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The shocking truth about fertility and NAD levels

Given the modern world’s accelerated human aging conditions, most of us know at least one person who has struggled or is struggling with fertility issues. 

But did you know that low fertility has recently been linked in academic studies to declining NAD levels? (Research link is at the bottom of the blog.) 

Here’s the nitty-gritty. 

The ovary—the crucial organ for female reproductive function—has a limited lifespan determined by the number of primordial follicles it possesses, established early in development. As females age, this ovarian reserve naturally decreases, leading to diminished fertility in the late 30s and menopause. 

Cells in the ovary require energy for folliculogenesis (which is just a fancy word for the process by which cells develop into a fertilizable egg). NAD plays a vital role in that energy generation, as well as cell signaling and tissue repair, so the decline in ovarian NAD levels with age is linked to reduced fertility. 

Understanding NAD and Ovarian Function: 

While NAD is a crucial component in the energy metabolism of ovarian cells—including those responsible for folliculogenesis and oocyte maturation—during ovulation, there’s a heightened demand for NAD to support various processes, including follicular rupture and DNA damage repair. The balance of NAD is essential for maintaining these ovarian functions. With decline in NAD levels due to health issues or simple aging, ovaries experience a decrease in egg quantity and quality. 

Role of CD38 in Ovarian NAD and Metabolism: 

One factor contributing to age-related decline in NAD levels is the gene CD38. CD38 is known for its diverse roles in regulating immune cell function and metabolic processes. As we age, an increase of CD38 gene expression and activity negatively correlates with tissue NAD levels in various organs. 

In mice studies, when mice lose the CD38 gene’s function, their ovaries have more resources and increased fertility when they’re young. But as they age, the levels of CD38 in ovaries go up, leading to decreased energy production and fertility. 

Which brings us to NAD. 

CD38 is a regulator that controls how much NAD is used in the ovaries, and NAD is crucial for reproductive functions. So when we look at mice without the CD38 gene, we notice that they have improved reproductive abilities, including more follicles and increased fertility. This led us to believe that these mice might have higher levels of NAD, and when we checked their ovaries, we discovered that the NAD levels were significantly higher in the mice without the CD38 gene compared to regular mice, especially in their reproductive prime. 

In summary, as we begin to understand the molecular mechanisms behind ovarian NAD loss, new avenues for enhancing reproductive longevity open up to us. 

We already knew that targeting NAD metabolism would have a dramatic effect on nearly every cellular process in the human body, but this new evidence is pointing us to potential solutions within one of the most challenging and heartbreaking conditions besieging our modern world: infertility. 

If someone you know is struggling with infertility, forward this email to them. NAD is integrally involved in over 500 cellular processes in the human body and is the foundational molecule of life. It should come as no surprise that we now see evidence of low NAD levels leading to infertility. 

Here at Jinfiniti, our flagship NAD supplement, the Accuri® Vitality Boost, is a patent-pending formulation that has been extensively tested in clinical studies by  hundreds of clinics and by thousands of consumers. It allows optimization of NAD in approximately 90% of users, a figure incomparable to any other NAD supplementation on the market. 

Lastly, if you’re interested in going deeper on health-related content, here are a few of our recent posts that you may want to read:

  1. What Does Peak Performance Look Like? 
  2. Why Optimized, Precision Medicine is the Future
  3. 9 Powerful Benefits of Optimizing Your NAD
  4. Andrew Huberman is Wrong About NAD, NMN & Longevity

Research Citation:

CD38 regulates ovarian function and fecundity via NAD+ metabolism from National Institute of Health.

9 Powerful Benefits of Optimizing Your NAD

No other molecule comes close to helping your cells function optimally as much as NAD. While there is still extensive research being done on all the benefits of NAD, we see nine benefits of optimizing your NAD constantly in test results at the Jinfiniti labs.

There are the given benefits right off the bat: the decrease of pain, inflammation and fatigue and the increase of mental clarity, stamina, recovery, energy, and youthfulness. But keep reading to discover how else the wonderful coenzyme of NAD can benefit you.

NAD is arguably the foundational molecule for all of life. Sadly, it declines as we age, but we can bring our NAD levels back to levels most of us haven’t experienced since we were teenagers, thus giving us a trickle-down effect for many of our age-related diseases (see graph below).

If you’re into health, peak performance, biohacking, or you’re just interested in feeling great, what I’m sharing today is relevant for you. Let’s dive into the cellular functions impacted by NAD.

9 Powerful Benefits of Optimizing Your NAD 


Telomere shortening and NAD+ levels are intricately connected in the context of cellular aging and health. Telomeres are the protective caps at the end of our chromosomes, and their gradual shortening over time is a hallmark of the aging process. As telomeres shorten, cells may lose their ability to divide and function properly. NAD+ plays a crucial role in this process by supporting the activity of enzymes called sirtuins, which are involved in DNA repair and maintenance. Sirtuins require NAD+ as a coenzyme to function effectively, and a decline in NAD+ levels can impair their ability to promote telomere stability and repair.


