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IS NMN MORE EFFECTIVE THAN NR

There’s a lot of research going on right now with Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR). It can be difficult to make sense of them all, so we summarize some results that lead us to believe NMN is more effective than NR.

DRAMATIC RESULTS WITH NMN IN ENDURANCE AND YOUTHFULLNESS

Below are the three studies that made the biggest splash’s about the potential for reversing aging by restoring NAD+ to youthful levels that have ALL been accomplished using NMN

After 6 days of NMN, 22 month old mice  had the muscle capacity, endurance and metabolism of 6 month old  mice (2013 Sinclair study)

NMN effectively mitigates age-associated physiological decline in mice (2016 Mills Long Term study)

“The old mice became as fit and strong as young mice” (Sinclair, 2018)

This third study recently published by Dr Sinclair is a  good example.

Mice that received NMN had nearly 100% increased endurance vs the control mice, and actually grew NEW blood vessels. This was after 60 days, in 20 month old mice (equivalent to 90 year old humans).

Along with the impressive increased endurance, the study shows  NAD+ increase is over 500% at 60 days

RESULTS NOT AS IMPRESSIVE WITH NR

In this 2016 study, 22-24 month old mice were given NR for 6 weeks.

Running distance and duration were improved approximately 20%.

The treatment duration was slightly shorter in this study than with NMN (6 weeks vs 8 weeks), there is a huge difference in the benefit with increased endurance from NMN nearly 100% vs the 20% with NR.

Treating Heart Disease

2 separate studies to treat a form of heart disease called Friedreich’s Ataxia with NR and NMN were published in 2017. Treatment with NMN was successful, while NR did not improve cardiac function.

“Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels. “(Martin, 2017)

“In conclusion, NAD+ supplementation with NR in the FRDA model of mitochondrial heart disease does not alter SIRT3 activity or improve cardiac function.”(Stram, 2017)

COMBATTING ALZHEIMERS DISEASE

Alzheimer’s disease (AD) pathogenesis is widely believed to be driven by the production and deposition of the β-amyloid peptide (Aβ). Evidence now indicates that the solubility of Aβ, and the quantity of Aβ in different pools is related to disease state (r).Researchers believe that flaws in the processes governing production, accumulation or disposal of beta-amyloid are the primary cause of Alzheimer’s (r).

In studies published in 2017 and 2018 NMN decreased β-amyloid buildup, while NR did not.

“NR lessened pTau pathology in both 3xTgAD and 3xTgAD/Polβ+/− mice but had no impact on amyloid β peptide (Aβ) accumulation”(Hou, 2018)

“NMN decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in AD-Tg mice” (Yao, 2017)

NMN was able to mitigate most age-associated physiological declines in mice Treatment of old mice with NMN reversed all of these biochemical aspects of aging

Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice (mills, 2016)

Raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse

Restore the mitochondrial homeostasis and key biochemical markers of muscle health in a 22-month-old mouse to levels similar to a 6-month-old mouse

Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)

DNA Repair

This study showed supplementation with NMN was able to repair the DNA in cells damaged by radiation

The cells of old mice were indistinguishable from young mice after just one week of treatment.

A conserved NAD+ binding pocket that regulates protein-protein interactions during aging (Sinclair, 2017)

WEIGHT

NMN was immediately utilized and converted to NAD+ within 15 min, resulting in significant increases in NAD+ levels over 60 min

Administering NMN, a key NAD+ intermediate, can be an effective intervention to treat the pathophysiology of diet- and age-induced T2D

Surprisingly, just one dose of NMN normalized impaired glucose tolerance

Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011)

NAD(+) levels were increased significantly both in muscle and liver by NMN

NMN-supplementation can induce similar reversal of the glucose intolerance

NMN intervention is likely to be increased catabolism of fats NMN-supplementation does mimic exercise

Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice (Uddin, 2016)

NMN significantly increased the level of NAD+ in the heart

NMN protected the heart from I/R injury

Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and repercussion (Yamamoto, 2014)

NMN reduces vascular oxidative stress

NMN treatment normalizes aortic stiffness in old mice

NMN represents a novel strategy for combating arterial aging

Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice (de Picciotto, 2016)

NMN can reduce myocardial inflammation NMN thus can cut off the initial inflammatory signal, leading to reduced myocardial inflammation

Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure (Zhang, 2017)

ENERGY

Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels.

