Most people nowadays are aware of the dire warnings about too much cholesterol in your blood.  With all of the pharmaceutical advertising for cholesterol lowering drugs; statins and a new outrageously expensive class of medication called PCSK9 inhibitors, you might think that simply lowering your cholesterol was the key to heart health and avoiding a heart attack.  But the evidence does not support that conclusion.  Although it is a contributing factor that should be taken into account, current evidence points to cholesterol being misidentified as the main cause of heart disease.

To get to the real underlying factor causing cardiovascular disease, you must become familiar with these two terms; the endothelium and glycocalyx.

The vascular endothelium is the lining of the arteries, veins, capillaries and the heart itself.  It is a single cell layer thick but, by area alone, it is one of the largest organs in the body.  It has multiple functions including the regulation of vascular tone to balance constriction and dilation which manages proper blood flow to various organs.  It regulates wound healing, new vessel formation, level of inflammation and balances thrombosis (clotting) and anticoagulation.  A healthy endothelium produces an abundance of nitric oxide (NO) to manage vascular tone, as well as inhibit platelet and inflammatory cell adhesion and activation.  A dysfunctional endothelium is compromised in its ability to generate NO, becomes stiff, damaged and susceptible to inflammation and plaque formation.   This endothelial dysfunction (ED) is the precursor to cardiovascular disease.  Notably, this ED is also the cause of the other ED, erectile dysfunction.  And studies have shown that erectile dysfunction predicts later cardiovascular events.[1]

The gycocalyx has only recently been recognized as a key element in maintaining vascular health and endothelial function.  It is a delicate, slippery gel meshwork lining the endothelium that provides a protective barrier allowing blood components, fats and cholesterol to glide freely along through your arteries.  Current studies suggest that damage to and dysfunction of the vascular glycocalyx may be the first step in the atherothrombotic process[2]

Factors that adversely affect the glycocalyx and, as a results, the endothelium include tobacco use, obesity, age, hypertension, hyperlipidemia, physical inactivity, and poor dietary habits.  Endothelial function can be measured directly with angiography or noninvasively in an office setting using flow-mediated dilation (FMD), peripheral artery tonometry (PAT) or accelerated plethysmography.  Each of these endothelial function tests measures an nitric oxide dependent process, is a predictive parameter of future cardiovascular events[3][4]and can assess the effectiveness of treatment.

Here are three simple steps to improve endothelial function and insure a healthy glycocalyx which will elevate the performance of your cardiovascular system:

  1. Lifestyle modifications

Mediterranean Diet – has consistently been shown to improve health outcomes, reduce the risk of cardiovascular events. A randomized controlled trial showed improved endothelial function and lowered blood pressure in participants that adhered to the Mediterranean diet over 6 months[5]

Exercise – regular aerobic exercise reduces blood pressure, cardiovascular evens and favorably modifies traditional risk factors.  Exercise helps maintain arterial flexibility as you age, elevates mood and is a great stress reliever.

Manage Stress  – mental stress is a well-known contributor to cardiovascular events.  Stress hormones, including cortisol, are believed to impair endothelial function by interfering with NO production and actions[6].

Avoid tobacco – smoking damages the glycocalyx thereby promoting platelet and inflammatory cell adhesion and impairs endothelial function through impaired NO production and bioavailability.  Smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes.[7]

  1. Improve Nitric Oxide (NO) production

Eat nitrate rich foods – This includes foods such as green leafy vegetables (kale, spinach, arugula, cabbage, lettuce, etc) and beets.  Avoid oral antiseptics because they kill the bacteria needed to convert these nitrates into NO.

L-Arginine – is the physiologic precursor to nitric oxide and has demonstrated clinical benefit in several studies in reducing blood pressure and improving endothelial function.  It must be stressed that the research doses of at least 6 grams/ day, which is much more than the typical L-arginine supplements  at local retailers.  Both Arginine Cardio and ProArgi9+ contain the research doses.

Neo-40 – restores NO through a secondary pathway.  After age 40 the L-arginine pathway can become less efficient in producing NO.  Neo-40’s clinical efficacy has been shown in 6 peer-reviewed, clinical trials. A recent 30 day study showed a 12mmHg drop in systolic blood pressure and 6 mmHg diastolic pressure as well as an improvement in exercise capacity. Professional strength formula  provides more nitric oxide production

  1. Sunlighten™ Infrared Sauna

Spending time in an infrared sauna has a variety of health benefits, including detoxification, relaxation, and post-workout recovery. There are many infrared saunas on the market but only one manufacturer, Sunlighten,  that has clinical trial data supporting its results and documenting significant cardiovascular benefits from their saunas.  A 2005 study at the University of Missouri showed that regular 30 minute sessions over 6 weeks significantly reduced participants’ blood pressure.  Another study published in the Journal of the American College of Cardiology demonstrated improvement of impaired endothelial function in individuals at risk for coronary artery disease over just a 2 week period of time.[8]

Cardiovascular disease remains the leading cause of death in the US and worldwide. We spend billions of dollars treating it and its complications every year. On the other hand, we have known for decades that more than 80% of cardiovascular disease is preventable with modifications in lifestyle. Adopting healthier strategies like those outlined here is a commitment to a forward looking approach to living. The choices you make now will directly influence how you live and function in the decades to come.

 

[1] Inman, BA, etal, A population-based, longitudinal study of erectile dysfunction and future coronary artery disease. Mayo Clin Proc. 2009 Feb;84(2):108-13. doi: 10.4065/84.2.108.

[2] Noble, MI, Drake-Holland, AJ, Vink, H, Hypothesis: arterial glycocalyx dysfunction is the first step in the atherothrombotic process. QJM. 2008 Jul;101(7):513-8. doi: 10.1093/qjmed/hcn024. Epub 2008 Mar 4.

[3] Yeboah J, Folsom AR, Burke GL, Johnson C, Polak JF, Post W, Lima JA, Crouse JR, Herrington DM. Predictive value of brachial flow-mediated dilation for incident cardiovascular events in a population-based study: The multi-ethnic study of atherosclerosis. Circulation. 2009;120(6):502–509.

[4] Anderson T, Charbonneau F, Title LM, Buithieu J, Rose MS, Conradson H, Hildebrand K, Fung M, Verma S, Lonn EM. Microvascular function predicts cardiovascular events in primary prevention: Long-term results from the firefighters and their endothelium (FATE) study. Circulation. 2011;123(2):163– 169.

[5] Davis, CR, Hodgson, J, et al, A Mediterranean diet lowers blood pressure and improves endothelial function: results from the MedLey randomized intervention trial. AJCN Volume 105, Issue 6, 1 June 2017, Pages 1305–1313

[6] Toda, N, Nagasishi How mental stress affects endothelial function. Pflugers Arch. 2011 Dec;462(6):779-94. doi: 10.1007/s00424-011-1022-6. Epub 2011 Sep 23

[7] Messner, B, Bernard, D Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arterioscler Thromb Vasc Biol. 2014 Mar;34(3):509-15

[8] Imamura, M, et al. Repeated thermal therapy improves impaired vascular endothelial function in patients with coronary risk factors. Journal of the American College of Cardiology. 2001, 38 (4): 1983-88.