High Cholesterol Wellness Protocol
Cholesterol is a lipoprotein — a waxy substance that’s found in the fats (lipids) in the blood.
There are two primary types of cholesterol:
Low-density lipoprotein (LDL-C) or “bad” cholesterol transports cholesterol throughout your body. LDL-C can build up in the walls of your arteries, making them hard and narrow, a process known as atherosclerosis. High LDL-C levels can increase your risk of heart disease, heart attack or stroke.
High-density lipoprotein (HDL-C) or “good” cholesterol picks up excess cholesterol and takes it back to your liver.
It is estimated that nearly 50% of adults in the U.S. have at least one lipid abnormality; for example, nearly 30% have either elevated LDL-C (bad cholesterol) levels, roughly 25% have low HDL-C (good cholesterol) levels, and about 10% have both.[1]
High LDL-C (bad cholesterol) increases fatty deposits in the blood vessels, which over time may lead to blockages in blood vessels. However, it is now understood that this is a slow and gradual process.
Of greater risk than the gradual blockage of the lumen is having a plaque that is unstable, because it may rupture and break off into the blood stream, causing a heart attack or stroke.[2],[3]
Thus rather than just enlarging the lumen of the blood vessel, more successful therapies address the factors which make a plaque unstable, including inflammation, increased reactive oxygen species, and immune activation.[4]
High blood cholesterol itself does not cause symptoms, so many people are unaware that their bad cholesterol level is too high. In addition to cholesterol levels, a more sophisticated analysis of blood lipids, including measures such as oxidized LDL, cholesterol subfractions, etc., can most effectively determine risk as well as which therapies will be most helpful.
A variety of things can affect cholesterol levels, including diet and lifestyle factors, lack of physical activity, age, gender, and heredity.
Foods high in saturated fat, trans fat, and cholesterol may have a negative impact, but even foods high in refined carbohydrates can have an impact. For example, a spike in blood sugar following a meal (known as postprandial hyperglycemia) is known to increase the proportion of small, dense LDL-C (bad cholesterol), the variant of this type of cholesterol associated with the greatest risk of plaque formation causing blockage in the coronary arteries, as well as arteries throughout the body.[5]
Similarly, consumption of fructose and high fructose corn syrup, which is commonly found in processed foods, has been shown to increase triglycerides, as well as both LDL-C and apoB levels, a strong predictor of future vascular events.[6]
Lack of physical activity and being overweight may also contribute to the inflammation which drives the atherosclerotic process. A large body of evidence has demonstrated an improvement in lipid levels and a reduction in cardiovascular risk with increasing amounts of physical activity.[7],[8]
Lastly, a number of toxins, including cigarette smoke and heavy metals such as lead and arsenic, not only have an adverse effect on lipid levels, they specifically increase cellular stress and inflammation which drive the process of plaque formation.[9],[10],[11],[12]
A blood test to check cholesterol levels (called a lipid panel or lipid profile) typically reports:
- Total cholesterol
- LDL cholesterol
- HDL cholesterol
- Triglycerides — another form of fat in the blood
For the most accurate results, don’t eat or drink anything (other than water) for nine to 12 hours before the blood sample is taken. There are other markers that contribute to plaque build-up. Ask your doctor for an advanced lipid profile that includes other markers of inflammations, as well as a micronutrient panel to see exactly what your individual supplement needs are. These tests include, but are not limited to:
- C-reactive protein: This is an important marker of inflammation, and independently predicts both primary and secondary adverse cardiovascular events.13 Also important, is that the benefit of statin medication may be limited to those with elevated levels of CRP, suggesting that it is the reduction in inflammation, rather than just the lowering of cholesterol, associated with benefit.14, 15
- Cholesterol particle size and number:
- A high particle number and small particle size (for LDL-C) has consistently been associated with greater risk, independently of other markers.16
- LDL-C size and density: very small and dense LDL-C particles have also been shown to be more atherogenic than more large and buoyant particles. These particles contain a higher amount of apoB and therefore are a better marker of risk than absolute LDL-C numbers.17,18 These smaller dense particles also are more likely to have sugar molecules attached to them, carrying that sugar all over the body, which is a factor that increases the risk and is a better marker of LDL.
- Lp(a) also increases the risk for heart disease, independently, which is another marker of inflammation, and appears to be largely inherited through your family genes.19
- Coronary calcium score: Coronary calcium scans use a special X-ray test called computed tomography (CT) to check for the buildup of calcium in plaque on the walls of the arteries of the heart (coronary arteries). Coronary calcium scans are also called cardiac calcium scoring. The coronary arteries supply blood to the heart.
