This page covers NAD IV Therapy and explains its benefits. IV League provides mobile NAD IV Therapy.
Nicotinamide adenine dinucleotide (NAD) is a coenzyme that can be synthesized from nicotinamide, a form of vitamin B3. Precursors to NAD are components that the body synthesizes in order to generate NAD.
In addition to its active form, nicotinamide adenine dinucleotide also exists in an inactive form. It is denoted by the symbols NAD+ and NADH, respectively, depending on whether it is in its active or inactive state.
Our body makes its own NAD+ from five dietary precursors:
- Nicotinamide (Nam)
- Nicotinamide mononucleotide (NMN)
- Nicotinamide riboside (NR)
- Nicotinic acid (NA)
Dietary foods rich in NAD+ precursors include:
Every single one of your cells contains NAD, a coenzyme that helps keep DNA intact and repairs damaged cells. The levels of NAD deplete with time because of:
- Environmental factors
There may be a variety of anti-aging effects associated with restoring these levels. When it comes to replenishing your body’s natural supply of NAD+, there is no better method than NAD IV therapy, which administers NAD+ and a combination of supportive vitamins (B-Complex Vitamins, Vitamin B12, Vitamin C, Magnesium, Glutathione).
NAD operates on mitochondria to lengthen telomeres, which are protective caps placed at the ends of chromosomes and get shorter as the body ages.
Telomeres are increased in length as a result of NAD’s action. The activity of the proteins SIRT1 and PARP 1, which are related with a slower pace of ageing and, respectively, an influence on DNA repair, are both increased when NAD is present.
The NAD IV therapy is used to reduce the natural ageing process, promote better general health and physical performance, enhance mental capacities, and even boost resilience to narcotics and addictive behaviors.
It does this by interacting with DNA on a molecular level to ensure that each cell has an adequate supply of energy.
What Are The Benefits Of NAD IV Therapy?
Given the importance of NAD+ to every major physiological activity in the body, as discussed above, maintaining healthy NAD+ levels is a must. IV NAD therapy may be necessary in cases when symptoms of NAD+ depletion are present, such as in pellagra, where symptoms include dermatitis, dementia, and diarrhea. In addition to symptoms of NAD+ insufficiency, there are a number of other situations in which intravenous NAD+ supplementation could be beneficial.
Increases Focus and Cognitive Ability
The word used to indicate difficulty in generating clear, concentrated ideas is the “brain fog”. Or perhaps you’ve observed a decline in your productivity at work or school, or you simply feel like you can’t focus on a single activity. Because it floods your brain’s cells with the nourishment they require, NAD IV treatment can help you think more clearly after a foggy day. The mental fog lifts when you take NAD, allowing you to concentrate on the current task.
Restores Skin from the Sun’s Effects
The DNA of our skin cells is altered by sun exposure, and the results can be seen on the surface in the form of wrinkles, discoloration, and, in the worst case scenario, cancer. As an essential cofactor, NAD+ is essential for fixing broken DNA.
Delays the onset of aging
We cannot stop the passage of time, we are able to slow it down. You will appear and feel younger thanks to this novel approach to vitamin therapy, which targets the molecular causes of ageing.
Therapy for Substance Abuse
Managing addiction is among the most typical cases in which intravenous NAD+ therapy is investigated. Patients detoxing from opioids, alcohol, chemicals, or prescription drugs may find relief from their withdrawal symptoms using intravenous NAD+. IV NAD+ is thought to help drain drugs out of the body and diminish cravings, though the mechanism by which it does this is still being researched.
Reduces Tiredness and Boosts Energy
When you get older, you lose a lot of energy and ambition. An internal cellular imbalance (decreasing NAD+ levels) is responsible for the fatigue we experience. The IV NAD+ Therapy treats this by giving your body the fuel it needs to repair its cells.
Improves the control of long-term illnesses
In addition to the many advantages for the brain, NAD IV therapy also has several other advantages. The pain-relieving effects of antioxidants and inflammation-reduction are both facilitated by the NAD coenzyme. Treatment with NAD can alleviate diabetes symptoms and help those with chronic pain. Since NAD treatment boosts serotonin levels, patients with depression may benefit from receiving an infusion of the compound.
Some athletes have found that increasing their cellular concentrations of NAD+ through intravenous infusion to improve their performance. There is some evidence that giving athletes an intravenous dose of NAD+ prior to a tournament or any other athletic event can raise their energy, cognition, and reaction times. Muscle hypertrophy and hyperplasia, the thickening and enlargement of muscle tissue, may also benefit from NAD+ supplementation, according to research.