Restoration of cardiac function and energy metabolism upon NMN supplementation

Remarkable decrease in whole-body EE and cardiac energy wasting

Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model

VISION

Exogenous NMN prevents photoreceptor degeneration and restores vision

NMN rescues retinal dysfunction in light-induced degeneration

 

NAMPT-mediated NAD+ biosynthesis is essential for vision in mice (lin, 2016)

Completed and pending publication

Beginning 2018

  • 2018 Sinclair Metrobio study – Phase 2

The Phase 1 study by Dr Sinclair has been completed, and they are ready to go forward with the Phase 2 study, so we can conclude there were positive results, and no negative side effects, else they would have to publish those immediately.

In the University of Washington study, participants are 50 healthy women between 55 and 70 years of age with slightly high blood glucose,BMI and triglyceride levels.

Using a dose of 2 capsules of 125mg NMN per day over a period of 8 weeks, researchers are testing for:

  • change in beta-cell function
  • works to control blood sugar
  • blood vessels dilate
  • effects of NMN on blood lipids
  • effects of NMN on body fat
  • markers of cardiovascular and metabolic health

The active supplementation portion of this study has ended, but testing of metabolic parameters will continue for 2 years after supplementation has ended.  So researchers know the immediate effects and  preliminary results are expected to be announced in 2018, with  final results expected in 2020.
 

Elevates NAD+ quickly throughout the body

In this 2016 study, mice were given a single dose of NMN in water.

NMN levels in blood showed it is quickly absorbed from the gut into blood circulation within 2’“3 min and then cleared from blood circulation into tissues within 15 min

Increases NAD+ and Sirt1 Dramatically in organs

The charts at left from 2017 study, NMN supplementation for 4 days significantly elevated NAD+ and SIRT1, which protected the mice from Kidney damage.

NAD+ and SIRT1 levels were HIGHER in OLD Mice than in YOUNG Mice that did not receive NMN.


REFERENCES:

