Cardiovascular Health and Lipoprotein(a): How to Address a Genetic Issue and Support Cardiovascular Health Naturally

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F1.largeA review article by Dr Carrie Decker ND. Anyone who has ever listened to their own heart with a stethoscope has likely found the lub-dub pattern reassuring, whether they are a doctor or not. The rhythmic regularity of the heart beat at rest can lull us into meditation, much like it helps an infant go to sleep, while the intense beating after exercise further spurs our energy like a beating drum. Our awareness of this internal rhythm often evades us, unless under a high level of exertion, or if an irregular beat sneaks through. Cardiovascular health for many only becomes a concern with age, unless familial factors or birth defects draw it to our attention earlier.


Lifestyle, genetics, and many other factors, several of which can be addressed, and some which cannot, influence the development of cardiovascular disease. The risk of cardiovascular disease increases with increasing age, and being male in gender.[i] Smoking is one well-established risk factor which can be eliminated with the support of smoking cessation programs, medications, counselling, and supplemental therapies. Diabetes, hypertension, and hypercholesterolemia also are well established factors which increase the risk of heart disease and can be addressed by both medications and natural therapies.[ii] A lack of exercise increases the risk of cardiovascular disease,[iii] and as exercise helps to increase high-density lipoprotein (HDL) cholesterol levels, decrease blood pressure, improve insulin sensitivity, and maintenance of a healthy body weight, this should not be surprising. Dietary changes such as reducing the glycemic index and intake of high fat dairy and red meat,[iv] as well as increasing consumption of fruits, vegetables, fiber, and healthy fats supports cardiovascular health.[v] Although light to moderate intake of alcohol reduces the risk of cardiovascular disease, heavy drinking is associated with worse cardiovascular outcomes.[vi]

As we learn more from the information obtained with genetic assessment, we further understand these markers of risk, and more importantly, how to make use of them as well. Elevated lipoprotein(a) levels are associated with coronary heart disease, stroke,[vii] and peripheral vascular disease,[viii] and are primarily dependent on genetics.[ix] And elevations of this protein are not uncommon, with one in five Americans having levels that put them at risk, approximately tripling the likelihood of having a heart attack or stroke at a young age.[x] Even the New York Times recently delved into discussion of this often unchecked risk marker, highlighting the story of Bob Harper, co-host of the hit show “The Biggest Loser,” who was found to have elevated levels of this protein after suffering a massive heart attack at the age of 52.

Despite the genetic predisposition for elevated lipoprotein(a), levels of this protein still can be impacted by natural supplement therapies. Coenzyme Q10, commonly known as CoQ10, is an antioxidant well known for its cardiovascular health supporting benefits. CoQ10 significantly reduces serum levels of lipoprotein(a), with reductions of 31% compared to 8.2% with placebo in one randomized double-blind placebo controlled trial.[xi] CoQ10 has been shown in meta-analysis to improve endothelial function,[xii] and in other studies to reduce LDL oxidation,[xiii] as well as systolic and diastolic blood pressure in patients with diabetes.[xiv] With the use of statin medications, which inhibit an enzyme known as HMG-CoA reductase, it is very important to include CoQ10 as a supplemental therapy as this enzyme is also necessary for production of CoQ10.[xv] Reductions of CoQ10 levels with statin therapies have been shown to be approximately 40%.[xvi] Although this only may contribute to symptomatic myopathy in a small fraction of this population, it is a dramatic decrease which may impact health long-term in many ways.

