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NMNH Triples NAD+ in First Human Trial: Here’s What That Means

The first NMNH human trial shows NAD+ levels increased up to 3x in 90 days. Here’s what the data actually reveal—and what’s still missing.
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The first human clinical trial results for NMNH are here. In this 90-day randomized, double-blind, placebo-controlled study, NMNH increased NAD+ levels up to 3x in healthy adults, with participants reporting improvements in energy and fatigue. But before you get too excited, there are important limitations to understand.
In this video, I break down the trial design, explain what the NAD+ increases actually mean, review the subjective outcomes like energy and emotional well-being (measured via SF-36), and discuss why the biological age claims are difficult to interpret. I also cover safety data and what we still need to know.
This is promising early data for NMNH vs NMN, but it’s unpublished, lacks key details, and needs independent replication. Here’s everything you need to know about what this trial does and doesn’t tell us.
Key topics: NMNH clinical trial, NAD+ boosters, NMN vs NMNH, longevity supplements, anti-aging research, NAD+ levels, UthPeak study, Phase I trial results.

📚 Chapters.
0:00 — Introduction & Trial Overview What this video covers and the trial basics.
1:39 — Trial Design & Methodology Study structure, participants, and objectives.
2:31 — NAD+ Results The primary outcome: dose-dependent increases.
3:18 — Subjective Outcomes & Limitations Energy, mood, biological age claims, and why interpretation is difficult.
6:26 — Safety & Final Thoughts Tolerability data and what comes next.

🌐Links in this video.
NMNH Clinical Trial https://www.clinicaltrials.gov/study/.… nicotinamide mononucleotide is a new and potent NAD+ precursor in mammalian cells and mice https://faseb.onlinelibrary.wiley.com… Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth https://pubmed.ncbi.nlm.nih.gov/33793… *************************************** Health claims Disclosure: Information provided on this video is not a substitute for direct, individual medical treatment or advice. Please consult with your doctor first. Products or services mentioned in this video are not a recommendation. Audio Copyright Disclaimer Please note that we have full authorization to the music that we used in our videos as they were created using the service WeVideo which provides the rights to the music. The rights are detailed in the terms of use that can be reviewed here https://www.wevideo.com/terms-of-use and any following inquiries should be addressed to [email protected]. ********************************************** #nmnh #nad #nmn.
Reduced nicotinamide mononucleotide is a new and potent NAD+ precursor in mammalian cells and mice.
https://faseb.onlinelibrary.wiley.com…
Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth.
https://pubmed.ncbi.nlm.nih.gov/33793…

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Inhibition of 15-hydroxy prostaglandin dehydrogenase promotes cartilage regeneration

Aging or injury to the joints can lead to cartilage degeneration and osteoarthritis (OA), for which there are limited effective treatments. We found that expression of 15-hydroxy prostaglandin dehydrogenase (15-PGDH) is increased in the articular cartilage of aged or injured mice. Both systemic and local inhibition of 15-PGDH with a small molecule inhibitor (PGDHi) led to regeneration of articular cartilage and reduction in OA-associated pain. Using single cell RNA-sequencing and multiplexed immunofluorescence imaging of cartilage, we identified the major chondrocyte subpopulations. Inhibition of 15-PGDH decreased hypertrophic-like chondrocytes expressing 15-PGDH and increased extracellular matrix-synthesizing articular chondrocytes. Cartilage regeneration appears to occur through gene expression changes in pre-existing chondrocytes, rather than stem or progenitor cell proliferation.

Clearing the brain of aging cells could aid epilepsy and reduce seizures

Temporal lobe epilepsy, which results in recurring seizures and cognitive dysfunction, is associated with premature aging of brain cells.

A new study by researchers at Georgetown University Medical Center found that this form of epilepsy can be treated in mice by either genetically or pharmaceutically eradicating the aging cells, thereby improving memory and reducing seizures as well as protecting some animals from developing epilepsy.

The study appears in the journal Annals of Neurology.

Aluminium in human brain tissue from donors without neurodegenerative disease: A comparison with Alzheimer’s disease, multiple sclerosis and autism

We present the first comprehensive data set for the aluminium content of brain tissue in donors without a diagnosis of neurodegenerative disease. All donors fulfilled recently revised criteria for control brain tissues. Approximately 80% of measured tissues have an aluminium content below 1.0 μg/g dry wt. (Table 1). There are some anomalies, 6 out of 191 tissues have an aluminium content ≥3.00 μg/g dry wt., and these are worth future investigation to identify possible neuropathology. There was no statistically significant relationship between brain aluminium content and age of donor and this observation is contrary to a previous investigation of brain aluminium in a neurologically normal population. An explanation may be that herein only two out of twenty donors were below 66 years old. The data do support a conclusion that a high content of brain aluminium is not an inevitability of ageing.