  1. Detection and pharmacological modulation of nicotinamide mononucleotide (NMN) in vitro and in vivo (Formentini, 2009)
  2. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity (Cato, 2009)
  3. A possibility of nutriceuticals as an anti-aging intervention: activation of sirtuins by promoting mammalian NAD biosynthesis (Imai, 2010)
  4. NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway (Zhuo, 2011)
  5. Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011)
  6. The NAD (+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity(Canto, 2012 )
  7. NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice. (Zhang, 2016)
  8. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)
  9. Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and repercussion (Yamamoto, 2014)
  10. NAD+ and sirtuins in aging and disease (Imai, 2014)
  11. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3 (Khan, 2014)
  12. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model (Long, 2015)
  13. NAD+ metabolism and the control of energy homeostasis – a balancing act between mitochondria and the nucleus (Canto, 2015)
  14. NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy (Yang, 2016)
  15. NAD+ replenishment improves lifespan and healthspan in ataxia telangiectasia models via mitophagy and DNA repair( Fang, 2016 )
  16. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans(Trammell, 2016a )
  17. Nicotinamide riboside opposes type 2 diabetes and neuropathy in mice(Trammell, 2016b )
  18. β-Nicotinamide Mononucleotide, an Anti-Aging Candidate Compound, Is Retained in the Body for Longer than Nicotinamide in Rats (Kawamura, 2016)
  19. The first human clinical study for NMN has started in Japan (Tsubota, 2016)
  20. Nicotinamide mononucleotide protects against β-amyloid oligomer-induced cognitive impairment and neuronal death (Wang, 2016)
  21. Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice (Uddin, 2016)
  22. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice (Mills, 2016)
  23. Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice (de Picciotto, 2016)
  24. Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease (Yao, 2017)
  25. Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model (Martin, 2017)
  26. Nicotinamide Mononucleotide, an NAD+ Precursor, Rescues Age-Associated Susceptibility to AKI in a Sirtuin 1-Dependent Manner (Guan, 2017)
  27. Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway (Wei, 2017)
  28. Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure (Zhang, 2017)
  29. Modulating NAD+ metabolism, from bench to bedside (Auwerx, 2017)
  30. Aspects of Tryptophan and Nicotinamide Adenine Dinucleotide in Immunity: A New Twist in an Old Tale. (Rodriguez, 2017)
  31. Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice (Williams, 2017)
  32. NAMPT-mediated NAD biosynthesis as the internal timing mechanism: In NAD+ World, time is running in its own way (Poljsak, 2017)
  33. Effect of “Nicotinamide Mononucleotide” (NMN) on Cardiometabolic Function (NMN)
  34. The dynamic regulation of NAD metabolism in mitochondria (Stein, 2012)
  35. Novel NAD+ metabolomic technologies and their applications to Nicotinamide Riboside interventions (Trammel, 2016)
  36. Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans (Meydayni, 2016)
  37. A high-fat, ketogenic diet induces a unique metabolic state in mice. (Kennedy, 2007)
  38. Ketone body metabolism and cardiovascular disease.(Cotter, 2013)
  39. Ketone bodies as signaling metabolites(Newman, 2014)
  40. The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease(Youm, 2015)
  41. The effect of the Spanish Ketogenic Mediterranean Diet on nonalcoholic fatty liver disease: a pilot study.(Guisado, 2011)
  42. β-Hydroxybutyrate: A Signaling Metabolite in starvation response(Morales, 2016)
  43. Physiological roles of ketone bodies as substrates and signals in mammalian tissues(Robinson, 1980)
  44. Ketone bodies mimic the life span extending properties of caloric restriction (Veech, 2017)
  45. Novel ketone diet enhances physical and cognitive performance(Murray, 2016)
  46. Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet.
  47. Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes(Cox, 2013)
  48. Neuroendocrine Factors in the Regulation of Inflammation: Excessive Adiposity and Calorie Restriction (Fontana, 2009)
  49. Beta-adrenergic receptors are critical for weight loss but not for other metabolic adaptations to the consumption of a ketogenic diet in male mice(August, 2017)
  50. A randomized trial of a low-carbohydrate diet for obesity(Foster, 2003)
  51. β-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation(Bae, 2016)
  52. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. (Maalouf, 2009)
  53. AMPK activation protects cells from oxidative stress‐induced senescence via autophagic flux restoration and intracellular NAD + elevation (Han, 2016)
  54. Regulation of AMP-activated protein kinase by natural and synthetic activators (Hardie, 2015)
  55. Effects of Exhaustive Aerobic Exercise on Tryptophan-Kynurenine Metabolism in Trained Athletes (Strasser, 2016)
  56. PARP-1 inhibition increases mitochondrial metabolism through SIRT1 activation(Bai, 2011)
  57. Carbohydrate restriction regulates the adaptive response to fasting (Klein, 1992)
  58. Interventions to Slow Aging in Humans: Are We Ready? (longo, 2015)
  59. Extending healthy life span–from yeast to humans (longo, 2010)
  60. Dietary restriction with and without caloric restriction for healthy aging (Lee, 2016)
  61. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan (Longo, 2015)
  62. Diet mimicking fasting promotes regeneration and reduces autoimmunity and multiple sclerosis symptoms (Longo, 2016
  63. Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle (Porter, 2015)
  64. Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice (Newman, 2017)
  65. The NAD(+)/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling.  (Mouchiroud, 2013)
  66. NAMPT- mediated NAD(+) biosynthesis is essential for vision in mice  (Lin, 2016)
  67. NAD+ replenishment improves lifespan and healthspan in ataxia telangiectasia models via mitophagy and DNA repair( Fang, 2016 )
  68. Inhibiting poly ADP-ribosylation increases fatty acid oxidation and protects against fatty liver disease (Gariani, 2017 )
  69. Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle(Canto, 2010)
  70. The NAD (+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity(Canto, 2012 )
  71. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans(Trammell, 2016a )
  72. Nicotinamide riboside opposes type 2 diabetes and neuropathy in mice(Trammell, 2016b )
  73. Dietary leucine stimulates SIRT1 signaling through activation of AMPK (Hongliang, 2012)
  74. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3 (Khan, 2014)
  75. NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway (Zhuo, 2011)
  76. The effect of different exercise regimens on mitochondrial biogenesis and performance (Philander, 2014)
  77. Dietary proanthocyanidins boost hepatic NAD+ metabolism and SIRT1 expression and activity in a dose-dependent manner in healthy rats (Aragon’s, 2016)
  78. NAD+ Deficits in Age-Related Diseases and Cancer (Garrido, 2017)
  79. Anti-diabetic and anti-lipidemic effects of chlorogenic acid are mediated by ampk activation (Ong, 2013)
  80. Chlorogenic Acid Improves Late Diabetes through Adiponectin Receptor Signaling Pathways in db/db Mice (Chang, 2015)
  81. Adenosine Monophosphate (AMP)-Activated Protein Kinase: A New Target for Nutraceutical Compounds (Marin-Aguilar, 2017)
  82. The Effects of Ramadan Fasting on Body Composition, Blood Pressure, Glucose Metabolism, and Markers of Inflammation in NAFLD Patients: An Observational Trial (Mazidi, 2014)
  83. Comparative effects of carbohydrate versus fat restriction on metabolic profiles, biomarkers of inflammation and oxidative stress in overweight patients with Type 2 diabetic and coronary heart disease: A randomized clinical trial. (Raygan, 2016)
  84. Normal fasting plasma glucose and risk of type 2 diabetes diagnosis (Nichols, 2008)
  85. Are We All Pre-Diabetic? (Stokel,2016)
  86. Hepatic NAD+ deficiency as a therapeutic target for non-alcoholic fatty liver disease in aging (Zhou, 2016)
  87. Effect of exercise intensity on post-exercise oxygen consumption and heart rate recovery (Mann,2014)
  88. A 45-minute vigorous exercise bout increases metabolic rate for 14 hours (Knab,2011)
  89. Effects of high-intensity resistance training on untrained older men. II. Muscle fiber characteristics and nuclei-cytoplasmic relationships (Gerontol, 2000)
  90. Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice (Newman, 2017)
  91. A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice (Roberts, 2017)
  92. NK cells link obesity-induced adipose stress to inflammation (Wensveen, 2015)
  93. The “Big Bang” in obese fat: Events initiating obesity-induced adipose tissue inflammation (Wensveen, 2015)
  94. The impact of the Standard American Diet in rats: Effects on behavior, physiology and recovery from inflammatory injury(Totsch, 2017)
  95. Bioenergetic state regulates innate inflammatory responses through the transcriptional co-repressor CtBP (Shen, 2017)
  96. The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders (Stafstrom, 2012)
  97. Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle (Fredrick 2016)
  98. Digestion and absorption of NAD by the small intestine of the rat (Henderson, 1983)
  99. Effects of a wide range of dietary nicotinamide riboside (NR) concentrations on metabolic flexibility and white adipose tissue (WAT) of mice fed a mildly obesogenic diet(Shi, 2017)
  100. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans (Brenner, 2004)
  101. Nampt Expression Decreases Age-Related Senescence in Rat Bone Marrow Mesenchymal Stem Cells by Targeting Sirt1 (Ma, 2017)
  102. NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR (Yoshino, 2017)

