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Impact on Aging

Genomic instability is a fancy way of describing accumulation of DNA damage. As cells age, their chromosomes become less stable. As repair mechanisms fail to correct DNA damage, mutations accumulate and lead to aging and disease. Genomic instability is a key hallmark of aging.

Impact on Aging

As cells divide, the telomere ends of chromosomes get shorter. Eventually, the enzyme that adds telomeric repeat sequences, telomerase, gets silenced and the telomeres are too short for cells to divide.

Impact on Aging

Epigenetic Alteration refers to damage that alters the interpretation of the genome, and not the sequence of the DNA. This happens as cells are exposed to environmental factors, and such changes accumulate over time. This has been correlated with the decline observed in aging cells.

Impact on Aging

As cells age, environmental stresses add up and mechanisms responsible for maintaining proper protein composition (autophagy) start to decline. Proteins lose their stability, autophagic processes start to fail, and misfolded proteins accumulate.

Impact on Aging

Metabolic activities can put stress on our cells. Too much activity, and changes in nutrient availability and composition cause cells to age faster. Metabolism and its byproducts, over time, damage cells via oxidative stress, ER stress, calcium signaling, and mitochondrial dysfunction. Therefore, organisms depend on multiple nutrient sensing pathways to make sure that the body takes in just the right amount of nutrition – not too much, not too little.

Impact on Aging

As cells age, their mitochondria start to lose their integrity due to the build-up of oxidative stress. Compromised mitochondrial function leads to a number of events, such as increased apoptosis induction, that correlate with aging.

Impact on Aging

Cellular senescence is the point at which our cells stop dividing and growing due to damage or lack of necessary components. As cells age, they lose their ability to actively divide and start to undergo senescence.

Impact on Aging

As we age, our stem cells eventually lose their ability to divide. Furthermore, we are unable to replace the stem cells that have migrated, differentiated, or died. As a result, we show outward symbols of aging, such as grey hair.

Impact on Aging

Cells, as they age, show an increase in self-preserving signals that result in damage elsewhere. Altered intercellular communication with aging contributes to decline in tissue health.

Nicotinamide adenine dinucleotide (NAD+) is a key coenzyme found in all living cells. It is a dinucleotide, which means that it consists of two nucleotides joined through their phosphate groups. One nucleotide contains an adenine base, and the other contains nicotinamide.

NAD+ is essential for life, one of the most versatile molecules in the body, and an important area of focus for aging research. Before we dive into the various things NAD+ does in the body, let’s take a quick look at its history.

NAD+ is important for the mitochondria, the powerhouses of our cells, to produce the energy our cells need. It functions as a coenzyme in the mitochondria, allowing the creation of chemical energy that our bodies can then use.

Metabolic processes such as glycolysis, the citric acid cycle (TCA/Krebs cycle), and the electron transport chain inside the mitochondria all rely on NAD+ in order to function.

In its function as a ligand, NAD+ binds to enzymes and transfers electrons between molecules.This means that NAD+ is found in two forms in the cell; NAD+ is an oxidizing agent that takes electrons from other molecules in order to become its reduced form, NADH. NADH can then become a reducing agent that donates the electrons it carries.

As electrons are the atomic basis of cellular energy, transferring them between molecules means that NAD+ works almost like recharging a battery. A battery goes flat because its electrons are used up to provide energy. The electrons cannot return to their charged state without a jolt, and it is the same in our cells. NAD+ gives the molecules the jolt they need to become active again, and in this way, NAD+ is able to increase or decrease enzyme activity, gene expression, and cell signaling.

Due to its critical importance in the body, most organisms can produce NAD+ in a few alternative ways. Humans like us have three major pathways to create NAD+: the de novo pathway, the Preiss–Handler pathway, and the salvage pathway.

In biochemistry, de novo means that a molecule is created directly from another molecule: in the case of NAD+, the niacin molecule is built from scratch using the essential amino acid L-tryptophan (TRP). The de novo is the only non-vitamin B3 pathway for the creation of NAD+.

The Preiss–Handler pathway is one of the vitamin B3 pathways and starts with either nicotinic acid (NA) or niacinamide (NAR). The NA or NAR present in the food we consume is then converted via a series of enzymatic reactions into NAD+. As the above diagram shows, this pathway and the de novo pathway both join at the point where they become NaNM and continue along the same path to become NAD+. Niacin is perhaps the best-known name for nicotinic acid, and as a 2020 human trial showed, niacin increases NAD+ significantly in muscle tissue.

Finally, the salvage pathway converts nicotinamide (NAM), also known as niacinamide, into NAD+. This pathway has nicotinamide mononucleotide (NMN) as an intermediate, and nicotinamide riboside (NR) also uses the same salvage pathway. This pathway is called the salvage pathway because instead of using the usual precursor molecules, such as TRP or Vitamin B3, to make NAD+, this pathway recycles (salvages) NAM, which is often generated from NAD+, back into NAD+ again.

Of the NAD+ pathways, perhaps the most recent focus has been on the salvage pathway and the NAD+ precursor molecules NMN and NR. 

• Boosting energy: Increases energy levels and reduces fatigue.

• Enhancing cognition: Improves focus, memory, and mental clarity.

• Supporting cellular health: Promotes DNA repair and overall cell function.

• Addressing aging: Replenishes declining NAD+ levels, potentially delaying aging.

• Strengthening immunity: Enhances immune system function and resilience.

• Aiding addiction recovery: Alleviates withdrawal symptoms and restores brain function.

The above statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

There are several ways to increase NAD+ levels in the body:

Dietary intake

Consuming foods rich in vitamin B3, such as fish, poultry, whole grains, mushrooms, and peanuts, can help increase NAD+ levels.

Supplements

Various supplements can boost NAD+ levels, including nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), which are both precursors to NAD+.

Exercise

Regular physical activity has been shown to increase NAD+ levels by stimulating cellular energy production and promoting mitochondrial biogenesis.

Caloric restriction

Reducing calorie intake without malnutrition can elevate NAD+ levels and activate sirtuins, leading to enhanced longevity and health span.

Intermittent fasting

Periodic fasting can increase NAD+ levels and stimulate autophagy, a cellular recycling process that promotes optimal cellular function.

Depending on your goals, you might get a:

Microdose (200 mg): Used by healthy folks to get an energy boost.

Low dose (400 mg): The starting dose for anti-aging and reducing fatigue.

Moderate dose (800 mg): Improved cognitive function.

High dose (1000 mg or more): Better neurotransmitter function, fewer withdrawal symptoms.

These rough figures are a starting point: your dose might take trial and error to pinpoint. But the effort is worth the benefits you experience once you nail it down.