According to the National Vital Statistics Reports, cardiovascular disease is the leading cause of death for both men and women in the United States.[1] Yet it’s estimated that up to 70% of cardiovascular disease, including heart attack and stroke, can be prevented or delayed with dietary choices and lifestyle modifications. Healthcare practitioners play a critical role in helping to reduce the burden of cardiovascular disease and improving our patients’ quality of life.
The role of diet and lifestyle in cardiovascular disease prevention and treatment
Diet and lifestyle play critical roles in cardiovascular disease prevention and treatment. Research supports the following dietary habits as being associated with decreased incidence of cardiovascular disease:[2]
Reduced caloric intake;
Reduced total fat, saturated fat, and trans fat intake;
Reduced cholesterol intake;
Total fat, saturated fat, and trans fat being replaced with monounsaturated, omega-3, and omega-6 fatty acids;
Increased dietary fiber
Increased intake of fruit and vegetables;
Increased intake of micronutrients, including vitamins B6, B9, and B12;
Increased plant protein in lieu of animal protein; and
Decreased portions of highly processed foods.
These dietary habits can be summed up by the saying, “Eat whole foods, mostly plants. Not too much.”
Research also supports the following lifestyle interventions for the prevention and reduction of cardiovascular disease:[2-3]
If applicable, utilize available resources to quit smoking, as this is a significant risk factor for cardiovascular disease;
Engage in physical activity, as this is associated with prevention and better health outcomes in cardiovascular disease;
Maintain ideal weight and blood pressure, as being overweight, obesity, and hypertension are important risk factors for cardiovascular disease;
Manage stress in an ideal way, as high stress levels can increase risk for hypertension and have been linked to cardiovascular disease; and
Get adequate sleep, as suboptimal quality and/or quantity of sleep can increase risk for hypertension and obesity, indirectly increasing risk for cardiovascular disease.
NAD+ levels, sirtuins, and cardiovascular disease
Another means of preventing or delaying the onset of cardiovascular disease involves nicotinamide adenine dinucleotide or NAD+. NAD+ is a cofactor that is present in each of our cells and is involved in multiple essential biological processes. It is important for DNA repair and for optimal health and longevity. Unfortunately, however, NAD+ levels decline as we age. As our patients’ NAD+ levels decrease with age, their risks for age-associated diseases such as cardiovascular disease increase.
The sirtuin family of nicotinamide adenine dinucleotide-dependent deacetylases
Sirtuins are a family of enzymes that are dependent on NAD+ to function. The enzymes in this family, referred to as SIRT1 through SIRT7, play significant roles in health and longevity. For example, SIRT1 activity has been associated with protection from cardiovascular disease and other chronic diseases, including Huntington’s disease, Parkinson’s disease, breast- and other forms of cancer, insulin resistance, diabetes, and hepatic steatosis.[4] Additionally, SIRT1 and SIRT7 control myocardial development and can help decrease stress- and aging-associated myocardial dysfunction [5] and SIRT6 activity has been associated with increased lifespan.[4]
Because sirtuins are dependent on NAD+ to function, their activity also decreases with age. By supporting optimal NAD+ levels in our older patients, we can enhance sirtuin activity and help reduce their risk for cardiovascular and other age-related diseases.
How can you support optimal NAD+ levels?
Some have attempted to support optimal NAD levels by oral supplementation with NAD+ or with NADH, which is the reduced form of NAD. However, research has not been able to demonstrate an appreciable increase in NAD levels after taking these supplements. This may be because NAD is changed into another substance when it passes through the gut and is metabolized or because it simply isn’t bioavailable and therefore absorption is limited.[6-8]
Supplementing with NAD precursors such as nicotinamide riboside, however, has been shown to lead to an increase in plasma NAD levels [9-10] and may be protective against cardiovascular disease.[11]
Another means of raising NAD levels is through intravenous administration of NAD. Because it bypasses the gut and isn’t changed through the metabolic process, intravenous NAD infusions can effectively increase NAD levels.
Conclusion
In conclusion, by encouraging our patients to eat more plant-based foods, limit animal products, quit smoking (if applicable), engage in physical activity, maintain optimal weight and blood pressure, manage stress in a healthy manner, and get adequate sleep, we can effectively reduce their risk for and even help address concerns of cardiovascular disease.
Because of its effect on sirtuin activity, maintaining optimal NAD levels may also offer protection against cardiovascular disease; however, NAD levels decline as we age. By supporting optimal NAD+ levels in our patients, either through NAD+ precursors like nicotinamide riboside or through intravenous administration of NAD, we can help promote longevity and decrease their risk for cardiovascular disease.
Heron, M. Deaths: Leading causes for 2017. National Vital Statistics Reports; vol 68 no 6. Hyattsville, MD: National Center for Health Statistics. 2019.
Forman, D. & Bulwer, B.E. Curr Treat Options Cardio Med (2006) 8: 47. https://doi.org/10.1007/s11936-006-0025-7
Agarwal S. K. (2012). Cardiovascular benefits of exercise. International journal of general medicine, 5, 541–545. https://doi.org/10.2147/IJGM.S30113
Hall, J.A., Dominy, J.E., Lee, Y., & Puigserver, P. (2013). The sirtuin family's role in aging and age-associated pathologies. The Journal of clinical investigation, 123(3), 973–979. https://doi.org/10.1172/JCI64094
Borradaile, N.M., & Pickering, J.G. (2009). NAD(+), sirtuins, and cardiovascular disease. Curr Pharm Des, 15(1), 110-117.
Kimura, N., Fukuwatari, T., Sasaki, R., et al. (2006). Comparison of metabolic fates of nicotinamide, NAD+ and NADH administered orally and intraperitoneally; characterization of oral NADH. J Nutr Sci Vitaminol (Tokyo). 52:142–148
Birkmayer, J.G., & Nadlinger, K. (2002). Safety of stabilized, orally absorbable, reduced nicotinamide adenine dinucleotide (NADH): a 26-week oral tablet administration of ENADA/NADH for chronic toxicity study in rats. Drugs Exp Clin, Res 28:185–192.
Birkmayer, J.G., Vrecko, C., Volc, D., et al. (1993). Nicotinamide adenine dinucleotide (NADH)—a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol Scand Suppl, 146:32–35.
Trammell, S.A., Schmidt, M.S., Weidemann, B.J., et al. (2016). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun, 7, 12948.
Martens CR, Denman BA, Mazzo MR, et al. (2018). Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat Commun, 9(1),1286.
Matasic, D. S., Brenner, C., & London, B. (2018). Emerging potential benefits of modulating NAD+metabolism in cardiovascular disease. American journal of physiology. Heart and circulatory physiology, 314(4), H839–H852. https://doi.org/10.1152/ajpheart.00409.2017