Slow Down Your Biological Aging
Aging is the ratio between damage accumulation and compensatory mechanisms. Damage accumulation occurs constantly in our biology and physiology. But over millions of years we have developed mechanisms that allow us to repair this damage. And when we cannot repair it, we can replace these molecules, we throw away the protein, we eliminate the DNA, and we create new DNA, new protein and so on. The ratio between damage accumulation and compensatory mechanisms gives us the rate of aging.
There is a very strong and evolutionary conserved developmental mechanism for compensation of damage inscribed in our DNA that is so redundant and so well maintained that we don’t see aging at the beginning of life.
Accumulation also occurs in the molecules that take care of the damage, and so slowly and progressively, this compensation becomes less effective, because damage accumulation also occurs in the molecules that take care of the damage, and so slowly and progressively more and more damage escapes from compensatory control and this manifests as aging.
Chronological age is one of the biggest risk factors for many common chronic diseases. Some in the field believe that aging itself is a disease, yet regulatory institutions like the Food and Drug Administration (FDA) and the World Health Organization (WHO) do not recognize aging as a disease. Where is the boundary between healthy aging and disease?
As our technologies became more developed and sophisticated, the boundaries between aging and diseases continued to blur. Understanding aging provides the strongest chance to prevent chronic diseases and expand healthspan. This shift creates incredible opportunities, and even private companies have started to become interested in studying aging.
Some people don’t realize, especially physicians, that when we talk about biological aging, it’s something that is occurring before the development of a disease, before the phenotypes are manifesting. And that’s why it’s so important to measure it. We can measure it in individuals that are apparently healthy, identify those that are on accelerated aging trajectory and intervene at the time when those compensatory mechanisms are still there.
The biology of aging is still a relatively young field, but it has grown tremendously over the last two or three decades.
NMN and NAD
Nicotinamide mononucleotide (NMN) and nicotinamide adenine dinucleotide (NAD+) are naturally present in every living organism. NAD+ molecule is central to energy metabolism. Everything happening in any life form, like breathing, moving, recovery is based on biochemical reactions. Every biochemical reaction requires energy. NAD+ is a key molecule in energy production and distribution. NAD+ can directly and indirectly influence many key cellular functions, including metabolic pathways, DNA repair, chromatin remodeling, cellular senescence and immune cell function. These cellular processes and functions are critical for maintaining healthy aging. Aging is accompanied by a gradual NAD+ decline. Decline in NAD+ levels is linked causally to numerous aging-associated diseases, including cognitive decline, cancer, metabolic disease, sarcopenia and frailty. Many of these aging-associated diseases can be slowed down by restoring NAD+ levels. Therefore, targeting NAD+ metabolism has emerged as a potential therapeutic approach to ameliorate aging-related disease, and extend the human healthspan and lifespan.
NAD+ levels can be increased by activating enzymes that stimulate synthesis of NAD+, by inhibiting an enzyme CD38 that degrades NAD+, and by supplementing with NAD precursors, including nicotinamide riboside (NR) and NMN.
NMN (Nicotinamide Mononucleotide)
NMN is one of the main precursors of NAD+. Precursor is a component that is needed to form another component. Taken orally, NMN is rapidly absorbed and converted to NAD+. NAD+ carries electrons from one molecule to another to help facilitate critical reactions and metabolic processes in the body.
NAD+ is an essential and commonly encountered molecule in our body because NAD+ participates in more than half of all biochemical reactions. NAD+ directly or indirectly contributes to cellular functions, such as the regulation of immune cells, metabolic pathways, cellular aging, DNA repair.
NAD+ is well known for its importance in the DNA repair mechanism. As we age, our DNA mutates, in simple terms, mistakes occur in our DNA that can lead to genetic diseases such as cancer. PARP is one of the critical DNA repair proteins. It is also a NAD+ dependent protein, which means that the PARP protein uses the NAD molecule as fuel. Thus, a sufficient amount of NAD is required to ensure the proper activity of PARP and to protect DNA from damage.
NAD+ also contributes to cellular metabolism and energy production. NAD+ is one of the main molecules in the production of cellular energy (ATP) in the Krebs cycle (TCA cycle).
Sirtuins is another group of proteins that gained a lot of scientific interest when it was discovered. Sirtuins have various functions but are best known for contributing to DNA repair, modulating oxidative stress, energy metabolism and increasing healthspan. Like the PARP protein, the sirtuins are also dependent on the NAD+ molecule, so the activity of sirtuins directly depends on the amount of NAD+ in the body.
Recent discoveries have demonstrated an age-dependent decrease in cellular and/or tissue NAD+ levels in laboratory animal models. Moreover, NAD+ depletion has been linked to multiple hallmarks of aging. In premature aging animal models, NAD+ levels are decreased, while NAD+ replenishment can improve lifespan and healthspan through DNA repair and mitochondrial maintenance. New evidence suggests that NAD+ precursors, such as nicotinamide, forestall pathology and cognitive decline in mouse models of Alzheimer’s disease. NAD+ supplementation can inhibit multiple aging features in animal models. This highlights essential roles for NAD+ in maintaining healthy aging, and suggests that NAD+ repletion may have broad benefits in humans.
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