- Vitamin D: Low 25-OH vitamin D levels have been shown in large epidemiological studies to increase the risk for heart disease, heart failure, abnormal lipids, and both all-cause and cardiovascular mortality.20,21,22,23
The most effective food program to help normalize cholesterol levels is a primarily plant-based diet, minimizing salt, sugar, soft drinks, sugar substitutes, alcohol, fatty meats, dairy products, and simple carbohydrates - such as baked goods, white bread and white rice.
Specific foods shown to lower LDL-C (bad cholesterol) are monounsaturated fats (e.g., olive oil) and nuts (including tree nuts, macadamia nuts, almonds, and pistachios), often combined as part of the Mediterranean or Paleo diets.[36],[37],[38],[39]
These diets emphasize fresh, lean meats (preferably grass-produced or free-range), fish, seafood, fresh fruits, vegetables, seeds, nuts, and healthy oils (olive, coconut, avocado, macadamia, walnut, and flaxseed), plant sterols, and viscous fibers, and are a powerful therapeutic intervention, causing significant reductions in LDL-C and blood pressure, with lipid-lowering effects similar to statins in terms of both LDL-C and LDL size.[40],[41]
In addition, Mediterranean, Paleo, and also vegetarian type diets are all low glycemic in composition, which is particularly important in managing high cholesterol, diabetes, and obesity, as sugar intake is linked to abnormal cholesterol, especially a low HDL-C (good cholesterol).[42]
Multiple nutritional supplements have been associated with improved cholesterol levels. This list contains those that have been shown to have the greatest evidence-based benefit.
Beta-Sitosterol (Plant Sterols)
Phytosterols have been found to effectively lower LDL-C (bad cholesterol), having a greater effect when combined with physical activity than either intervention alone.[34],[35]
Suggested dose:
1-2g per day, sometimes incorporated as part of a trans-fat free spread.
Omega-3 Fatty Acids
Increased consumption of DHA and EPA has been associated with reductions in subclinical atherosclerosis and significant improvements in a number of cardiovascular risk factors, including lipids, blood pressure, and inflammatory markers.[24],[25],[26] For individuals with high cholesterol, EPA lowered the risk of heart disease, especially for those patients who had both low HDL-C and elevated triglycerides.[27]
Suggested dose:
EPA/DHA 1-2g per day in a 2:1 or 1:1 ratio. Dosage should be increased to 3g per day if triglycerides are also high.
N-Acetyl Cysteine and L-Arginine
These two nutrients appear to target cellular stress and improve the health of the endothelium (the inner lining of blood vessels). Taken together, they improved LDL-C and HDL-C, blood pressure, as well as oxidized LDL-C.[33]
Suggested dose:
N-Acetyl Cysteine - 600mg twice per day.
L-Arginine - 2-4g per day (in divided doses)
Coenzyme Q10 (CoQ10) - Ubiquinol
This mitochondrial nutrient not only improves cardiovascular risk, at a dosage of 100-200mg per day, it reduces the muscle damage associated with statin drug therapy.[31],[32]
Suggested dose:
100-200 mg per day
Niacin
This B vitamin has been found to improve the composition of LDL-C (bad cholesterol), leading to more large and buoyant particles and less small and dense ones. It is also the most potent agent for raising HDL-C (good cholesterol) levels, which usually increase by 15-35%.[28],[29],[30]
Suggested dose:
1.5-3g of an intermediate or extended release product (not a sustained or immediate release niacin). Because of the current dosing, and sometimes mixed reviews in medical literature, this should only be taken after consulting with your physician.
[1] Ghandehari H, Kamal-Bahl S, Wong ND. Prevalence and extent of dyslipidemia and recommended lipid levels in U.S. adults with and without cardiovascular comorbidities: the National Health and Nutrition Examination Survey 2003-2004. Am Heart J. 2008 Jul;156(1):112-9.
[2] Mallika V, Goswami B, Rajappa M. Atherosclerosis pathophysiology and the role of novel risk factors: a clinicobiochemical perspective. Angiology. 2007 Oct-Nov;58(5):513-22.
[3] Falk E. Pathogenesis of atherosclerosis. J Am Coll Cardiol. 2006 Apr 18;47(8 Suppl):C7-12.
[4] Halvorsen B, Otterdal K, Dahl TB, Atherosclerotic plaque stability--what determines the fate of a plaque? Prog Cardiovasc Dis. 2008 Nov-Dec;51(3):183-94
[5] Blackburn P, Côté M, Lamarche B, et al. Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size. Metabolism. 2003 Nov;52(11):1379-86.