 

25 thoughts on “IS NMN MORE EFFECTIVE THAN NR

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  6. Donald Myck says:

    What do you say about this?
    1. NR is a vitamin. NMN is not.
    NR is a proven form of vitamin B3 which is required to sustain healthy living. It’s shown in multiple human studies to effectively increase NAD levels.

    NMN is not a form of vitamin B3, and there are no clinical trials to prove it increases NAD in humans. NMN is also not the type of molecule that would ever be considered as a vitamin as it contains a phosphate, which affects its ability to enter cells.

    2. NR can enter the cell. NMN cannot.
    NR is the largest part of NAD that can enter the cell. This is why NMN supplements turn into NR first before they are able to make NAD.

    3. NMN makes NAD in 3 steps. NR requires only 2.
    In its supplement form, NMN must become NR first before entering the cell. Then once inside the cell, it converts back into NMN to make NAD. This is a 3-step and rather inefficient process.

    NR can directly access the cell, so it only requires two steps to begin creating NAD.

    SHOP TRU NIAGEN®
    4. NR has 4 published human clinical studies. NMN has 0.
    NMN’s only published trials are in mice and rats.* NR has at least 4 published clinical trials and all of them confirm NR is a safe and effective way of increasing NAD in people.

    5. NR is taken orally. NMN is mostly studied by injection.
    Despite NMN being sold as a pill to people, NMN is frequently studied through injections in rodents. In preclinical NR trials, it’s most commonly added to food or water. Plus, in all of NR’s published human trials it was administered in capsule form, which represents the recommended way of taking NR as a vitamin.*

    6. NR increases NAD by up to 60% in humans. NMN may not.
    In this 2018 study, 1000mg/day of NR increased NAD levels by 60% on average in older adults. There is no published data to show how NMN affects human NAD levels.*

    “There is no published data to show how NMN affects human NAD levels.*”
    7. NR has at least 4 published trials confirming it’s safe for humans. NMN has 0.
    There are no data available stating whether or not NMN is safe for human consumption.* Careful analysis of all the preclinical and clinical information available on NR confirms it is safe and well-tolerated.

