Understanding heart diseases, particularly the risk of heart attack, strokes, valvular diseases requiring stents or cardiac surgery, is a dynamic field. Heart diseases, particularly coronary heart disease (CHD), remain the #1 risk of disability and death in western countries in both men and women. The traditional risk factors for early CHD are smoking, diabetes mellitus, hypertension, elevated cholesterol, and a family history of early CHD. The standard lipid profile has served as a mainstay of CHD risk assessment for decades.
What is Lipoprotein(a) cholesterol?
Lipoprotein(a) (Lp[a]) is a type of cholesterol particle that is not measured on standard lab panels. Measure Lp(a) can help refine strategies of CHD risk assessment. Lp(a) has huge importance as it is estimated to be elevated in approximately 20% of the world's population and is genetically determined. It is a complex structure that has a low-density lipoprotein (LDL) particle with an added apolipoprotein(a) via a totally different hepatic pathway than LDL cholesterol. If inherited, the level of Lp(a) in the blood is elevated and has the potential to do harm by 1-2 years of age! Ongoing strategies to lower Lp(a) in patients at risk or with proven CHD are a recent focus of pharmaceutical companies but none are approved for use at this time. This case study indicates that “natural” approaches using diet and supplements may have a profound impact on the level of Lp(a).
Case Study of Lowering Lp(a) With Natural Therapies
A 60 year old woman referred herself to the Kahn Center for Cardiac Longevity. She had no known CHD but reported a cholesterol as high as 270 mg/dl in the past. Before her visit she had adopted a whole food plant-based (WFPB) diet and lost 40 pounds in 2 years. She brought her most recent cholesterol panel on that diet demonstrating a total cholesterol of 214 mg/dl, a LDL cholesterol of 117 mg/dl, a HDL cholesterol of 82 mg/dl and triglycerides of 75 mg/dl. She had normal measurements of blood sugar, liver, and thyroid function. She weighed 135 pounds and did not smoke. Her mother had a stroke.
After our initial visit she had a coronary artery calcium CT scan demonstrating a score of 178 spread across all of her coronary arteries. This score was in the >90%tile for women her age, so very abnormal. A carotid intimal medial thickness ultrasound (CIMT) showed bilateral carotid plaques <20%. Additional labs demonstrated a Lp(a) level of 162 nmol/L (normal <75). Her Astrocharm score calculated a 10-year risk of heart attack or stroke of 1.5% which is quite low overall. She was presented data on statin cholesterol medication, niacin therapy and other alternatives and chose niacin along with aged garlic (Kyolic), vitamin K2, and an 81 mg aspirin.
After three months on that program of titrating her niacin (Enduracin) to 1,500 mg a day, her repeat laboratory studies demonstrated a Lp(a) of 131 nmol/L, a cholesterol of 216 mg/dl and a normal liver and glucose/insulin panel. She then increased her niacin to 1,000 mg twice a day along with bergamot polyphenol tablets (Bergamet MEGA) twice a day. She did not experience any disabling hot flashes. After 3 months on this combination therapy of a WFPB diet and supplements, repeat fasting labs demonstrated a total cholesterol of 169 mg/dl, HDL of 80 mg/dl, LDL of 75 mg/dl, triglycerides of 67 mg/dl, an apoB of 60 mg/dl, and a Lp(a) 74 nmol/L. Repeat liver and glucose measures remained normal.
Discussion of Natural Cholesterol Lowering
Inherited and elevated levels of Lp(a) are considered both risk factors for CHD, stroke and aortic valvular disease and also causal through pathways that are proatherosclerotic, proinflammatory, and prothrombotic. Currently there is no consensus on the optimal treatment for an elevated Lp(a). Ongoing research on a promising pharmacologic agent with a novel mechanism is hopeful. The usual recommendation in a patient with a high Lp(a) and CHD is to use a statin medication to lower the LDL cholesterol. However, statin medications do not lower Lp(a) levels and frequently cause them to increase through mechanisms that are not known.
Conclusions About Cholesterol Lipoprotein(a) Lowering
The woman reported in this case study from my clinic was offered statin therapy but chose not to initiate it. Therefore, we created a program of diet and supplemental agents that have data for optimizing arterial health and lower both LDL cholesterol and Lp(a). Her most recent laboratory studies show both and optimal LDL and Lp(a) cholesterol values. Not all patients demonstrate the >50% drop in Lp(a) that she demonstrated but many due. Patient education about managing flushing on niacin, watching for skin rashes, and careful monitoring of liver and glucose levels is mandatory. Until therapies are studied with long-term outcome data, as are currently underway but not to be completed for 4-5 years, this case report indicates that there are “natural” approaches that have the capacity to make significant improvements in the lab risk markers of patients with Lp(a) and CHD.
