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Revitalise Your Wellness: Explore NAD+ Therapy

Unlock the fountain of youth with NAD+ Therapy at ACCA Longevity Clinic. Our longevity clinic is at the forefront of cutting-edge treatments, and we’re excited to introduce you to the incredible benefits of NAD+ Therapy. Nicotinamide Adenine Dinucleotide (NAD+) is a natural coenzyme that plays a crucial role in cellular energy production and DNA repair, both of which are fundamental to the ageing process. As we age, our NAD+ levels decline, but with NAD+ Therapy, you can replenish and rejuvenate your cells, enhancing your overall well-being and potentially extending your lifespan. 

NAD+'s Role in Your Metabolism

NAD+ works on mitochondria and increases the length of telomeres, which are the protective caps located at the ends of chromosomes that become shorter as the body ages. NAD+ increases the activity of SIRT1 and PARP 1 proteins, which are linked with a slower rate of ageing and influencing DNA repair respectively. – source

What are the Benefits of NAD+ Therapy?

NAD+ IV Drip Therapy offers a myriad of benefits that can significantly enhance one’s overall well-being. As a coenzyme found in every cell of the body, NAD+ plays a crucial role in various biological processes, including energy production, DNA repair, and cellular regeneration.  Moreover, NAD+ therapy has been linked to potential anti-ageing effects, promoting longevity and overall vitality. 

NAD+ Intramuscular (IM) Injections offer a convenient and effective way to replenish cellular levels of this essential coenzyme, promoting numerous health benefits. By directly injecting NAD+ into the muscle tissue, the body can quickly absorb and utilise this vital compound for optimal cellular function. From enhancing energy production and metabolism to supporting DNA repair mechanisms, NAD+ IM injections provide a holistic approach to wellness. 


NAD+ IM Shot

60 mg Injection
£ 45 single shot
  • NAD+ 5 x IM Shots - £180
  • NAD+ 10 x IM Shots - £340

NAD+ IM Shot

120 mg injection
£ 90 single shot
  • NAD+ 5 x IM Shots - £360
  • NAD+ 10 x IM Shots - £680

NAD+ IV Drip

250 mg IV Drip
£ 175 single IV drip
  • NAD+ 5 x IV Drips - £745
  • NAD+ 10 x IV Drips - £1400

NAD+ IV Drip

500 mg IV Drip
£ 225 single IV drip
  • NAD+ 5 x IV Drips - £955
  • NAD+ 10 x IV Drips- £1800

The above prices are for Non-members. Members receive 20% off the above prices.

If this is your first NAD+ infusion please book the 250mg dose. Please allow up to 90 mins as some people can take the dose of NAD+ faster than others. You are more than welcome to bring along your phone or laptop, to work while you drip!

NAD+ Home Kits 2g Vial

2 Months Supply of NAD+

Introducing the ACCA NAD+ Home Kit – an innovative injectable supplement designed to enhance performance and well-being from the convenience of home, offering a viable alternative to conventional NAD+ IV drips. Each vial holds 2 grams of highly bioavailable NAD+.

Our suggested regimen involves a monthly dosage of 1 gram, divided and administered every other day. With a two-month supply of pure, active NAD+ and included subcutaneous injection equipment, you can easily self-administer the treatment, empowering you to optimise your health and vitality on your own terms. 

Harnessing its anti-ageing capabilities, NAD+ facilitates energy restoration, bolsters cognitive resilience, and counteracts cellular ageing. Our supplement is crafted to fortify natural defences, amplify performance, and invigorate youthful vigour.

For initial usage, we propose administering the NAD+ solution on two consecutive days, followed by alternate-day doses thereafter. With 32 doses per pack, our kit furnishes approximately 8 weeks’ worth of NAD+ supplementation. We maintain the recommendation of an initial loading dose, for discernible effects, which is administered at our clinic

NAD+ Home Kit

2g Vial
£ 495 One time purchase - Subscription 20% Discount
  • 2000 mg Vial of NAD+
  • 40 x Micro Needles
  • 40 x Antibacterial Wipes
  • 1 x Sharps Bin (for disposing of needles)
  • 1 x Instruction Guide (for self injecting subcutaneously)

Please note that NAD + therapy is not recommended for the following people:
Those in active cancer treatment, in recent remission or have not yet been discharged from care and are still undergoing annual reviews.

Speak to our team for more personalised advice if:
You live with an autoimmune disorder, including long COVID. Please bear in mind that this treatment can occasionally intensify your symptoms and make side effects from the NAD + therapy more pronounced.

