The Ultimate Guide to NAD Therapy: Combat Fatigue and Low Energy

There is a molecule inside every cell in your body that quietly determines how well those cells function. Not how they look. Not how old you are chronologically. But how efficiently they convert fuel into energy, repair damage, regulate inflammation, and support cognitive performance.

That molecule is NAD+.

Most patients who present with persistent fatigue, brain fog, or a recovery that is no longer what it used to be are not imagining those changes. Something in the underlying biology has shifted. Very often, NAD+ is part of that picture.

But before we get to the molecule, we need to start where the conversation actually belongs: with longevity medicine, what it is, what it is not, and why it matters to anyone who wants to understand what is actually happening as they age.

Part One: What longevity medicine actually is

Most people arrive at longevity medicine through a single question. Not a grand philosophical question about living forever. A practical, personal one. Something along the lines of: why does my skin look so different from how I feel inside? Or: why am I recovering more slowly than I used to? Or simply: why does everything feel harder to maintain than it did ten years ago?

These questions sound like aesthetic concerns. They are not. They are biological ones.

Longevity medicine is the clinical science of slowing biological ageing, extending healthspan, and maintaining vitality across the decades. It is not biohacking. It is not six-figure protocols for wealthy early adopters. It is a clinical framework grounded in established biochemistry, applied preventively rather than reactively.

"Longevity medicine is what happens when you stop asking how to treat the symptoms of ageing and start asking what is driving the biology underneath them. It's the same shift that happened in cardiology when we stopped just treating heart attacks and started measuring the factors that cause them." — Nurse Marina, EMSc Longevity, Geneva College of Longevity Science

The distinction between lifespan and healthspan is the one that matters most. Lifespan is how long you live. Healthspan is how long you live well, with sufficient energy, cognitive function, physical capacity, and resilience to do the things that make life worth living. These two numbers are not the same. In the UK, they are diverging.

According to the Health Foundation's 2025 analysis, the gap in healthy life expectancy between the most and least deprived deciles in England is now 19.4 years for males and 20.3 years for females. In Richmond, healthy life expectancy for men is 69.3 years. In Blackpool, it drops to 50.9. The biology of ageing does not just vary by age. It varies by postcode.

Longevity medicine is the clinical discipline that asks: why does this happen, what drives the gap, and what can be done about it?

Part Two: The biology of healthspan inequality

I want to be specific about the mechanisms, because the mechanism is important and it connects directly to the clinical science I practise every day.

The gap in healthy life expectancy is not primarily genetic. Genetics accounts for roughly 20 to 30% of how we age. The rest is driven by modifiable biological factors: chronic inflammation, hormonal decline, mitochondrial function, sleep quality, metabolic health, and the accumulated effects of psychological stress.

These factors do not affect everyone equally. Chronic stress from financial insecurity elevates cortisol consistently and measurably. Ultra-processed food is cheaper and more accessible in deprived areas. Sleep is harder to protect under sustained economic pressure. The biological markers of accelerated ageing, elevated high-sensitivity CRP, lower NAD+ levels, disrupted cortisol rhythms, impaired sleep architecture, cluster in the same populations that experience the poorest health outcomes.

"Longevity medicine is not a luxury. It is not a product for wealthy early adopters. The biology it addresses is the same biology driving the 19-year healthy life expectancy gap in England. The expensive interventions are one part of the picture. The most important principles, sleep, movement, nutrition, stress management, are available to everyone. The framing of healthy ageing as inherently elite is not just commercially irritating. It is scientifically dishonest." — Nurse Marina

The interventions that most reliably extend healthspan are, at their foundation, not expensive. Consistent quality sleep. Regular zone 2 cardiovascular exercise. A diet low in ultra-processed food and refined sugar. Stress regulation. SPF. Resistance training. These are the foundations, and they are accessible. Clinical interventions, blood panels, IV therapies, hormonal optimisation, NAD+ supplementation, extend and accelerate what the foundations make possible. They do not replace them.

Part Three: NAD+ and why it matters

NAD+ is nicotinamide adenine dinucleotide. It is not simply an energy molecule. It governs DNA repair, cellular senescence, mitochondrial function, and the sirtuins: a family of proteins that function as the body's longevity regulators.