History of NAD+ IV Therapy
In 1906, when they were conducting research on alcohol fermentation, two British biochemists made the initial discovery of NAD+. Over the course of the following century, numerous biological activities of NAD+ were progressively identified.
NAD+ has been the subject of research in the field of medicine over the past few decades, which has resulted in the development of an IV form of NAD+ therapy.
Although there is a lot that is known about NAD+, researchers are still trying to figure out what role it plays in the brain. Some hypothesize that NAD+ could be a new type of neurotransmitter.
The chronological discovery of NAD+ is given below:
- Arthur Harden And William John Young Discovered NAD in 1906:
In their seminal research, Arthur Harden and William John Young attempted to gain a better understanding of the role that yeast play in the fermentation process. They made an attempt to replicate the procedure outside of the yeast cells. They were able to crack open yeast cells and separate the contents of the yeast cells into two distinct portions by using laboratory techniques. One of the fractions was heat sensitive, which meant that exposure to heat rendered it incapable of carrying out the fermentation reaction. The remaining portion was not affected by the heat. Harden and Young were able to demonstrate, by the process of separating the fractions and then recombining them, that the fermenting capacity of the heat-sensitive portion was dependent on the heat stable fraction. They came to the conclusion that the heat-sensitive fraction included the proteins that were responsible for fermentation, whereas the heat-stable fraction contained cofactors (such as NAD molecules) and other stable molecules which assisted the proteins in carrying out their operations.
- Hans Von Euler-Chelpin Won The Nobel Prize With Arthur Harden For Their Investigation Into Fermentation in 1929:
Hans von Euler-Chelpin was a student of art at the beginning of his career, but he continued the work of Harden and Young by researching the specific chemical processes that take place throughout the fermentation process. Throughout the course of this research, von Euler-Chelpin was successful in further fractional distillation of the heat-stable component of the yeast cells. As a result of his actions, the NAD molecule was made more pure. The first information regarding the chemical shape and qualities of the co-factor that permitted fermentation reactions to progress is credited to von Euler-Chelpin. This information was discovered by von Euler-Chelpin.
- Otto Heinrich Warburg Demonstrated How NAD Functions In Fermentation Reactions in 1936:
Otto Heinrich Warburg conducted research on fermentation processes in chemistry and made the discovery that NAD is required for a certain kind of chemical reaction that is referred to as a hydride transfer. In hydride transfer processes, an atom of hydrogen and the electrons that normally accompany it are traded for one another. These kinds of reactions are very important to cellular metabolism as well as a wide variety of other chemical activities that are necessary for maintaining life. The research done by Warburg shown that during fermentation, the nicotinamide component of NAD+ accepts the hydride to create NADH, which then enables the reaction to continue.
- Conrad Elvehjem Discovered “Anti-Black Tongue Factor,” The First Vitamin Precursors Of NAD in 1938:
In the 20th century, Pellagra was a widespread condition that was characterized by a variety of unpleasant symptoms, including dementia and diarrhea. Joseph Goldberger is credited with carrying out the preliminary research that established pellagra as a dietary shortage; nevertheless, the results of his studies involving human participants have been criticized. His subsequent studies were unethical since they caused pellagra in prisoners by excluding certain nutritional items from their diets. He did this to see what would happen.
Conrad Elvehjem contributed significantly to this line of research by conducting controlled studies on dogs. Elvehem observed that the tongues of dogs suffering from pellagra, which is caused by an inadequate diet, become dark in color. Elvehjem was able to determine which food extracts assisted dogs recover from the “black tongue” sickness by using this model animal system, which involved giving dogs a different food extracts. Elvehjem observed that nicotinic acid, which he found by carefully purifying the food extracts, was able to heal pellagra, also known as “black tongue illness,” in dogs.
- Arthur Kornberg Discovered The First NAD Biosynthetic Enzyme in 1948:
Following Hans von Euler-early Chelpin’s purification of NAD and Conrad Elvehjem’s exploration of nicotinic acid as the nutrient that deterred pellagra, Arthur Kornberg learned about the process by which NAD is made in the body. Both of these discoveries came after Hans von Euler-early Chelpin’s purification of NAD. At this point in time, the procedures for the synthesis of protein and co-enzymes had reached the stage that scientists were able to purify all of the components that they believed would be required for a reaction. They may then put their hypotheses to the test by recombining the components after they had been cleaned and searching for signs that the reaction had taken place.