Published Science Articles and References

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor in all living cells that is involved in fundamental biological processes. NAD+ depletion has been associated with hallmarks of aging and may underlie a wide-range of age-related diseases, such as metabolic disorders, cancer and neurodegenerative diseases. Emerging evidence implicates that elevation of NAD+ levels may slow or even reverse the aspects of aging and also delay the progression of age-related diseases. Here we discuss the roles of NAD+-synthesizing and -consuming enzymes in relationships to aging and major age-related diseases. Specifically, we highlight the contribution of NAD+ depletion to aging and evaluate how boosting NAD+ levels may emerge as a promising therapeutic strategy to counter aging-associated pathologies and/or accelerated aging.

Nicotinamide plays a protective role in hypoxia-induced cardiomyocyte dysfunction. However, the underlying molecular mechanisms remain poorly understood. The purpose of this study was to investigate these and the effect of nicotinamide pretreatment on hypoxic cardiomyocytes.

Poly(ADP-ribose)-1 (PARP-1) is a key mediator of cell death in excitotoxicity, ischemia, and oxidative stress. PARP-1 activation leads to cytosolic NAD(+) depletion and mitochondrial release of apoptosis-inducing factor (AIF), but the causal relationships between these two events have been difficult to resolve. Here, we examined this issue by using extracellular NAD(+) to restore neuronal NAD(+) levels after PARP-1 activation. Exogenous NAD(+) was found to enter neurons through P2X(7)-gated channels. Restoration of cytosolic NAD(+) by this means prevented the glycolytic inhibition, mitochondrial failure, AIF translocation, and neuron death that otherwise results from extensive PARP-1 activation. Bypassing the glycolytic inhibition with the metabolic substrates pyruvate, acetoacetate, or hydroxybutyrate also prevented mitochondrial failure and neuron death. Conversely, depletion of cytosolic NAD(+) with NAD(+) glycohydrolase produced a block in glycolysis inhibition, mitochondrial depolarization, AIF translocation, and neuron death, independent of PARP-1 activation. These results establish NAD(+) depletion as a causal event in PARP-1-mediated cell death and place NAD(+) depletion and glycolytic failure upstream of mitochondrial AIF release.


lzheimer’s disease (AD) is a major neurodegenerative disease of old age, characterised by progressive cognitive impairment, dementia and atrophy of the central nervous system. The pathological hallmarks include the accumulation of the peptide β-amyloid (Aβ) which itself is toxic to neurons in culture. Recently, it has been discovered that Aβ activates the protein poly(ADP-ribosyl) polymerase-1 (PARP-1) specifically in astrocytes, leading indirectly to neuronal cell death. PARP-1 is a DNA repair enzyme, normally activated by single strand breaks associated with oxidative stress, which catalyses the formation of poly ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD(+)). The pathological over activation of PARP-1 causes depletion of NAD(+) and leads to cell death. Here we review the relationship between AD and PARP-1, and explore the role played by astrocytes in neuronal death. AD has so far proven refractory to any effective treatment. Identification of these pathways represents a step towards a greater understanding of the pathophysiology of this devastating disease with the potential to explore novel therapeutic targets.


A G-protein-coupled receptor [GPR109A/HM74A, mouse PUMA-G (protein upregulated in macrophages by interferon-gamma)] was found to mediate the antilipolytic effect of niacin via inhibition of adenylyl cyclase in adipocytes. The same receptor in skin Langerhans cells mediates the common flushing side effect. The endogenous ligand for the receptor may be beta-hydroxybutyrate. Among nine controlled clinical trials using niacin, mostly combined with other drugs, statistically significant positive impact on clinical or anatomic cardiovascular end-points was found in seven, which represents a remarkably consistent record of benefit. Although niacin induces insulin resistance, deterioration of glycemic control in diabetes is usually minor, and there is no evidence of increased incidence of new onset diabetes. Hepatic toxicity is common with higher doses of sustained-release niacin but rare with immediate-release and extended-release niacin at doses up to 2000 mg/day. Extended-release and immediate-release niacin do not substantially potentiate myopathic effects when given in combination with statin.


