What’s This NAD All About? NAD—Why Is It So Important?

NAD (Nicotinamide Adenine Dinucleotide) is a coenzyme found in every cell in our bodies. It is essential to metabolism, the life-sustaining chemical reactions needed to convert energy in food to the energy to run our body’s cells. NAD is also required to turn food into the building blocks of proteins, lipids, nucleic acids (DNA and RNA), and some carbohydrates, as well as elimination of wastes. Normal NAD levels are essential to proper functioning of virtually every metabolic activity, and decreases in NAD are associated with aging, fatigue, decreased cognitive function, increased cholesterol, and may have a role in development of certain cancers.

NAD was first discovered by British scientists in 1906 while researching alcohol fermentation. After this initial discovery, researchers continued to study the details of NAD function in the body. NAD production decreases as we age, with physical and cognitive declines. NAD is critical to so many bodily processes on a cellular level that inadequate NAD levels can affect:

·         Aging

·         Neuologic function

·         Energy and metabolism

·         Regulation and reduction of inflammation and DNA damage/repair

·         Drug/Antibiotic/Anti-cancer pharmacology

·         Overall Health

Thus far, we’ve discussed how NAD is fundamental to a person’s cellular-level well-being, and how inadequate amounts of NAD could negatively affect so many critical functions. But what is the basic process by which this occurs? Let’s delve into cellular building blocks for part of the answer.

Mitochondria are the energy-producing organelles found in large numbers in most cells, and mitochondrial damage is associated with many of the negative things on the list above. This is primarily because mitochondrial DNA is highly susceptible to mutations, since it does not have the better DNA repair mechanisms seen elsewhere in the cell’s nucleus, and because mitochondria are a major producer of free radicals which damage the mitochondrial DNA. One result (of many not-so-good things) of dysfunctional mitochondria is damaged (shortened) telomeres. Telomeres are the protective caps on the ends of chromosomes, and shortened telomeres are associated with the aging process. Recent studies have demonstrated that patients with critically short telomeres exhibit lower NAD levels, and how increasing NAD may help combat one factor in the aging process.

Even though our bodies naturally produce NAD, it is unfortunately not enough to keep up with the demands that occur as we age. This is why Hydrate IV Therapy NAD infusions exist!

Let’s discuss a bit about the different administration routes NAD can be given. These include intravenous (IV), intramuscular (IM) shots (jabs if you’re British), nasal spray, and oral. Each of these routes has differences in how effectively and quickly NAD is absorbed into the body.

The fastest, most direct, and most complete route is IV. This allows the NAD to be directly introduced into the bloodstream for immediate absorption into the body’s cells, bypassing the digestive process which breaks down nutrients and medications. In addition, since the NAD is put into IV fluids, this aids the kidneys’ elimination of wastes and toxins as well.

IM shots require a needle injection into a large muscular area where it is broken down and absorbed. This also bypasses the digestive system, but takes much longer to reach the bloodstream, and may delay the desired effects of the NAD.

Nasal sprays work by introducing a mist/spray into the nostril where the NAD is absorbed via the mucous membrane. This route has a slower rise in NAD levels, which can be beneficial for those who need to maintain NAD levels over longer periods of time, but who will not see the more rapid rise in levels as with IV use. Some find nasal administration of NAD (or any substance, for that matter) uncomfortable.

Lastly is the oral route. This would involve taking NAD as a pill or a drink. This route involves breakdown by stomach acid and the digestive process before reaching the bloodstream. Not all of the NAD given by this route will be available for utilization, as a fair amount is lost through the digestive process. Orally is also the slowest route of absorption, leading to delayed and diminished response in seeing results.

While all routes can be effective in their own way, please remember this. Even though NAD naturally occurs in our body, NAD supplements are manufactured in a laboratory. Although reactions are quite rare when taking NAD, the only route of administration that can be stopped immediately is an IV, as the infusion is shut off and discontinued. All the other routes do not have the same advantage that IV infusions do since they cannot be stopped once they are introduced into the body.

Overall;, NAD is a superb way to aid in many changes we all see as we progress through life’s ups and downs. Although NAD is not a “cure” for aging, it is a tool that can be used to potentially help with many of the issues listed above. Below is a video that further discusses NAD and its advantages.

Telomeres are specialized nucleoprotein structures that form protective caps at the ends of chromosomes. Short telomeres are a hallmark of aging and a principal defining feature of short telomere syndromes, including dyskeratosis congenita (DC). Emerging evidence suggests a crucial role for critically short telomere-induced DNA damage signaling and mitochondrial dysfunction in cellular dysfunction in DC. A prominent factor linking nuclear DNA damage and mitochondrial homeostasis is the nicotinamide adenine dinucleotide (NAD) metabolite. Recent studies have demonstrated that patients with DC and murine models with critically short telomeres exhibit lower NAD levels, and an imbalance in the NAD metabolome, including elevated CD38 NADase and reduced poly (ADP-ribose) polymerase and SIRT1 activities. CD38 inhibition and/or supplementation with NAD precursors reequilibrate imbalanced NAD metabolism and alleviate mitochondrial impairment, telomere DNA damage, telomere dysfunction-induced DNA damage signaling, and cellular growth retardation in primary fibroblasts derived from DC patients. Boosting NAD levels also ameliorate chemical-induced liver fibrosis in murine models of telomere dysfunction. These findings underscore the relevance of NAD dysregulation to telomeropathies and demonstrate how NAD interventions may prove to be effective in combating cellular and organismal defects that occur in short telomere syndromes.