. https://www.cdc.gov/cholesterol/facts.htm
    NIH. 2018. Hypercholesterolemia. https://ghr.nlm.nih.gov/condition/hypercholesterolemia;
  4. CDC. 2019. High Cholesterol Facts. https://www.cdc.gov/cholesterol/facts.htm
  5. Michael Gurven, Aaron D. Blackwell, Daniel Eid Rodríguez, Jonathan Stieglitz, and Hillard Kaplan. Does Blood Pressure Inevitably Rise With Age? Longitudinal Evidence Among Forager-Horticulturalists. Hypertension, 2012 DOI: 10.1161/HYPERTENSIONAHA.111.189100
  6. Daniel Lemogoum, William Ngatchou, Christophe Janssen, Marc Leeman, Luc Van Bortel, Pierre Boutouyrie, Jean Paul Degaute, and Philippe Van de Borne. Effects of Hunter-Gatherer Subsistence Mode on Arterial Distensibility in Cameroonian Pygmies. Hypertension, May 21 2012 DOI: 10.1161/HYPERTENSIONAHA.111.187757
  7. Soliman G. A. (2018). Dietary Cholesterol and the Lack of Evidence in Cardiovascular Disease. Nutrients, 10(6), 780. doi:10.3390/nu10060780
  8. Nettleton, J. A., Brouwer, I. A., Geleijnse, J. M., & Hornstra, G. (2017). Saturated Fat Consumption and Risk of Coronary Heart Disease and Ischemic Stroke: A Science Update. Annals of nutrition & metabolism, 70(1), 26-33.de Souza RJ, Mente A, Maroleanu A, Cozma AI, et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015;351:h3978.
  9. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010;91:535–546.
  10. Sachdeva, A., Cannon, C.P., Deedwania, P.C., LaBresh, K.A., Smith, S.C., Dai, D., Hernández, A.V., & Fonarow, G.C. (2009). Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. American heart journal, 157 1, 111-117.e2
    12. Sniderman AD. Differential response of cholesterol and particle measures of atherogenic lipoproteins to LDL-lowering therapy: implications for clinical practice. J Clin Lipidol. 2008; 2(1):36-42. https://www.lipidjournal.com/article/S1933-2874(08)00004-4/fulltext
  11. Cromwell WC, Otvos JD, Keyes MJ. LDL particle number and risk of future cardiovascular disease in the Framingham Offspring Study—Implications for LDL management. J Clin Lipidol. 2007; 1(6):583–592. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720529/pdf/nihms36287.pdf
  12. Otvos JD, Mora S, Shalaurova I, et al. Clinical implications of discordance between low-density lipoprotein cholesterol and particle number. J Clin Lipidol. 2011; 5(2):105–113. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070150/pdf/nihms-274658.pdf
  13. Degoma EM, Davis MD, Dunbar RL, et al. Discordance between non-HDL-cholesterol and LDL-particle measurements: Results from the Multi-Ethnic Study of Atherosclerosis. Atherosclerosis. 2013; 229(2):517-523. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066302/pdf/nihms-462449.pdf
  14. Toth PT, Grabner M, Punekar RS, et al. Cardiovascular risk in patients achieving low-density lipoprotein cholesterol (LDL-C) and particle (LDL-P) targets. Atherosclerosis. 2014; 235:585-591. https://www.atherosclerosis-journal.com/article/S0021-9150(14)01164-2/pdf
  15. Kronenberg F, Utermann G. Lipoprotein(a): resurrected by genetics. J Intern Med. 2013; 273(1);6–30. https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1365-2796.2012.02592.x
    18. Kolata, G. 2004. Experts Set Lower Low for Levels of Cholesterol. New York Times. https://www.nytimes.com/2004/07/13/us/experts-set-lower-low-for-levels-of-cholesterol.html
  16. Scandinavian Simvastatin Survival Study Group. 1994. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). The Lancet. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(94)90566-5/abstract
  17. Ballantyne, C. 2009. Clinical Lipidology. https://www.sciencedirect.com/science/book/9781416054696
    21. Pollack, A. 2015. Eli Lilly Abandons Heart Disease Drug in Final Stage of Trials. New York Times. https://www.nytimes.com/2015/10/13/business/eli-lilly-abandons-heart-disease-drug-in-final-stages-of-trials.html
  18. Golomb, B. A., & Evans, M. A. (2008). Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism. American Journal of Cardiovascular Drugs: Drugs, Devices, and Other Interventions, 8(6), 373–418.
  19. John Munkhaugen, Elise Sverre, Jan E Otterstad, Kari Peersen, Erik Gjertsen, Joep Perk, Lars Gullestad, Torbjørn Moum, Toril Dammen, Einar Husebye. Medical and psychosocial factors and unfavourable low-density lipoprotein cholesterol control in coronary patients. European Journal of Preventive Cardiology, 2017; 204748731769313 DOI: 10.1177/2047487317693134
    24. Karlsson, F. H., Fåk, F., Nookaew, I., Tremaroli, V., Fagerberg, B., Petranovic, D., Bäckhed, F., … Nielsen, J. (2012). Symptomatic atherosclerosis is associated with an altered gut metagenome. Nature communications, 3, 1245.
    25. Jingyuan Fu. 2015. The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids. Circulation Research. 117 (9): 817–824. https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.115.306807