Tocotrienols are the lesser studied fraction of the naturally occurring vitamin E isoforms, with tocopherols, which are commonly found in nature, dominating scientific research.[xvii] However, tocotrienols are potent antioxidants, quoted in some research as having 40 – 60 times the antioxidant potential of tocopherols, and with this they bring a variety of benefits particularly where cardiovascular health is concerned.[xviii] In addition to helping reduce lipoprotein(a) levels,[xix] tocotrienols have been shown to improve total cholesterol and its fractions, reduce low-density lipoprotein (LDL) oxidation, and improve arterial compliance, that is, the ability of arterial walls to be flexible which directly impacts blood pressure.[xx]

One of the reasons elevated lipoprotein(a) levels may be associated with an increase risk of cardiovascular disease is through its relationship with fibrinogen,[xxi] the glycoprotein in the blood that is converted by thrombin into fibrin, forming a clot in the setting of vascular injury. Nattokinase and lumbrokinase are two potent fibrinolytic enzymes which are used for supporting a healthy balance of circulation and coagulation, and help to address this issue. Both can be useful to help decrease fibrinogen and disintegrate clots by breaking down fibrin, promoting healthy blood flow in not only arteries but also the small capillaries.[xxii],[xxiii] This not only can be helpful for reducing risk of a clot or dissolving an existing one, but also for supporting healthy circulation in any condition in which the other critical elements of Virchow’s triad are compromised.[xxiv] Parameters associated with bleeding should be monitored during nattokinase and lumbrokinase use.

Cardiovascular health is critically important, and for many, addressed all to late. Taking proactive measures to evaluate and support cardiovascular health will help to reduce the risk of future detrimental events.

Dr. Decker is a certified Naturopathic Doctor, graduating with honors from the National College of Natural Medicine (now the National University of Natural Medicine) in Portland, Oregon. Prior to becoming a naturopathic physician, Dr. Decker was an engineer, with graduate degrees in biomedical engineering as well as mechanical engineering from the University of Wisconsin-Madison and University of Illinois at Urbana-Champaign. Having had her own experience of healing from chronic disease conditions with the support of naturopathic medicine, she chose to pursue a career in this healing realm so she could help others as well. Dr. Decker sees patients at her office in Portland, OR, as well as remotely, with a focus on gastrointestinal and liver disease, allergies, mood imbalances, eating disorders, autoimmune disease, chronic fatigue, thyroid dysfunction, women’s health, and skin conditions.


[i] Jousilahti P, Vartiainen E, Tuomilehto J, Puska P. Sex, age, cardiovascular risk factors, and coronary heart disease: a prospective follow-up study of 14 786 middle-aged men and women in Finland. Circulation. 1999 Mar 9;99(9):1165-72.

[ii] Khot UN, Khot MB, Bajzer CT, et al. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA. 2003 Aug 20;290(7):898-904.

[iii] Powell KE, Thompson PD, Caspersen CJ, Kendrick JS. Physical activity and the incidence of coronary heart disease. Annu Rev Public Health. 1987;8:253.

[iv] Bernstein AM, Sun Q, Hu FB, et al. Major dietary protein sources and risk of coronary heart disease in women. Circulation. 2010;122(9):876.

[v] Satija A, Bhupathiraju SN, Spiegelman D, et al. Healthful and Unhealthful Plant-Based Diets and the Risk of Coronary Heart Disease in U.S. Adults. J Am Coll Cardiol. 2017;70(4):411.

[vi] Di Castelnuovo A, Costanzo S, Bagnardi V, et al. Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies. Arch Intern Med. 2006;166(22):2437.

[vii] Emerging Risk Factors Collaboration, Erqou S, Kaptoge S, et al. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009 Jul 22;302(4):412-23.

[viii] Hopewell JC, Clarke R, Parish S, et al. Lipoprotein(a) genetic variants associated with coronary and peripheral vascular disease but not with stroke risk in the Heart Protection Study. Circ Cardiovasc Genet. 2011 Feb;4(1):68-73.

[ix] Boerwinkle E, Leffert CC, Lin J, et al. Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J Clin Invest. 1992 Jul;90(1):52-60.

[x] Rallidis LS, Pavlakis G, Foscolou A, et al. High levels of lipoprotein (a) and premature acute coronary syndrome. Atherosclerosis. 2017 Dec 7;269:29-34.

[xi] Singh RB, Niaz MA. Serum concentration of lipoprotein(a) decreases on treatment with hydrosoluble coenzyme Q10 in patients with coronary artery disease: discovery of a new role. Int J Cardiol. 1999 Jan;68(1):23-9.

