Understanding the Role of NAD+ and NO in COVID-19 Cardiovascular Risks

In the wake of the COVID-19 pandemic, the world has been grappling with the virus's lingering impact on survivors. One particularly concerning trend that has emerged is the increased risk of cardiovascular disease (CVD) among COVID-19 survivors. Recent research from the University of Colorado Boulder sheds light on this issue and offers a potential solution – replenishing NAD+.

The Cardiovascular Connection

COVID-19 has evolved into one of the leading causes of death worldwide. What's intriguing, however, is the link between COVID-19 severity and the subsequent risk of cardiovascular disease. This link became the focus of a study conducted by Freeberg and colleagues, as reported in Nitric Oxide.

While India's medical research body, the Indian Council of Medical Research (ICMR), continues to investigate the connections between heart attacks and both COVID recovery and vaccination, international studies have been yielding noteworthy insights. These studies suggest a concrete association between COVID-19 and a heightened likelihood of heart attacks. Even individuals who experience a less severe COVID-19 infection and recover may face increased prospects of developing heart-related issues or encountering early-onset cardiovascular challenges. A study based in Italy, for instance, highlights the alarming risk of acute myocardial infarction, which was found to be 93 percent higher among COVID-19-recovered individuals when compared to the general population. Furthermore, even those who had experienced mild forms of the disease seem to remain at an elevated risk of heart problems up to a year after their initial infection, as indicated by one of the largest investigations into the long-term cardiovascular consequences of COVID-19. These findings underscore the importance of comprehending the potential impacts of the virus on heart health, even in cases where the infection is relatively mild.

The severity of COVID-19 infection correlates with a higher risk of cardiovascular complications. To investigate this connection, researchers examined the effect of the virus on human aorta endothelial cells (HAECs), the innermost layer of the body's largest artery, the aorta. These cells play a pivotal role in producing nitric oxide (NO), a critical signaling molecule that dilates blood vessels.

The Oxidative Stress Dilemma

Upon infecting HAECs with the SARS-CoV-2 virus, researchers observed a concerning phenomenon. COVID-19-infected HAECs displayed elevated levels of reactive oxygen species (ROS), which are known to cause cellular damage – a condition referred to as oxidative stress. Additionally, these infected cells produced less NO and had reduced levels of NAD+, a coenzyme involved in various cellular processes.

The key takeaway here is that low NAD+ levels are closely associated with blood vessel dysfunction in the context of COVID-19 infection.

NAD+ Precursors to the Rescue

In their quest to rejuvenate COVID-19-affected HAECs, Freeberg and colleagues turned to NAD+ precursors. Specifically, they treated these cells with nicotinamide riboside (NR), a compound that boosts NAD+ levels. The results were promising – NR successfully restored NO and ROS levels to normal. This suggests that NR has the potential to rejuvenate COVID-19-affected HAECs.

However, NR wasn't the only contender in this fight. Another NAD+ precursor, nicotinamide mononucleotide (NMN), was also put to the test. NMN exhibited remarkable results, almost completely restoring NO production to normal levels and significantly reducing ROS production. The implication is clear: NMN can rejuvenate COVID-19-affected HAECs just as effectively as NR.


A Promising Approach for Cardiovascular Health

In summary, the findings of Freeberg and colleagues open a promising avenue in the battle against COVID-19-related cardiovascular risks. Replenishing NAD+ through precursors like NR and NMN can effectively combat oxidative stress and the depletion of NO in COVID-19-affected HAECs. This, in turn, may help prevent cardiovascular dysfunction and disease in survivors of the virus.

NMN's Unique Potential

A separate study highlighted the remarkable capabilities of NMN. Not only did NMN reduce ROS levels in human endothelial cells, but it also addressed senescence, a pro-inflammatory state associated with aging. This suggests that NMN might have broader health benefits beyond COVID-19-related concerns.

NMN vs. NR: The Ongoing Debate

The question remains: is NMN or NR the superior NAD+ precursor? While NMN came very close to restoring NO levels to normal, statistical differences were noted. This discrepancy could be attributed to the number of cells tested for each precursor. More cells were treated with NMN, potentially resulting in more statistically accurate results.

Comparative studies between NMN and NR in humans are still relatively scarce. However, some research has suggested similar metabolic improvements with both compounds in healthy adults. Bryan Johnson's walking longevity experiment also yielded comparable results for NMN and NR. Until more studies emerge to definitively compare these NAD+ precursors, it's premature to conclude that one is superior to the other.

In conclusion, the intricate dance between NAD+ and NO, alongside the havoc wreaked by ROS in human artery cells infected with SARS-CoV-2, unveils a profound story of cellular resilience. NR, acting as a shield, steps in to thwart the loss of NO production and the surge in ROS levels, effectively combating oxidative stress. Meanwhile, NMN takes on the role of a vigilant guardian, preventing the dangerous elevation of ROS and almost single-handedly rescuing NO production from its COVID-19-induced decline. These revelations not only offer a glimmer of hope in the fight against COVID-19-related cardiovascular complications but also shed light on a broader path toward fortifying our cardiovascular health in the face of viral adversaries.