When we compared the new control data set with data produced in an identical manner in donors dying with diagnoses of sporadic Alzheimer’s disease (sAD)16, familial Alzheimer’s disease (fAD)11, autism spectrum disorder (ASD)13 and multiple sclerosis (MS)12 all of these disease groups had significantly higher brain aluminium content. The differences were always highly significant regardless of the method of statistical analysis (Table 4). The largest disease group, designated as sAD, was actually composed of approximately equal numbers of donors previously described by a brain bank as controls and donors diagnosed with sAD. Unfortunately, information discriminating between control and sAD donors was not made available to us17. However, the observation that the aluminium content of brain tissue in this group as a whole was significantly higher than the similarly aged control group emphasised the likelihood that brain aluminium content is increased in sAD.

Why Your Lifespan Could Be Thousands of Years — New DNA Research Explained

Can humans live for thousands of years? New DNA and longevity research suggests that aging may not be fixed—it may simply be the result of imperfect cellular repair. In this video, we explore how DNA damage, genetic repair mechanisms, and modern longevity science are reshaping our understanding of human lifespan.

This content is based on current research from USA and Europe, focusing on emerging breakthroughs in genetics, DNA repair therapies, and anti-aging science.
If you’re interested in health, biology, or the future of human longevity, this video is for you.

Disclaimer:
This video is for educational purposes only, is not intended to diagnose, treat, or cure any condition, and does not replace professional medical advice. Always consult a qualified healthcare provider for guidance related to your health.

#LongevityScience.
#DNARepair.
#AntiAging.
#GeneticsResearch.
#HealthFacts.
#BioLogicHealth.
#ScienceExplained.
#HealthyAging

Control of aging-associated neurodegeneration via hypothalamic extracellular vesicles containing parathymosin

Jung, Yu, Choi et al. reveal a critical neuroprotective role of PTMS, while loss of this protein causes severe neurodegeneration. Hypothalamic neural stem cell-derived extracellular vesicles carrying PTMS protect neurons by preventing DNA damage and offer therapeutic benefits against aging-related neurodegenerative and Alzheimer’s-like conditions in animal models.

Cardiovascular risk score identifies risk for ocular disease

The Pooled Cohort Equations (PCE) cardiovascular risk score stratifies risk for multiple ocular diseases, according to a study published online in Ophthalmology.

Deyu Sun, Ph.D., from the David Geffen School of Medicine at the University of California Los Angeles, and colleagues conducted a historical prospective cohort study using electronic health record data from the “All of Us” Research Program to examine whether the PCE cardiovascular risk score is associated with future age-related macular degeneration (AMD), glaucoma, diabetic retinopathy (DR), retinal vein occlusion (RVO), and hypertensive retinopathy (HTR).

A total of 35,909 adults aged 40 to 79 years with complete variables for PCE calculation within a six-month period were included in the study. Individual-level PCE score was classified into four risk categories.

Scientists Uncover How Aging Brains Turn a Vital Amino Acid Toxic

Scientists have uncovered how aging alters tryptophan metabolism in the brain, linking a longevity protein to neurodegeneration. Tryptophan is often associated with sleep, but its role in the body extends far beyond that reputation. This essential amino acid serves as a foundational building bloc

High risk of sleep apnea linked to poorer mental health in adults over 45

Researchers at Ottawa Hospital Research Institute and University of Ottawa found that high risk of obstructive sleep apnea was associated with approximately 40% higher odds of a composite poor mental health outcome at baseline and follow-up among adults aged 45–85 years in the Canadian Longitudinal Study on Aging.

Identifying factors associated with mental health outcomes is an important goal on several fronts. Mental health conditions rank among the leading contributors to global disease burden, with anxiety and depressive disorders described as most common. Individuals living with mental health conditions face higher risks of cardiometabolic diseases, unemployment, homelessness, disability, and hospitalizations. Economically, mental disorders carry an estimated $1 trillion annual global cost in lost productivity.

Obstructive sleep apnea (OSA) involves repeated upper airway narrowing during sleep. Disturbed breathing can break up sleep (sleep fragmentation), trigger a stress response in the nervous system (sympathetic activation), and cause episodes of low oxygen in the blood (intermittent hypoxemia).

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