The story of NMN
<LifeSpan-Why We Age, and Why We Don't Have To> by David A. Sinclair, Ph. D.
"A NEW YORK TIMES BESTSELLER
“Brilliant and enthralling.” —The Wall Street Journal"
< LifeSpan-Why We Age, and Why We Don't Have To> by David A. Sinclair, Ph. D.
A NEW YORK TIMES BESTSELLER
“Brilliant and enthralling.” —The Wall Street Journal
NMN(β-nicotinamide mononucleotide)
ANTI-AGING REVOLUTION
SLOWS DOWN THE TIME OF AGING
A paradigm-shifting book from an acclaimed Harvard Medical School scientist and one of Time’s most influential people.
It’s a seemingly undeniable truth that aging is inevitable. But what if everything we’ve been taught to believe about aging is wrong?
What if we could choose our lifespan?
In this groundbreaking book, Dr. David Sinclair, leading world authority on genetics and longevity, reveals a bold new theory for why we age. As he writes: “Aging is a disease, and that disease is treatable.”
NMN
(β-nicotinamide mononucleotide)
ANTI-AGING REVOLUTION
SLOWS DOWN THE TIME OF AGING
As a person gets older, their skin changes. It becomes thinner and more easily damaged. The epidermis becomes slower at replacing dead skin cells and the process of healing slows. Overall, a person will have less skin, and it becomes less elastic. Older adults may find that their skin becomes more dry, irritated, and thin. The skin may itch more, bruise, and become infected more easily. There are several reasons why the skin goes through these changes as a person ages, these include environmental, genetic, and cellular factors. Hormonal changes can also impact the skin, as well as exposure to UV rays, which increases the risk of skin damage.Recommended skin care for aged skin adult places particular emphasis on moisturizing, strengthens skin barrier, improves water resistance, reduces oxidation, and keeping it protected from the sun.
NMN (β-Nicotinamide mononucleotide), NMN was researched and presented in many journals like Nature, Science, and Cell metabolism
as a key to anti-aging and it shows the result NMN has the effect of improving ageing.
As we aged, metabolism—how our body converts food to energy—becomes less efficient as our cell’s powerhouses, the mitochondria, decline.
As the result, the creation and utilization of cellular energy, cellular renewal, and the ability of our cells to respond to their changing environment are all impacted.
"NMN targets metabolic aging by supplying declining metabolites and acting to preserve and help generate new mitochondria.
Promotes healthy metabolic aging by: Increasing levels of the critical coenzyme NAD+ via the highly efficient precursor NMN,
Protects and generates new mitochondria to support cellular energy."
FIGURE. Hypothetic molecule mechanisms of NAD+ decreased with aging.
"Oxidative stress, DNA damage, and chronic inflammation are increased with aging, which results in accelerated NAD degradation via activation of CD38 and PARPs, or dysregulation of NAMPT. Finally, decreased levels of NAD+ lead to various metabolic and age-associated diseases. "
Oxidative DNA Damage Accumulates with Age
DNA is vulnerable to oxidative damage which, if not repaired, can trigger mutagenesis and/or cell death via energy restriction.
Phosphorylated-H2AX as a marker for DNA
Phosphorylated-H2AX as a marker for DNA damage in male subjects show a significant correlation with age. Line a represents the correlation for subjects aged between 0–77 years (p = 0.0095; n = 27). Line b shows post-pubescent data (males only) (p = 0.0286; n = 19).
Phosphorylated-H2AX as a marker for DNA
Damage in post-pubescent female subjects shows a significant positive correlation with age (36–76 years) (p = 0.003; n = 22).
NMN (β-nicotinamide mononucleotide) is a key of anti-aging.
As we age, metabolism—how our body converts food to energy—becomes less efficient as our cell’s powerhouses, the mitochondria, decline. As the result, the creation and utilization of cellular energy, cellular renewal, and the ability of our cells to respond to their changing environment are all impacted.
"NMN targets metabolic aging by supplying declining metabolites and acting to preserve and help generate new mitochondria.
Promotes healthy metabolic aging by:Increasing levels of the critical coenzyme NAD+ via the highly efficient precursor NMN,Protects and generates new mitochondria to support cellular energy."
Mitochondria play crucial roles in energy production, metabolism, apoptosis, and intracellular signaling.
Figure. Mitochondria can metabolize fuels, such as fatty acids, amino acids and pyruvate, derived from glucose.
