As we age, our bodies begin to deteriorate, leading to a variety of age-related diseases. One of the most common conditions that come with aging is cellular aging, which can lead to a decline in eyesight and hearing.
Currently, treatments are available to help slow the progression of these conditions, but they are not always effective. However, recent research has shown that a compound called nicotinamide mononucleotide (NMN) may hold the key to improving eyesight and hearing in those affected by age-related diseases.
NMN is a naturally occurring compound that has neuroprotective effects and can improve overall physiological function.
In this article, we will explore the potential of NMN as a treatment for age-related diseases, specifically regarding improving eyesight and hearing. We will also discuss the current state of treatments for these conditions and their limitations.
Age-related diseases, also known as geriatric diseases, are a group of disorders that occur primarily in older individuals. These diseases are caused by a combination of genetic and environmental factors, with the most significant contributor being the aging process itself.
One of the leading causes of age-related diseases is cellular aging, which is characterized by the gradual deterioration of cells and the decline in their ability to function properly.
One of the most common age-related diseases that affect eyesight is age-related macular degeneration (AMD), which is the leading cause of blindness in people over the age of 60.
Similarly, age-related hearing loss is also a common condition that affects older individuals. Both of these conditions can significantly impact a person's quality of life and independence.
Currently, the main treatments for age-related diseases are focused on slowing the progression of the condition and managing symptoms.
However, these treatments are only sometimes effective and can have a variety of side effects. Additionally, there needs to be more treatments that can actually improve the function of cells and reverse the effects of cellular aging.
NMN for Overall Physiological Function
NMN is a naturally occurring compound found to have neuroprotective effects and can improve overall physiological function.
It is a precursor to nicotinamide adenine dinucleotide (NAD+), which is a coenzyme that plays a critical role in energy metabolism and cellular signalling.
As we age, NAD+ levels decline, leading to a decline in cellular function. NMN has been found to increase NAD+ levels, thus improving cellular function and protecting against age-related diseases.
A recent study found that administering the NAD+ intermediate, nicotinamide mononucleotide (NMN), to mice over a 12-month period effectively mitigated age-associated physiological decline (3).
The study found that orally administered NMN was quickly utilized to synthesize NAD+ in the mice's tissues, suppressing age-associated body weight gain, enhancing energy metabolism, improving physical activity, improving insulin sensitivity and plasma lipid profile, and improving eye function, among other benefits.
The study suggests that NAD+ intermediates, such as NMN, have the potential to be effective anti-aging interventions in humans.
NMN for Improving Eyesight
Recent research has shown that NMN can improve eyesight and hearing in animal models (1). The study found that when NMN was administered after a retinal detachment, it resulted in a significant reduction of damage to the cells in the eye called photoreceptors, as well as a reduction in inflammation.
It also found that NMN helped to preserve the thickness of a layer in the eye called the outer nuclear layer. Additionally, the study found that NMN increased levels of a molecule called NAD+ and increased the activity of two proteins, SIRT1 and heme oxygenase-1 (HO-1), which are essential for protecting cells from damage.
The study suggests that NMN may have therapeutic potential for treating photoreceptor degeneration, which is a type of damage to the cells in the eye that can cause vision loss. It also suggests that the protective effects of NMN may be related to the SIRT1 and HO-1 proteins.
NMN for Hearing Loss
Noise-induced hearing loss is a common condition that affects both young and older individuals. It occurs when loud noise exposure damages the hair cells in the inner ear, leading to a decline in hearing.
Age-related hearing loss is also a common condition that is caused by the gradual deterioration of the auditory system. Both of these conditions can greatly impact a person's quality of life and independence.
The NAD+ precursor NMN has been shown in recent research to prevent noise-induced hearing loss (2). Despite being exposed to noise, mice who were given NN still had their spiral ganglia neurites (which innervate their cochlear hair cells) intact, suggesting that this treatment may be effective in preventing hearing loss.
Also, SIRT3-overexpressing mice were shown to be resistant to noise-induced hearing loss, suggesting that SIRT3, an NAD+-dependent mitochondrial sirtuin, mediates this protective effect.
These results demonstrate that NMN administration activates the NAD+-SIRT3 pathway, therefore decreasing the degeneration of neurites brought on by noise exposure, suggesting a treatment strategy for avoiding this kind of hearing loss.
NMN has been shown to have neuroprotective effects and mechanisms of action in animal models, specifically in regard to improving eyesight and hearing.
It has the potential to improve cellular function and protect against age-related diseases. While more research is needed to fully understand the potential of NMN as a treatment for age-related diseases, the current studies suggest that it may be a promising solution for those affected by cellular aging.
1. Chen, Xiaohong, et al. “Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment.” Aging vol. 12,24 (2020): 24504-24521. doi:10.18632/aging.202453.
2. Brown, Kevin D et al. “Activation of SIRT3 by the NAD⁺ precursor nicotinamide riboside protects from noise-induced hearing loss.” Cell metabolism vol. 20,6 (2014): 1059-68. doi:10.1016/j.cmet.2014.11.003
3. Mills, Kathryn F et al. “Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice.” Cell metabolism vol. 24,6 (2016): 795-806. doi:10.1016/j.cmet.2016.09.013