    8. NR has 3 FDA safety notifications. NMN has 0.
    The only commercially available form of NR, NIAGEN®, has twice been successfully reviewed under FDA’s new dietary ingredient (“NDI”) notification program and has also been successfully notified to the FDA as generally recognized as safe (“GRAS”). NMN has no safety notifications from the United States FDA.*

    “Published data shows NR is a safe and more efficient way of increasing NAD levels than NMN.”
    There aren’t any human studies comparing NR to NMN (because NMN doesn’t have any clinical trials), but we do have them in animal models. And there the evidence is clear: NR is a more efficient way of increasing NAD. That’s because NR and NMN are structurally different in one very important way: NR can get directly into the cell, and NMN can’t. [1–4]

    NAD is getting a lot publicity lately for its potential impacts on human health. Recent publications include TIME, Fast Company, The Atlantic, AARP The Magazine, and more. If you think NAD is as important as some leading biochemists and nutritionists believe it is, it’s worth making sure you’re investing in the most effective way to increase NAD. After all, isn’t that why all of us keep up with the news surrounding aging and science? We care about things like that.

    More in SCIENCE
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    1 NIKIFOROV, A., ET AL., 2011
    2 RATAJCZAK, J., ET AL., 2016
    3 FLETCHER, R.S., ET AL., 2017
    4 VAUR, P., ET AL., 2017
    *As of September 2018

    SCIENCE, LIFE, HEALTH

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  13. Len says:

    The July 2018 issue of Scientific American has an article about ChronoBioloogy (The Clocks Within Our Cells). They show how the time of day you take a medicine, nutrient, etc. can make a big difference in how it affects the body. and how this can explain the differences in results from clinical trials using the exact same dosages and patient profiles. Trials done with dosing in the morning can have radically different and otherwise unexplainable outcomes than ones where the subjects took the drug in the evening. i.e. mice given a dangerously large dose of Acetaminophen in the morning nothing untoward happens. The same dose in the evening and the liver is kaput. Fluorouracil given to cancer patients at midnight resulted in a 5 fold reduction in inflamation and 3 fold reduction in hospitalizations for side effects.
    My question is: do you have any data on the time of day for taking NMN for the greatest effect? If not you should look into getting that data from your ongoing trials and finding out when people are taking it. That can be responsible for several hundred per cent differences in outcomes. If some people don’t see an effect that could be caused by the time of day they typically take it, conversely some that get a large effect may be taking it at another time of day. The author of the above article estimates that over 80% of drugs are affected by the time of day they’re taken. Transcription factors and the genes that encode them can be very chrono dependent.

  14. dluber says:

    I’ve not tried either but am going with ABN based on this page and the misinformation given on the Tru Niagen blog: https://blog.truniagen.com/home/2018/3/16/8-key-differences-between-nmn-nr (which does not have a user comment feature, or else I would tag them over there).
    Note first that their 16 points really collapse into 8 points, they just give the vice versa for each. E.g. #1 and #2 obviously. In fact, you can collapse all four points #3–6 into one point: NR and NMN are interconverted by phosphorylation/dephosphorylation – which is what the diagram above illustrates (and as a chemist, I’ll pick nits about the one-way arrow; all reactions are reversible and should show a two-way arrow).

    However, according to this PLOS-One article, the preferred direction is apparently NR –> NMN. So they have the diagram backwards, meaning the reality is the opposite of their statement supporting the use of NR over NMN.
    Airhart et al. 2017
    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0186459

    “Nicotinamide riboside (NR) is a pyridine nucleoside form of vitamin B3 that is naturally found in milk and is available as a nutraceutical. NR is converted by nicotinamide riboside kinases (NRK1,2) to NMN, which is subsequently converted to NAD+ by nicotinamide mononucleotide adenylyltransferase (NMNAT).”

    They also say that there are no published clinical human studies with NMN, but there are 6 listed above on this ABN page in pre-publication; all that means is that the NR studies were completed earlier. At the bottom, they falsely say that “NMN doesn’t have any clinical trials”.

  15. Jerre Levy says:

    The Martin study gave 500 mg/kg of NMN. In a 70 kg person, this translates to a dose of 35,000 mg twice weekly or 70,000 mg per week! You suggest 250 mg daily for people (1750 mg over the course of a week). What possible relevance does such a massive dosage in rodents have to do with 250 mg daily in people?

  16. wandawilmoth95 says:

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