At the most fundamental level, NAD+ sits at the centre of cellular energy metabolism. Every time your mitochondria convert nutrients into ATP, the energy currency your cells use for every function, NAD+ acts as a co-factor and electron carrier. Without sufficient NAD+, this conversion slows. Cells are surrounded by fuel they cannot use. They starve in the presence of plenty.

NAD+ also activates sirtuins, which regulate inflammation, DNA repair, stress response, and which genes are expressed. Research published in PMC confirms that sirtuins act as NAD+-dependent regulators of metabolism, cell survival, and circadian rhythm. When NAD+ declines, sirtuin activity falls with it and the cellular maintenance programme that keeps tissues healthy goes quiet.

NAD+ activates PARP enzymes, your cells' primary DNA repair machinery. Every day, your DNA sustains thousands of small errors and breaks. PARP enzymes find and fix them. Research published in PubMed demonstrates that as NAD+ falls, PARP activity becomes substrate-limited. DNA damage accumulates. Cellular senescence increases. Tissues begin ageing faster biologically than they are ageing chronologically.

In cardiac nursing, I watched how cellular energy failure shows up in the heart long before it becomes visible anywhere else. Mitochondrial decline is not a cosmetic concern. It is a systemic one.

NAD+ role	Mechanism	What declines when NAD+ falls
Cellular energy production	Electron carrier in mitochondrial oxidative phosphorylation	ATP output; persistent fatigue despite adequate rest
DNA repair	Substrate for PARP enzymes	Accumulation of DNA damage; accelerated biological ageing
Longevity regulation	Sirtuin activation	Metabolic regulation, inflammation control, circadian rhythm
Inflammatory modulation	Cytokine pathway regulation	Increased baseline inflammation; slower tissue recovery
Cognitive function	Neuronal energy supply	Brain fog; word retrieval difficulties; processing speed

Why NAD+ declines with age

The decline is not a single mechanism. Several converging factors make it both progressive and hard to reverse through lifestyle alone by the time it becomes symptomatic.

CD38, an enzyme that becomes increasingly active with age, is an NAD+ consumer: it breaks the molecule down faster than it is being synthesised. Chronic inflammation, UV exposure, poor sleep, and the cumulative DNA damage that comes with time all increase PARP activation and burn through NAD+ reserves faster than the baseline decline alone would predict. By around sixty, most people have roughly half the NAD+ of a healthy twenty-year-old.

The symptom picture overlaps significantly with what most people attribute to middle age, which is precisely why it goes unidentified for years. Persistent fatigue that does not respond to rest. Cognitive dulling. Recovery that takes longer than it used to. Skin that does not respond to regenerative treatments as expected, because collagen synthesis and fibroblast activity are downstream of cellular energy availability.

Part Four: IV NAD+ therapy versus NMN supplements

This is the distinction that matters most practically, and it determines which approach is right for which patient.

NMN, nicotinamide mononucleotide, is the most direct precursor to NAD+. The body uses it via the salvage pathway to synthesise NAD+ without needing to build the molecule from scratch. Scientists including David Sinclair at Harvard have described NMN research as a genuine breakthrough in our understanding of cellular ageing. The evidence for NMN raising cellular NAD+ levels is substantial and growing.

The critical issue is bioavailability. Most NMN capsules dissolve in the stomach and a significant fraction is degraded before reaching the bloodstream in useful quantities. At Juvenology, we stock HINNAO NMN specifically because its sublingual liposomal delivery achieves bioavailability that standard capsules cannot match. The product bypasses the digestive tract, absorbing directly through the oral mucosa. For maintenance and long-term prevention, this is the most accessible and practical approach.

IV NAD+ therapy delivers pharmaceutical-grade NAD+ directly into the bloodstream: 100% bioavailability, immediate systemic distribution, precise dose control. There is no digestive process, no conversion step, no guessing at absorption rates. Cells absorb it immediately for ATP production, sirtuin activation, and PARP-mediated DNA repair.