Nicotinamide (NAM) at doses far above those recommended for vitamins is suggested to be effective against a wide spectrum of diseases and conditions, including neurological dysfunctions, depression and other psychological disorders, and inflammatory diseases. Recent increases in public awareness on possible pro-longevity effects of nicotinamide adenine dinucleotide (NAD+) precursors have caused further growth of NAM consumption not only for clinical treatments, but also as a dietary supplement, raising concerns on the safety of its long-term use. However, possible adverse effects and their mechanisms are poorly understood. High-level NAM administration can exert negative effects through multiple routes. For example, NAM by itself inhibits poly(ADP-ribose) polymerases (PARPs), which protect genome integrity. Elevation of the NAD+ pool alters cellular energy metabolism. Meanwhile, high-level NAM alters cellular methyl metabolism and affects methylation of DNA and proteins, leading to changes in cellular transcriptome and proteome. Also, methyl metabolites of NAM, namely methylnicotinamide, are predicted to play roles in certain diseases and conditions. In this review, a collective literature search was performed to provide a comprehensive list of possible adverse effects of NAM and to provide understanding of their underlying mechanisms and assessment of the raised safety concerns. Our review assures safety in current usage level of NAM, but also finds potential risks for epigenetic alterations associated with chronic use of NAM at high doses. It also suggests directions of the future studies to ensure safer application of NAM.


Chronic fatigue syndrome (CFS) is a chronic and extremely debilitating illness characterized by prolonged fatigue and multiple symptoms with unknown cause, diagnostic test, or universally effective treatment. Inflammation, oxidative stress, mitochondrial dysfunction, and CoQ10 deficiency have been well documented in CFS. We conducted an 8-week, randomized, double-blind placebo-controlled trial to evaluate the benefits of oral CoQ10 (200 mg/day) plus NADH (20 mg/day) supplementation on fatigue and biochemical parameters in 73 Spanish CFS patients. This study was registered in (NCT02063126). A significant improvement of fatigue showing a reduction in fatigue impact scale total score (p<0.05) was reported in treated group versus placebo. In addition, a recovery of the biochemical parameters was also reported. NAD+/NADH (p<0.001), CoQ10 (p<0.05), ATP (p<0.05), and citrate synthase (p<0.05) were significantly higher, and lipoperoxides (p<0.05) were significantly lower in blood mononuclear cells of the treated group. These observations lead to the hypothesis that the oral CoQ10 plus NADH supplementation could confer potential therapeutic benefits on fatigue and biochemical parameters in CFS. Larger sample trials are warranted to confirm these findings. Antioxid. Redox Signal. 22, 679–685.



Nicotinamide adenine dinucleotide (NAD+) participates in redox reactions and NAD+-dependent signaling processes, which involve the cleavage of NAD+ coupled to posttranslational modifications of proteins or the production of second messengers. Either as a primary cause or as a secondary component of the pathogenic process, mitochondrial dysfunction and oxidative stress are prominent features of several neurodegenerative diseases. Activation of NAD+-dependent signaling pathways has a major effect in the capacity of the cell to modulate mitochondrial function and counteract the deleterious effects of increased oxidative stress. Recent Advances: Progress in the understanding of the biological functions and compartmentalization of NAD+-synthesizing and NAD+-consuming enzymes have led to the emergence of NAD+ metabolism as a major therapeutic target for age-related diseases.Accordion Content.


Frequently Asked Questions

NAD+ is a coenzyme found in all living cells. It’s responsible for transferring electrons and hydrogen in the Krebs cycle, making it a vital component for producing all of the energy your body uses. It’s involved in over 100 metabolic processes, and is considered one of the most essential building blocks for life. Unfortunately, NAD+ levels decrease as you age and in response to psychological illnesses. This negatively impacts your health in many ways. Boosting your NAD+ can help restore your natural and healthy levels, enhancing your physical and mental wellbeing. 

NAD+ infusion therapy promotes healthier aging and can help several mental illnesses, including substance abuse disorders, mood disorders, anxiety, and PTSD. It can also treat Lyme disease due to its ability to aid enzymatic functions. 

Restorative processes depend on NAD+, and shortages can cause problems such as metabolic decline, cognitive issues, and a lowered immune system. An NAD+ infusion helps counteract this, preventing issues before they arise. It also helps protect your neurons against the effects of neurodegenerative diseases. 

NAD+ is necessary for optimal mental health and recovery. NAD+ protects your neurons from damage, and improves your cognitive function and mental clarity. It also combats stress, fatigue, exhaustion, and a lack of motivation. 

NAD+ infusion therapy is a completely safe treatment option. It’s a natural substance used in the body and is readily incorporated. 

We highly recommend that you consult with our psychiatrist, although a referral is only required if you are seeking treatment for substance abuse. 

You can eat and drink before your infusion, although eating junk food is not recommended. 

During the infusion, NAD+ can cause side effects such as nausea, brain fog, cramping, and muscle fatigue. However, these can often be relieved through slowing the IV drip. 

Yes. There aren’t any lasting amnesiac or psychoactive effects of the infusion, so it’s safe to drive home afterward. 

To find out more about NAD+ therapies or any of our other wellness services you can contact us, by email, using the button below. Alternatively please call us on (028) 9013 4407.
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