The critical role of NAD+
NAD+ is an essential housekeeping molecule found in every cell of the body, participating in numerous metabolic pathways. It serves as a vital cofactor and driving force for various critical cellular processes, such as energy metabolism, mitochondrial function, biosynthesis, gene expression, DNA repair, immune function, and ageing.
As a coenzyme, NAD+ performs two crucial functions: it acts as an electron transporter in cellular respiration and adenosine triphosphate (ATP) production, and it also serves as a substrate for poly (ADP-ribose) polymerase (PARP) and sirtuin (SIRT) enzymes, which are involved in DNA repair, gene regulation, and cell signalling – as well as being a substrate for CD38 ectoenzymes.
A sustained imbalance in NAD+ metabolism can disrupt physiological functions, potentially leading to diseases such as metabolic disorders, cancer, premature ageing, and neurodegenerative conditions. The impact of NAD+ deficiency on various diseases through the manipulation of cellular communication networks can be mitigated by NAD+ therapeutic intervention.
In essence, without NAD+, we would die. NAD+ is as vital to our bodies as oxygen. By enhancing and optimising NAD+ levels through therapeutic intervention, we can improve both mental and physical human performance and extend our lifespan.
WHAT IS NAD+ USED FOR PHYSIOLOGICALLY?
- Energy Production (ATP)
- Chromosome Stability
- DNA Repair (PARP 1)
- Immune Cell Signalling
- Telomere Elongating
- Neurotransmitter (Brain Health)
- Longevity Mechanisms
NAD+ & GLYCOLYSIS
Figure a. shows the series of steps that make up glycolysis. These steps all happen in the cytoplasm of a cell.
- Glycolysis is the splitting, or lysis, of glucose. It takes place in the cytoplasm of a cell. • Glycolysis is a series of reactions (steps) in which a glucose molecule is eventually split into pyruvate (links Glycolysis to Krebs cycle).
- Hydrogen is transferred to the carrier molecule NAD (nicotinamide adenine dinucleotide). The NAD is now reduced NAD. Two molecules of reduced NAD are produced for each molecule of glucose entering Glycolysis. The hydrogens carried by reduced NAD can easily be transferred to other molecules.
THE LINK REACTION & KREBS CYCLE
NAD+ participates in energy creation by acting as a delivery mechanism. This molecule donates and accepts electrons to and from enzymes in the mitochondrial membrane.
It is these electrons that fuel chemical reactions in the mitochondria. Without a sufficient supply of NAD+, the mitochondria can’t adequately convert the nutrients from the foods we eat into usable energy.
The crucial role of NAD+ in different biological functions such as ageing, metabolism, mitochondrial function, immunological pathways, oxidative stress, gene expression, and apoptosis has been extensively investigated. Many studies have found that altered and reduced NAD+ levels play an important role in stimulating metabolic disorders, neurodegenerative disorders and tumorigenesis.
ELECTRON TRANSPORT CHAIN & OXIDATIVE PHOSPHORYLATION
Cells obtain energy during cellular respiration by oxidising food molecules such as glucose. The energy derived from these actions is used to form ATP. The two forms of NAD constitute a redox couple. This term is used to describe reduced and oxidised forms of the same molecule. The NAD+ is the oxidised form, that is, a state in which it loses an electron. NADH is a reduced form of the molecule, which means that it gains the electron lost by NAD+. The redox reaction described in Figure 1 involves electron transfers which play a central role in energy creation. NAD+ is the main carrier of electrons in the energy-producing processes that take place in a cell’s mitochondria. Mitochondria are known as the “powerhouses of the cell. ” These membrane-bound organelles are found in almost every living cell in the body, including the heart, brain, muscles, and lungs. They generate most of the energy needed to power the cell’s biochemical reactions. The energy produced by the mitochondria is stored in the adenosine triphosphate molecule (ATP).
NAD+ THERAPY TARGETS ALL KIND OF MITOCHONDRIAL DISEASES
NAD+ participates in energy creation by acting as a delivery mechanism. This molecule donates and accepts electrons to and from enzymes in the mitochondrial membrane. It is these electrons that fuel chemical reactions in the mitochondria. Without a sufficient supply of NAD+, the mitochondria can’t adequately convert the nutrients from the foods we eat into usable energy. The crucial role of NAD+ in different biological functions such as aging, metabolism, mitochondrial function, immunological pathways, oxidative stress, gene expression, and apoptosis has been extensively investigated. Many studies have found that altered and reduced NAD+ levels play an important role in stimulating metabolic disorders, neurodegenerative disorders and tumorigenesis.
NAD+ THERAPY HELPS DIRECTLY REPLENISH NAD+ LEVELS
NAD+ BIOSYNTHESIS
To compensate for a reduction in natural NAD levels, most NAD+ is recycled via salvage pathways from nicotinamide riboside (NR), nicotinamide (NAM) and nicotinic acid (NA), which are the three main B3 vitamins that function as precursors of NAD+ (Figure 2). Each contributes to the generation of NAD+ via distinct metabolic pathways but which may be inadequate to support healthy NAD+ levels.
These precursors appear to have differing efficacy as primary sources of sufficient quantities of NAD+ particularly to tissues in which there is high metabolic stress and consequent high demand. Most cells and tissues utilise NR to produce NAD+, however where a deficiency exists, tryptophan catabolism through the kynurenine pathway is the sole route for de novo NAD+ synthesis and interestingly, altered kynurenine pathway activity has frequently been linked to ageing and some age-associated diseases.
CAN DECLINING NAD+ LEVELS BE RESTORED?
Low levels of NAD can be caused by a deficiency in the synthesis/salvage pathways, excessive DNA damage due to free radicals or ultraviolet light, or chronic immune activation. Activation of PARPs in the presence of excessive or accelerated DNA damage leads to depletion of NAD.
When NAD levels become critically low, adenosine triphosphate (ATP) production decreases, ATP stores are utilised and eventually, cell death ensues. The increased activity of CD38 and other NAD- consuming ectoenzymes in chronic immune activation similarly depletes NAD.
Decreased NAD levels may be a major factor in ageing and age-related degenerative diseases of the heart, brain, liver, kidney, and skin.
NAD+ is constantly being consumed by all physical and mental functions and unfortunately, our physiological system consumes NAD+ faster than it can reproduce it once we are into our thirties.
The ageing process, increases chance of DNA damage, inflammation and reduced mitochondrial function which parallelly negatively affects the body’s ability to produce NAD+. Emerging anecdotal and science-based evidence has implicated dysregulated NAD+ metabolism in the age-related functional decline of various tissues and organs, with lower levels of NAD+ correlated with diseases of ageing, other metabolic disorders and neurodegenerative diseases.
On average, NAD+ levels drop by 50% between the ages of 40 and 60 which is the scientific trigger for the decline of many basic physiological and physical functions. Therefore, therapeutically intervening and elevating NAD+ levels offers a solution for preventive health and cellular health optimisation.
WHAT CAUSES DECREASE IN NAD+?
LIFESTYLE CHOICES
SUBSTANCE ABUSE
AGEING
CHRONIC DISEASES
NAD+ IV solution
YuBoost produces and supplies NAD+IV as an intravenous solution, the most effective and efficient way of increasing the body’s own NAD+ levels. Studies prove that restoring levels of NAD+ in your cells has benefits for your brain and body, helping repair DNA, protect brain cells from damage, reduce inflammation and prevent ageing.
