NMN Supports Cardiovascular Health in 3 Surprising Ways

Declining heart health is a leading cause of death amongst both men and women in the United States, with 1 in 4 deaths per year being attributed to the various cardiovascular conditions. While increasing age is a top risk factor for poor heart health, there are ways to support the cardiovascular system as we grow older.

The compound NMN, or nicotinamide mononucleotide, is a promising supplement for protecting the heart against this age-related dysfunction. Emerging research suggests that NMN supports healthy blood pressure levels and overall cardiovascular health.

In addition to new clinical trials to evaluate the impact of NMN on blood pressure, the potential impacts of NMN on cardiovascular health is well documented. Research has indicated that NMN is cardioprotective in several ways, including improving blood vessel integrity and reducing oxidative damage — the buildup of inflammatory compounds called reactive oxygen species that damage cells.

What Is NMN? An Overview

NMN is important for health and longevity, as it is a precursor to NAD+ (nicotinamide adenine dinucleotide), an essential molecule needed by all cells in the body.

Although essential, levels of NAD+ tend to decline with age, contributing to premature aging — both internally and externally — and disease development. NAD+ also regulates a family of proteins called sirtuins, which play a crucial role in longevity.

NMN has been linked to increased lifespan in animals, improved cognitive and metabolic support, DNA repair, healthy weight management, and support to cardiovascular health.

How Does NMN Support Cardiovascular Health?

Due to its ability to quickly and efficiently enter cells and convert into NAD+, NMN is involved in many cellular and biochemical processes, including those of the heart and vascular systems.

1. NMN Supports Blood Vessel Health

Damage to the vascular endothelium, a thin layer of cells that line the inside of blood vessels, is a leading cause of poor cardiovascular health.

Endothelial damage precedes a buildup of plaque in the arteries that restricts blood flow, which damages cardiovascular function.

With age, both the number and quality of vascular endothelial cells decline. Researchers believe that the subsequent age-related decline in NAD+ levels and sirtuin activity are, in part, responsible for this dysfunction in blood vessel integrity.

In a March 2018 study published in Cell, older mice who received supplemental NMN experienced improved blood flow and capillary density, similar to levels of young mice. This process was mediated by an increase in the activity of sirtuins (specifically, SIRT1) in their endothelial cells.

Similar results were found in a June 2016 paper published in Aging Cell, which looked at older mice with impaired endothelium‐dependent dilation, a measure of endothelial function. After NMN supplementation, the endothelial function of the mice was significantly improved by reducing arterial stiffness and activation of SIRT1. The study also indicates promising implications for NMN to support healthy blood pressure.

Lastly, an August 2019 study published in GeroScience found that NMN-supplemented older mice had improved vascular function, including reductions in plaque buildup and epigenetic rejuvenation of microRNA profiles in the heart. Alterations in microRNA profiles are thought to play a large role in vascular aging and dysfunction. Additionally, the study showed that NMN showed promise for the positive regulation of blood pressure.

Together, these animal studies indicate that supplemental NMN may be an option for reducing the commonly seen age-related vascular dysfunction, thereby supporting cardiovascular health with age.

2. NMN Supports Heart Health by Reducing Oxidative Damage

The blood vessels’ endothelium is often a target of oxidative damage, including a buildup of free radicals and reactive oxygen species (ROS). These harmful molecules also contribute to plaque buildup because oxidized cholesterol particles are responsible for arterial plaque.

In addition, high levels of ROS reduce the availability of nitric oxide, which dilates blood vessels and regulates healthy blood pressure.

Oxidative damage tends to increase with age, as the accumulation of these inflammatory molecules can compound over the years. In the vascular system, oxidative damage can ultimately lead to the senescence, or irreversible growth arrest, of endothelial cells. However, there are ways to mitigate this cellular stress.

In the previously mentioned study published in Aging Cell, NMN supplementation significantly reduced levels of an oxidative compound called superoxide and increased nitric oxide production in older mice.

As discussed in a January 2019 review published in Antioxidants & Redox Signaling, the sirtuin SIRT1 acts as a sensor for ROS, which can offer cardioprotection by inducing oxidative cell death. Upregulating SIRT1 through supplemental NMN and its subsequent conversion into NAD+ may activate this oxidative sensor.

3. NMN Exhibits Cardioprotective Activity

The heart requires a steady supply of energy via ATP to maintain its primary function of circulating blood. The cells’ energy powerhouses, the mitochondria, produce over 95% of the heart’s ATP. Therefore, a breakdown in mitochondrial function is linked to declining cardiovascular function. Mitochondrial dysfunction is common with age and occurs more rapidly when oxidative stress is present.

In a November 2017 study published in the Journal of Molecular and Cellular Cardiology, mice that were genetically susceptible to cardiac stress received short-term administration of NMN. Supplemental NMN protected the mice against failing heart function, preserved mitochondrial structure, and reduced the prevalence of ROS in the heart.

Another condition of declining heart health is ischemia — when blood flow and oxygen to the heart are blocked. A complication after ischemia is called reperfusion injury, or ischemia followed by reperfusion (I/R). I/R is the tissue damage that occurs when blood supply returns to the tissue after a period of ischemia and is a life-threatening event.

A June 2014 study published in PLoS One aimed to determine if NMN could protect the heart against the damage associated with ischemia and I/R. In mice, NMN preserved heart function and reduced damage from I/R injury when injected before an ischemic event, as well as before and during the reperfusion injury. This effect was mediated by sirtuins, as mice whose genes were modified not to contain SIRT1 did not experience the same cardiac benefits.

The results from these studies indicate that NMN may exhibit cardioprotective effects during times of low oxygen and blood flow to the heart, as well as with cases of high oxidative stress or mitochondrial dysfunction. With its ability to reduce oxidative stress, NMN may also play a role in supporting healthy blood pressure levels.

Key Takeaway

• Older adults are more likely to experience declining heart and vascular function with age.
• Supplemental NMN has been shown in animal studies to support blood vessel health and integrity, reduce oxidative damage in the heart and blood vessels, and protect the heart against damaging events. Studies also suggest a connection between NMN and blood pressure.
• However, more research is needed to determine if these cardioprotective benefits apply to humans and the aging population.