In order to demonstrate that the yeast cells contained the components necessary for the NAD-generating reaction, Kornberg isolated and purified those components before combining them in an experiment to show that they were the ones responsible for producing NAD. His research were the first to explain the chemical pathway that cells use to make NAD from the precursor molecule nicotinamide mononucleotide. His experiments were also the first to highlight the importance of NAD (NMN).
- Jack Preiss And Philip Handler Revealed The Pathway Through Which Nicotinic Acid Is Transformed Into NAD in 1958:
Conrad Elvehjem demonstrated that nicotinic acid was the agent that stopped pellagra, but Arthur Kornberg’s work demonstrated only how nicotinamide mononucleotide, and not nicotinic acid, was used by cells to create NAD. Elvehjem’s findings contradicted Kornberg’s findings, which only demonstrated how cells used nicotinamide mononucleotide. Jack Preiss and Philip Handler undertook research to find the process that turned nicotinic acid into NAD. Through their research, they demonstrated that there are three stages involved in the conversion of nicotinic acid to NAD and isolated the enzymes that are responsible for each step. We now call the “route” that nicotinic acid takes to become NAD the Preiss-Handler pathway. This was not the case in the past.
- Mandel And Colleagues Defined The First Chemical Reaction In Which NAD Was Decomposed To Its Constituent Parts in 1963:
Researchers had previously demonstrated that NAD played a vital role in the fermentation process in yeast, as well as in the health of both people and animals. They have discovered many different pathways that the cell utilized in order to produce NAD. No research up to this point had demonstrated a chemical reaction during which the NAD molecule was chosen to take apart, or broken into its constituent parts. Despite the fact that quite a lot was identified about the forms that the NAD molecule was “built” in the cell, no research had demonstrated a chemical reaction up until this point. Through his research, Mandel discovered a process that split NAD into its component molecules, nicotinamide and ADP-ribose.
- Scientists Discovered That Sirtuin Enzymes Break The NAD Molecule Into Its Component Parts in 2000:
In yeast, the enzymes known as sirtuins were found to have the remarkable capacity to lengthen the organism’s lifespan. The finding that yeast sirtuins use NAD to help keep some genes in the cell “quiet” so that they cannot function was made as a result of biochemical studies that analyzed how yeast sirtuins influence the lifespan of yeast. In order to accomplish this, the sirtuin enzymes first cleave NAD into its component parts and then use those parts to “deacetylate” other proteins found in the cell. For instance, deacetylating histone proteins that are connected with DNA can alter the way in which the cell accesses neighboring genes in the DNA.
- Charles Brenner And Colleagues Discovered The Pathway Through Which Nicotinamide Riboside Is Converted Into NAD in 2004:
Brenner and colleagues first uncovered a new precursor or basic structure of NAD, similar to how Conrad Elvehjem and Preiss and Handler discovered nicotinic acid, and then found the enzymes that eukaryotic cells were using to transform that precursor to NAD. This discovery follows in the footsteps of the discoveries of nicotinic acid made by Preiss and Handler. This study revealed a route that converts nicotinamide riboside (NR) to nicotinamide adenine dinucleotide (NAD) in two stages. In further research, it was demonstrated that providing cells with nicotinamide riboside led to increased levels of NAD as well as a longer lifespan in yeast.
- Contemporary – Scientists around the Globe Endure To Research NAD:
As scientists continue their investigation of NAD, our knowledge of this molecule and the myriad ways in which cells can make it and put it to use also continues to expand. As a result of the outcomes of their experiments, researchers from all over the globe are diligently pursuing new avenues of inquiry into potential methods for boosting levels of NAD and its positive impact on human health. Even in the consumer arena, NAD supplementation is beginning to become more popular; this can take the form of IV therapy or the use of supplements that enhance NAD levels. There is nearly a new study published every week that investigates the consequences of NAD precursors like NR and NAM. In addition, registered human trials that are currently in various stages of completion promise to assist us in gaining a more comprehensive understanding of the possible influence that NR and other precursors may have on human health.
The Mechanisms of Action for NAD IV Therapy
The process by which NAD+ and its precursors are absorbed up by cells and tissues is not completely known and is currently the focus of a significant amount of research as well as some disagreement. It is commonly accepted that SLC7A5 and SLC36A4 are responsible for the uptake of tryptophan, whilst SLC5A8 and SLC22A13 are responsible for the uptake of NA.
The rapid diffusion of NAM, which is an uncharged molecule, throughout the plasma and mitochondrial membranes is consistent with the notion that NA and NAM have effects that are additive when it comes to elevating NAD+ levels in cells. There must be specialized transporters in order to move bigger charged molecules.