[xii] Gao L, Mao Q, Cao J, et al. Effects of coenzyme Q10 on vascular endothelial function in humans: a meta-analysis of randomized controlled trials. Atherosclerosis. 2012 Apr;221(2):311-6.

[xiii] Thomas SR, Neuzil J, Stocker R. Inhibition of LDL oxidation by ubiquinol-10. A protective mechanism for coenzyme Q in atherogenesis? Mol Aspects Med. 1997;18 Suppl:S85-103.

[xiv] Hodgson JM, Watts GF, Playford DA, et al. Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes. Eur J Clin Nutr. 2002 Nov;56(11):1137-42.

[xv] Hargreaves IP, et al.  The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications. Drug Saf. 2005;28(8):659-76.

[xvi] Ghirlanda G, Oradei A, Manto A, et al. Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study. J Clin Pharmacol. 1993 Mar;33(3):226-9.

[xvii] Peh HY, Tan WS, Liao W, et al. Vitamin E therapy beyond cancer: Tocopherol versus tocotrienol. Pharmacol Ther. 2016 Jun;162:152-69.

[xviii] Prasad K. Tocotrienols and cardiovascular health. Curr Pharm Des. 2011;17(21):2147-54.

[xix] Theriault A, Chao JT, Wang Q, et al. Tocotrienol: a review of its therapeutic potential. Clin Biochem. 1999 Jul;32(5):309-19.

[xx] Rasool AH, Rahman AR, Yuen KH, Wong AR. Arterial compliance and vitamin E blood levels with a self-emulsifying preparation of tocotrienol rich vitamin E. Arch Pharm Res. 2008 Sep;31(9):1212-7.

[xxi] Heinrich J, Sandkamp M, Kokott R, et al. Relationship of lipoprotein(a) to variables of coagulation and fibrinolysis in a healthy population. Clin Chem. 1991 Nov;37(11):1950-4.

[xxii] Hsia CH, Shen MC, Lin JS, et al. Nattokinase decreases plasma levels of fibrinogen, factor VII, and factor VIII in human subjects. Nutr Res. 2009 Mar;29(3):190-6.

[xxiii] Cao YJ, Zhang X, Wang WH, et al. Oral fibrinogen-depleting agent lumbrokinase for secondary ischemic stroke prevention: results from a multicenter, randomized, parallel-group and controlled clinical trial. Chin Med J (Engl). 2013 Nov;126(21):4060-5.

[xxiv] Milner M, Makise K. Natto and its active ingredient nattokinase: A potent and safe thrombolytic agent. Alt Comp Therapies. 2002 Jun 1;8(3):157-64

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2 Comments. Leave new

  • Kelly Meadows
    January 6, 2019 8:52 pm

    Thank you for this information. I have high Lp(a) 131 mg/dL but all my other lipids levels are good. I do take water-soluble CoQ10, as well as a myriad of other nutraceuticals but my Lp(a) is still very high. I do not have any polymorphisms in my two main Lp(a) SNPs (rs10455872 and rs3798220), and I am aware that polymorphisms in these SNPs can cause serious health problems like aortic stenosis. I would like to find out if having normal Lp(a) SNPs with high Lp(a) is still dangerous. My CAC score is 36 (out of 4000) and my carotids are clear.
    Would you know who can answer my question about the SNPs?


    • Hi Kelly,
      I have a Lipoprotein(a) score of 249.9 – High.
      Values greater than or equal to 75.0 nmol/L may
      indicate an independent risk factor for CHD,
      but must be evaluated with caution when applied
      to non-Caucasian populations due to the
      influence of genetic factors on Lp(a) across
      How did you have the test to see if you had polymorphisms in your two main LP(a) SNP’s?
      Can my primary doctor check for this or do I need to go to my cardiologist? What is the name
      of the specific blood test that needs to be ordered? I can’t seem to find the answer to these questions online.
      Thank you,


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