During cellular stress or damage, mitochondria release a variety of signals to the cytosol and the nucleus to alert the cell of changes in mitochondrial function.
Nicotinamide adenine dinucleotide (NAD+) levels in the cells deplete with aging and it is associated with downregulation of energy production in mitochondria, oxidative stress, DNA damage, and inflammatory conditions.
However, NMN, as the precursor of NAD+, can slow down this process by elevating NAD+ levels in the body.
Chronic inflammation and oxidative stress, which come along with aging, are the causes for reduction and inhibition of NAD+ biosynthesis. A number of in vivo studies have indicated affirmative results of therapeutic effects for various age-induced complications with NMN.
NAD+ Biosynthetic Pathways Decline With Age
FIGURE. Hypothetic molecule mechanisms of NAD+ decreased with aging.
"Oxidative stress, DNA damage, and chronic inflammation are increased with aging, which results in accelerated NAD degradation via activation of CD38 and PARPs, or dysregulation of NAMPT. Finally, decreased levels of NAD+ lead to various metabolic and age-associated diseases. "
Nicotinamide adenine dinucleotide (NAD) is a vital metabolic redox coenzyme found in eukaryotic cells and is necessary for over 500 enzymatic reactions. In mammalian cells, NAD+ is synthesized predominantly through NMN, to replenish the consumption by NADase participating in physiologic processes including DNA repair, metabolism, and cell death.
NMN plays a crucial role in various biological processes, including metabolism, aging, cell death, DNA repair, and gene expression.
Oxidative DNA Damage Accumulates with Age
DNA is vulnerable to oxidative damage which, if not repaired, can trigger mutagenesis and/or cell death via energy restriction.
NAD+ related metabolism
Nicotinamide adenine dinucleotide (NAD+) levels in the cells deplete with aging and it is associated with downregulation of energy production in mitochondria, oxidative stress, DNA damage, and inflammatory conditions.
However, NMN, as the precursor of NAD+, can slow down this process by elevating NAD+ levels in the body.
Chronic inflammation and oxidative stress, which come along with aging, are the causes for reduction and inhibition of NAD+ biosynthesis. A number of in vivo studies have indicated affirmative results of therapeutic effects for various age-induced complications with NMN.
THE RESULT OF AGING
Depletion and reduction of NAD+ biosynthesis
Downregulation of energy production in mitochondria
Chronic inflammation and oxidative stress
The thickness of the whole skin layer was significantly thicker in the mice in the NMN+UVB group than in those in the UVB group.
Figure Photomicrograph of skin sections. H&E staining of the skin; epidermal thickness of skin. *p < 0.05 compared to the UVB group; **p < 0.01 compared to UVB group; ***p < 0.001 compared to the UVB group. → ← in indicate the thickness of dermis. Abbreviations: VC+UVB, mice treated with vitamin C(300mg/kg) and UVB irradiation; NMN+UVB, mice treated with nicotinamide mononucleotide (300mg/kg) and UVB irradiation.
The thickness of the whole skin layer was significantly thicker in the mice in the NMN+UVB group than in those in the UVB group.
Figure Photomicrograph of skin sections. H&E staining of the skin; epidermal thickness of skin. *p < 0.05 compared to the UVB group; **p < 0.01 compared to UVB group; ***p < 0.001 compared to the UVB group. → ← in indicate the thickness of dermis. Abbreviations: VC+UVB, mice treated with vitamin C(300mg/kg) and UVB irradiation; NMN+UVB, mice treated with nicotinamide mononucleotide (300mg/kg) and UVB irradiation.
"According to the Toluidine blue staining results, significantly more mast cells were present in the dermal layer in the UVB group (p < 0.05), indicating that UVB irradiation induced the production of mast cells in the skin, thereby resulting in skin inflammation.
The VC+UVB group showed decreased mast cells in mouse skin than the UVB group. After the mice were treated with NMN, the mast cells in mouse skin were significantly reduced (p< 0.05), and the results were similar to the control group."
Figure Photomicrograph of skin sections. H&E staining of the skin; epidermal thickness of skin. *p < 0.05 compared to the UVB group; **p < 0.01 compared to UVB group; ***p < 0.001 compared to the UVB group. → ← in indicate the thickness of dermis. Abbreviations: VC+UVB, mice treated with vitamin C(300mg/kg) and UVB irradiation; NMN+UVB, mice treated with nicotinamide mononucleotide (300mg/kg) and UVB irradiation.