Neurons are the sole type of cell that are capable of absorbing NAD+, as all other cells are incapable of doing so. Nobody really knows how neurons get their hands on NAD+. ATP/ADP translocase is the mechanism by which NAD+ is transported in bacteria; however, a corresponding NAD+ transporter in human cells has not yet been discovered.
Both NR and NAR are transported in yeast by the nucleoside transporter Nrt1, as well as the equilibrative nucleoside transporter FUN26. This could be true in mammals based on a fall in cellular NAD+ levels that occurs when the nucleoside transporter is suppressed by dipyridamole, despite the fact that there is no direct proof of a particular transporter.
Both serum and the extracellular space contain NAD+, and there is evidence to imply that the same is true for the extracellular space and NMN. Based on these findings, it appears that the circulation of NAD+ precursors may play a role in coordinating the production of NAD+ and functioning as mediators of signals across organs.
Even though some people believe that NMN cannot be detected in the extracellular milieu and that circumstances do not promote catalytic activity, it has been shown that the enzyme that generates NMN, known as eNAMPT, can be found in serum.
This finding is consistent with the model. Oral administration of NMN or NR can increase the levels of NAD+ and NAM in extracellular fluids like blood plasma, which are in the micromolar range under physiological settings. These concentrations can be increased to higher levels.
Transmembrane glycohydrolases CD38 and CD157 can also act as ADP-ribosyl cyclases that catalyze the hydrolysis of NAD+ to generate NAM, and cADPR, a cell-cell messenger that makes it appear to mediate activated monocyte-induced Ca2+ signaling, ROS production, and apoptosis. Extracellularly, nucleotide pyrophosphatases (NPPs) such as CD.
The question of whether or not NMN will be adopted by a transporter is one that is being discussed at the moment. Brenner, Canto, and their colleagues contend that NMN is not taken up at a rate that is fast enough to infer the presence of a transporter, and that both NAD+ and NMN undergo extracellular degradation to create permeable precursors that can be taken up by cells.
They argue that this demonstrates the existence of transporters. On the other hand, Imai contends that this is most likely a phenomenon that is unique to a certain type of cell and that some cell types are able to rapidly take up NMN.
If this is the case, the characterization of the putative transporter will assist in putting an end to the controversy and will assist in determining which cell types and tissues are capable of transporting NMN across the plasma membrane. These problems should be easier to answer if further research is conducted using isotopically labeled NAD+ precursors to track the uptake and metabolism of the compounds in question.
It is not fully understood how the metabolism and biodistribution of NAD precursors work in the various tissues and inside the cells themselves. It is abundantly obvious that the system is complicated due to the fact that there is a variance in the expression of transporter genes, enzymatic machinery, extracellular degradation, and resynthesis.
Although NAMPT is expressed in every tissue of the body, the quantities of expression vary greatly from one tissue to the next. The metabolic profiling of mouse tissues reveals that the activity of NMNAT isoforms, which is considered necessary for amidated NAD+ salvage pathways that utilize NR or NAM, is significantly higher than that of NAMPT and is not rate-limiting in the majority of tissues, with the exception of blood.
This is the case for all tissues except for blood. NADS activity, which is necessary for the deamidated pathway that makes use of NA, it seems to be rate limiting in lung and skeletal muscle, where levels are difficult to detect and the substrate for the enzyme, NAAD, accumulates.
This activity is required for the deamidated pathway that makes use of NA. In order to generate NAD+, the NAMPT-dependent pathway is the preferred mechanism of salvage in the brain and the heart. On the other hand, the NRK-dependent salvage pathways are the primary method of salvage in skeletal muscle.
In addition, the expression study of NRK subtypes reveals that NRK1 is represented everywhere, whereas NRK2 is primarily prevalent in skeletal muscle. This finding supports the first point. In line with this observation, chronic NR administration enhances NAD+ levels in muscle, but not in the brain or in white adipose tissue.
It is interesting to note that the CD38 inhibitor 78c increases NAD+ in mouse liver by more than five times but only increases it by more than one and a half times in muscle, which suggests that CD38 activities are also tissue dependent.
It is not yet known whether the capacity of CD38 to boost NAD+ levels in tissues is attributable to activities inside or outside of the cells themselves; this must be investigated further.
How Is NAD+ IV Therapy Used To Treat Inflammatory Bowel?
The term “inflammatory bowel syndrome” refers to a group of disorders that might manifest themselves in the digestive tract. For instance, Crohn’s disease can affect any region of the gastrointestinal tract, from the mouth all the way down to the anus. Ulcerative colitis, on the other hand, only causes inflammation of the lining of the large intestine and the rectum.