[6] Stanhope KL, Bremer AA, Medici V, et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. J Clin Endocrinol Metab. 2011 Oct;96(10):E1596-605.
[7] Kokkinos P. Physical activity and cardiovascular disease prevention: current recommendations. Angiology. 2008 Apr-May;59(2 Suppl):26S-9S.
[8] Moholdt T, Wisløff U, Nilsen TI, Physical activity and mortality in men and women with coronary heart disease: a prospective population-based cohort study in Norway (the HUNT study). Eur J Cardiovasc Prev Rehabil. 2008 Dec;15(6):639-45.
[9] Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004 May 19;43(10):1731-7.
[10] Navas-Acien A, Guallar E, Silbergeld EK, et al. Lead exposure and cardiovascular disease--a systematic review. Environ Health Perspect. 2007 Mar;115(3):472-82.
[11] Weiss N. Mechanisms of increased vascular oxidant stress in hyperhomocysteinemia and its impact on endothelial function. Curr Drug Metab. 2005 Feb;6(1):27-36.
[12] Prozialeck WC, Edwards JR, Nebert DW, et al. The vascular system as a target of metal toxicity. Toxicol Sci. 2008 Apr;102(2):207-18.
[13] Wilson AM, Ryan MC, Boyle AJ. The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen. Int J Cardiol. 2006 Jan 26;106(3):291-7.
[14] Ridker PM, Danielson E, Fonseca FA, et al; JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207.
[15] Mora S, Ridker PM. Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)—can C-reactive protein be used to target statin therapy in primary prevention? Am J Cardiol. 2006;97(2A):33A-41A.
[16] Ip S, Lichtenstein AH, Chung M, Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern Med. 2009 Apr 7;150(7):474-84.
[17] Davidson MH. Apolipoprotein measurements: is more widespread use clinically indicated? Clin Cardiol. 2009 Sep;32(9):482-6.
[18] Shin MJ, Krauss RM. Apolipoprotein CIII bound to apoB-containing lipoproteins is associated with small, dense LDL independent of plasma triglyceride levels in healthy men. Atherosclerosis. 2010 Feb 24. [Epub ahead of print]
[19] Rasouli M, Kiasari AM. Interactions of lipoprotein(a) with diabetes mellitus, apolipoprotein B and cholesterol enhance the prognostic values for coronary artery disease. Clin Chem Lab Med. 2008;46(5):667-73
[20] Kim DH, Sabour S, Sagar UN, et al. Prevalence of hypovitaminosis D in cardiovascular diseases (from the National Health and Nutrition Examination Survey 2001 to 2004). Am J Cardiol. 2008 Dec 1;102(11):1540-4.
[21] Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2007 Jun 11;167(11):1159-65.
[22] Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008 Jun 23;168(12):1340-9.
[23] Wang TJ, Pencina MJ, Booth SL Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008 Jan 29;117(4):503-11.
[24] Jung UJ, Torrejon C, Tighe AP, et al. n-3 Fatty acids and cardiovascular disease: mechanisms underlying beneficial effects. Am J Clin Nutr. 2008 Jun;87(6):2003S-9S.
[25] Bhatnagar D, Durrington PN. Omega-3 fatty acids: their role in the prevention and treatment of atherosclerosis related risk factors and complications. Int J Clin Pract. 2003 May;57(4):305-14.
[26] He K, Liu K, Daviglus ML, Mayer-Davis E, et al. Intakes of long-chain n-3 polyunsaturated fatty acids and fish in relation to measurements of subclinical atherosclerosis. Am J Clin Nutr. 2008 Oct;88(4):1111-8.
[27] Saito Y, Yokoyama M, Origasa H, et al. Effects of EPA on coronary artery disease in hypercholesterolemic patients with multiple risk factors: sub-analysis of primary prevention cases from the Japan EPA Lipid Intervention Study (JELIS). Atherosclerosis. 2008 Sep;200(1):135-40.
[28] Hausenloy DJ, Yellon DM. Targeting residual cardiovascular risk: raising highdensity lipoprotein cholesterol levels. Heart. 2008 Jun;94(6):706-14.
[29] Kuvin JT, Dave DM, Sliney KA, et al. Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease. Am J Cardiol. 2006 Sep 5;98(6):743-5.
Beta-Sitosterol
Coenzyme Q10 (CoQ10) - Ubiquinol
N-Acetyl Cysteine (NAC)
L-Arginine
Omega-3 Fatty Acids
Multiple nutritional supplements have been associated with improved cholesterol levels. This list contains those that have been shown to have the greatest evidence-based benefit.