Feature	HINNAO NMN (sublingual liposomal)	IV NAD+ therapy
Delivery method	Sublingual, bypasses digestion	Direct intravenous infusion
Bioavailability	High (significantly better than standard capsules)	100%
Speed of effect	Hours to days for measurable cellular impact	Immediate systemic effect
Best suited for	Maintenance, prevention, ongoing support between infusions	Therapeutic restoration for significant depletion
Onset of noticeable benefit	Days to weeks	Often within 24 to 48 hours
Practical use	Daily at home	Clinic-based, 2 to 4 hours per session
Cost	Accessible	Higher per session; course investment

For patients with significant depletion and clear clinical symptoms, IV delivery is the therapeutic intervention. NMN is the maintenance strategy between and after sessions. Many patients use both: an IV course to restore levels, followed by sublingual NMN to sustain them.

Part Five: Testosterone and why it belongs in this conversation

NAD+ is not the only molecule whose decline shapes how we age. Testosterone is another, and its connection to longevity medicine is one that most patients, including most clinicians, do not fully appreciate.

Testosterone belongs to the androgen family. Both sexes produce it throughout life, though in very different quantities. Dermal fibroblasts are androgen-sensitive. As testosterone declines from the mid-thirties onward in both men and women, collagen synthesis slows, dermal density reduces, muscle mass decreases, and the overall anabolic environment that supports tissue repair and maintenance deteriorates.

There is a wound healing paradox worth noting here. Male skin turns over cells more quickly than female skin at equivalent ages, which might suggest faster healing. The evidence shows the opposite: older men heal cutaneous wounds more slowly, and serum testosterone levels are negatively correlated with healing rate. DHT, the more potent testosterone metabolite, suppresses the inflammatory resolution phase that allows tissue repair to complete. This is clinically relevant for anyone considering regenerative aesthetic treatments: if the hormonal environment is significantly depleted, the cells receiving biostimulation lack the metabolic resources to respond fully.

For women, the picture is equally significant. As oestrogen falls during perimenopause, the relative effect of testosterone on sebaceous gland activity and hair follicles changes. Androgenetic alopecia in women presents as diffuse thinning at the crown and temples, driven by the same DHT-mediated follicular miniaturisation seen in men, but without the oestrogen counterbalance that previously modulated it.

"Testosterone is a variable that most aesthetic consultations never consider. But when a patient arrives whose regenerative treatments are not producing the results I would expect, hormonal status, including testosterone and SHBG bioavailability, is one of the first things I want to understand. The biology is always telling you something. You just have to be asking the right questions." — Nurse Marina

The SHBG caveat is clinically important. A standard blood test showing technically normal total testosterone can mask significant functional deficiency if SHBG, sex hormone binding globulin, is elevated and binding most of the available hormone away from tissue. Free testosterone, the fraction available to cells, is what matters clinically. This is why the Advanced Blood Panel at Juvenology includes free testosterone, SHBG, DHEA-S, and related markers, interpreted in the context of symptoms and stage of life rather than against a generic reference range.

Part Six: What the longevity medicine approach looks like at Juvenology

Longevity medicine at Juvenology is not a single treatment or a package. It is a clinical framework applied individually, starting with understanding what is actually happening in your biology before making any recommendations.

The Advanced Blood Panel provides the foundation. It covers:

• Hormonal markers: oestradiol, free and total testosterone, DHEA-S, SHBG, FSH, LH, progesterone

• Thyroid function: TSH, Free T3, Free T4

• Metabolic markers: HbA1c, fasting glucose, full lipid profile

• Inflammatory load: high-sensitivity CRP

• NAD+ pathway indicators: relevant metabolic markers informing cellular energy status

• Nutritional markers: vitamin D, B12, ferritin, folate, zinc

From that picture, the protocol is built. IV NAD+ therapy for patients with significant cellular energy deficit. HINNAO NMN as ongoing maintenance. Hormonal optimisation where indicated. Red light therapy for mitochondrial support and inflammaging reduction. Regenerative aesthetics for the dermal consequences of what the blood panel has identified systemically. The goal is not to treat multiple separate concerns. It is to restore the biological environment in which every treatment, every cell, every system in the body, works more effectively.