A deficiency in NAD+ causes an erosion of the protective mucus that lines the walls of the intestinal tract, as well as inflammation of the intestinal cells. Experiments have demonstrated that raising the amount of NAD+ in the body can reduce inflammation in the intestinal tract and improve the health of the intestinal wall.
How Is NAD+ IV Therapy Used To Treat Rheumatoid Arthritis?
NAD+ is a compound that has recently drawn the interest of researchers who are trying to determine the factors that contribute to ageing and disorders associated with old age. Recent research from a number of different sources has found a correlation between low NAD+ levels and the advancement of rheumatoid arthritis:
- A recent analysis of related studies in 2018 sheds light on the part that enzymes related to NAD+ play in the development and progression of rheumatoid arthritis (RA), and it investigates the possibility that NAD+ supplementation could be used as a therapeutic cure for RA.
- Supplemental NAD+ boosters may prove to be a viable therapeutic treatment for rheumatoid arthritis, according to the findings of a study that was conducted in 2021 and explored the ability of NAD+ boosters to decrease the oxidative, apoptotic, and inflammatory profiles of RA.
- Another study suggests that fasting is useful in lowering the symptoms of RA, while another study analyses the possibility of a ketogenic diet for decreasing inflammation caused by RA and slowing the progression of the disease.
There is no question that the association between low NAD+ levels and the emergence and development of RA will proceed to intrigue the curiosity of researchers seeking an answer for the rheumatoid arthritis treatment. And we can anticipate that in the future there will be more research that relates NAD+ to autoimmune abnormalities like RA.
How Is NAD+ IV Therapy Used To Treat Multiple Sclerosis?
The immune system is responsible for the erosion of the myelin sheath, which is a protective layer of the nerve cells, in multiple sclerosis. As a direct consequence of this, the signals that are sent between these cells take significantly longer. This is the root source of the symptoms that are connected with the condition, which include numbness, poor balance, and difficulties walking.
Researchers have shown that NAD+ can bring the immune system back into equilibrium and counteract the harm that is caused by autoimmune responses. Some medical professionals have voiced their support for the research and development of NAD-based treatments for those living with multiple sclerosis based on the findings of studies like these.
Intravenous IV NAD+ vs. Oral Supplementation
If you are interested in adding NAD+ to your diet, it is best to check with your doctor first to make sure it is safe for you to do so.
Intravenous: The only approach to guarantee full bioavailability of NAD+ is through intravenous infusion i.e. a drip. If you take high-quality coenzyme supplements, your body will be able to absorb and use all the molecular energy they contain.
Cell regeneration can be sped up using intravenous nicotinamide adenine dinucleotide (NAD) IV therapy. NAD is a coenzyme that helps your body function more efficiently by binding to other substances; this has numerous health benefits, including alleviated withdrawal symptoms during addiction treatment and improved mental acuity.
The NAD coenzyme is injected into the bloodstream, where it may be utilized most effectively by the organism. The NAD coenzyme is essential for proper cell activity, and without it, your body may be lacking the necessary components.
NAD molecules infused into the body connect with proteins to produce enzymes used for fuel metabolism and cellular rejuvenation. Niacin, or vitamin B3, is produced when NAD coenzymes are combined with other substances; it is this vitamin that is responsible for reviving cells from the inside-out.
Your medical condition will determine how often you need to receive NAD+ treatments. Patients with severe exhaustion, for instance, may need therapy once or twice weekly until their energy levels are recovered, and then once a month going forward, as needed.
However, for overall health maintenance, NAD+ doses once a month are frequently adequate.
Oral: Though NAD supplements can be taken orally, it’s not easy for your system to absorb NAD+ this way, making it hard to ensure any positive effects. The most reliable and effective method of increasing your body’s supply of coenzyme right now is intravenous treatment.
Molecular Structure of NAD+ IV
NAD+ is a molecule that exists in living organisms and is composed of atoms of carbon, hydrogen, oxygen, nitrogen, and phosphorus, among other elements. A molecule of ATP, which is an adenosine molecule connected to three phosphate groups, is bonded to a molecule of vitamin B3, which results in the formation of the NAD+ molecule. Niacin is the common name that you will see attached to vitamin B3 on product labels.
In other words, it can be said that ribosylnicotinamide 5′-diphosphate coupled to adenosine 5′-phosphate by pyrophosphate linkage geenrates NAD+. Its molecular formula is C21H28N7O14P2 while average mass is 664.432 Da.