Deregulated nutrient sensing and NAD+ levels are closely intertwined in the context of metabolic health and aging.  NAD+ serves as a critical cofactor of enzymes like sirtuins (sirtuins + NAD are intricately connected to many aspects of aging), which are key regulators of nutrient sensing pathways. When nutrient sensing becomes dysregulated, often due to overnutrition and sedentary lifestyles, it can lead to metabolic dysfunction and age-related diseases. Maintaining adequate NAD+ levels is crucial to support sirtuin activity and restore balance in nutrient sensing.


Stem cell exhaustion and NAD+ levels are intimately interconnected in the context of aging and tissue homeostasis. Stem cells are essential for the regeneration and repair of various tissues, and their capacity to divide and differentiate declines with age. NAD plays a pivotal role in maintaining stem cell function by supporting critical processes like DNA repair and energy production. When NAD levels are low, it contributes to reduced sirtuin activity, leading to inefficient DNA repair and genomic instability within stem cells, which in turn accelerates stem cell exhaustion and compromises tissue repair. By bolstering NAD levels, it’s possible to enhance sirtuin function and potentially rejuvenate stem cell activity.


Disabled microautophagy and NAD levels are intricately related in the context of cellular quality control and overall health. Microautophagy is a cellular process responsible for degrading and recycling damaged organelles and proteins through direct engulfment by lysosomes. NAD plays a crucial role in regulating the activity of sirtuins, which are involved in the maintenance of cellular quality control mechanisms, including autophagy. When NAD levels decline, sirtuin activity may be compromised, impacting microautophagy and other autophagic processes. This can result in the accumulation of cellular debris, impaired organelle quality, and ultimately contribute to cellular dysfunction and aging. By sustaining optimal NAD levels, it may be possible to support the efficient functioning of microautophagy and maintain cellular health, offering potential beefits for overall well-being and longevity.


Inflammaging, the chronic low-grade inflammation that accompanies the aging process, is closely intertwined with NAD levels in the context of immune function and age-related diseases. NAD is a critical cofactor for enzymes known as sirtuins, which play a pivotal role in regulating inflammation and immune responses. As NAD levels naturally decline with age, sirtuin activity may decrease, leading to a state of chronic inflammation. This persistent low-grade inflammation is associated with a range of age-related conditions, including neurodegenerative diseases, cardiovascular issues, and metabolic disorders. By replenishing NAD levels, it is possible to potentially enhance sirtuin-mediated anti-inflammatory mechanisms and mitigate inflammaging, offering a promising approach to promote healthier aging and reduce the risk of age-related diseases.


Mitochondrial dysfunction and NAD levels are intricately linked in the realm of cellular energy production and overall health. Mitochondria are the powerhouse of our cells, responsible for generating ATP, the cellular energy currency. NAD plays a critical role as a coenzyme in the electron transport chain, a fundamental process in mitochondrial ATP synthesis. However, as NAD levels decline with age, the efficiency of mitochondrial function may deteriorate, leading to impaired energy production and an increase in oxidative stress. By maintaining optimal NAD levels, it’s possible to support the function of key enzymes involved in mitochondrial energy production, potentially mitigating mitochondrial dysfunction, and promoting cellular vitality, which is crucial for overall health and longevity.


Cellular senescence and NAD levels are interconnected in the context of aging and tissue function. Cellular senescence is a state where cells lose their ability to divide and function properly, often as a response to various stressors or DNA damage contributing to aging-related diseases and tissue dysfunction. Sirtuins, which play a crucial role in regulating and controlling the process of senescence. Declining NAD levels with age can impair sirtuin function, potentially promoting the accumulation of senescent cells in tissues. These senescent cells release proinflammatory signals.


Loss of proteostasis, the failure to maintain the correct balance of properly folded and functional proteins, is intricately connected with NAD levels in the context of cellular health and aging. NAD is essential for the activity of sirtuins so by replenishing NAD levels, it may be possible to enhance sirtuin-mediated protein quality control mechanisms and maintain proteostasis, potentially mitigating age-related protein aggregation and related diseases, thus supporting overall cellular health.


Altered cellular communication and NAD levels are closely linked in the context of aging and age-related diseases. NAD plays a pivotal role in the regulation of intercellular signaling and communication processes. As NAD levels naturally decline with age, sirtuin activity may diminish, disrupting the finely tuned cellular communication network. By maintaining optimal NAD levels, it is possible to support sirtuin-mediated mechanisms that help restore proper cellular communication and signaling pathways, potentially mitigating age-related cellular dysfunction and promoting healthier aging.

Additional blogs you may enjoy:

Lastly, if you’re interested in going deeper on health-related content, here are a few of our recent posts that you may want to read:

  1. What Does Peak Performance Look Like? 
  2. 9 Powerful Benefits of Optimizing Your NAD
  3. Why Optimized, Precision Medicine is the Future
  4. Andrew Huberman is Wrong About NAD, NMN & Longevity

P.S. Want to boost your intracellular NAD levels? Try a 2 week trial of our Jinfiniti Vitality Boost (do 2 scoops per day), use the discount code welcome20 if you’re a new customer for 20% off your 1st order).