My postgraduate training in longevity medicine at the Geneva College of Longevity Science, alongside my qualification in hormonal health from the Marion Gluck Academy, shapes how I approach this work. Not as a collection of interventions, but as a clinical system.

Frequently asked questions

How do I know if my NAD+ levels are low?

There is no standard clinical test for NAD+ levels currently available in routine UK practice. The clinical picture, persistent fatigue, poor recovery, cognitive dulling, and skin that does not respond to regenerative treatment as expected, alongside relevant blood markers, guides the decision. The Advanced Blood Panel identifies the metabolic and hormonal variables most closely connected to NAD+ pathway function.

Is IV NAD+ therapy safe?

NAD+ is an endogenous molecule your body produces and uses constantly. Replenishing it parenterally has a strong safety profile in the published literature. The most common effects during infusion are warmth, flushing, and mild chest sensation, all transient and rate-dependent. Every infusion at Juvenology is conducted with vital signs monitored throughout and a full medical history taken before any treatment is agreed.

Can NMN supplements replace IV NAD+ therapy?

They serve different purposes rather than competing. Oral NMN raises NAD+ via the salvage pathway and is appropriate for maintenance and prevention. IV NAD+ delivers the coenzyme directly into circulation with immediate bioavailability for therapeutic restoration. For significant depletion or specific clinical goals, IV delivery provides a therapeutic dose that oral precursors cannot match. The most effective approach for many patients is a course of IV infusions followed by sublingual NMN maintenance.

Is longevity medicine only for older patients?

No. The most effective time to intervene is before biological thresholds are crossed, not after. Patients in their thirties and forties benefit substantially from the preventive and maintenance dimensions of longevity medicine. The biology is always moving. Working with it before it moves significantly is considerably more effective than addressing the consequences afterwards.

Does testosterone really affect skin ageing?

Yes, through specific and measurable biological mechanisms. Dermal fibroblasts are androgen-sensitive. Testosterone decline reduces collagen synthesis, dermal density, and the anabolic environment that supports tissue repair. For both men and women, addressing hormonal status alongside aesthetic treatment consistently produces better and longer-lasting results than treating the surface while the underlying biology works against it.

Book a longevity medicine consultation at Juvenology

We see patients from across Kent including Maidstone, Tonbridge, Sevenoaks, Kings Hill, West Malling, Medway, and Chatham.

External references

1. NAD+ and sirtuins in ageing and disease — PMC: pmc.ncbi.nlm.nih.gov/articles/PMC4112140

2. The NAD+/PARP1/SIRT1 axis in ageing — PubMed: pubmed.ncbi.nlm.nih.gov/28537485

3. Sirtuins and NAD+ in metabolic and cardiovascular diseases — PMC: pmc.ncbi.nlm.nih.gov/articles/PMC6206880

4. UK healthy life expectancy gap: 19.4 years male, 20.3 years female by deprivation — Health Foundation, 2025

5. ONS healthy life expectancy data 2022 to 2024 — ONS

6. Oestrogen and skin ageing: collagen loss post-menopause — PMC: pmc.ncbi.nlm.nih.gov/articles/PMC3772914

About Me

I’m Nurse Marina, founder of Juvenology Clinic in Maidstone, Kent. I’ve been a nurse for 25 years, which probably explains why I’m obsessed with precision, safety, and understanding how the body works.

I’m an NMC Registered nurse, JCCP Verified, a BACN Member, ACE Group Registered, a member of the Royal College of Nursing, and recognised by the Professional Standards Authority.

If you want to see more of what I do day to day, I share education, clinic insights, and the occasional behind-the-scenes moment here.

Instagram: https://www.instagram.com/juvenologyclinic/

TikTok: https://www.tiktok.com/@juvenologyclinic

References

1. NAD+ and sirtuins in ageing and disease — PMC: pmc.ncbi.nlm.nih.gov/articles/PMC4112140

2. Sirtuins and NAD+ in metabolic and cardiovascular diseases — PMC: pmc.ncbi.nlm.nih.gov/articles/PMC6206880

3. The NAD+/PARP1/SIRT1 axis in ageing — PubMed: pubmed.ncbi.nlm.nih.gov/28537485