Is Basis by Elysium Health a Hoax?

As we age, levels of the co-enzyme Nicotinamide Adenine Dinucleotide NAD+ drop significantly in multiple organs, which disrupts our bodies ability to fight inflammation, disease, and physiological decline  (5,8,10).

NAD+ decrease is described as a trigger in age-associated decline(23), and perhaps even the key factor in why we age (5).

In 2013, Research published by Dr Sinclair  of Harvard stunned researchers by showing that short term supplementation with Nicotinamide MonoNucleotide (NMN)  reversed many aspects of aging, making the cells of old mice resemble those of much younger mice, and greatly improving their health.

Since then, dozens of other studies have been published investigating the efficacy of supplementation with NAD+ precursors such as NMN and Nicotinamide Riboside (NR) in treatment and prevention of a wide range of disease including cancer, cardiovascular disease, diabetes, Alzheimers, Parkinsons, and more (5,6,7,9,10,11,13,14,15,16,23).

BASIS USES NICOTINAMIDE RIBOSIDE

NR and NMN are precursors that are used by our bodies to replenish NAD+ levels.

In 2004 Dr Charles Brenner published a paper showing that the enzyme Nrk1 can catalyze NR directly to NMN (100) which might make it a much more effective precursor to NAD+.  Although NR is unstable by itself, Dartmouth University has patented production methods that combine it with Chloride which makes it stable.

Chromadex has licensed this technology and has been selling NR commercially since 2014 under the brand name “Niagen”.

Basis is the brand name used by Elysium Health to market their Nicotinamide Riboside product.

WHAT IS NAD+

NR benefits chartNAD+ is a key co-enzyme that the mitochondria in every cell of our bodies depend on to fuel all basic functions. (3,4)

NAD+ play a key role in communicating between our cells nucleus and the Mitochondria that power all activity in our cells (5,6,7)

NAD+ LEVELS DECREASE WITH AGE

NAD+ levels decreaseAs we age, our bodies produce less NAD+ and the communication between the Mitochondria and cell nucleus is impaired. (5,8,10).

Over time,  decreasing NAD+ impairs the cell’s ability to make energy, which leads to aging and disease (8, 5) and perhaps even the key factor in why we age (5).

NAD+ METABOLISM IN HUMANS

NAD+ is synthesized in humans by several different molecules (precursors), thru 2 different pathways:
De Novo Pathway

  • Tryptophan
  • Nicotinic Acid (NA)

Salvage Pathway

  • NAM – Nicotinamide
  • NR – Nicotinamide Riboside
  • NMN – Nicotinamide MonoNucleotide

The NAD+ supply is not stagnant – it is constantly being consumed and replenished, with the entire NAD+ pool being turned over 2-4 times per day (14).

This recycling is through the salvage pathway, where the enzyme Nampt catalyzes NAM to NMN, which is then metabolized to NAD+.


Nampt is the rate-limiting step in the salvage process (97).

Many studies have confirmed the importance of Nampt in maintaining sufficient NAD+ levels, such as the quote below from a 2016 study that used mice lacking Nampt in muscle fiber:

“NAD content of muscle was decreased by ~85% confirmed the prevailing view that the salvage route of NAD synthesis from NAM sustains the vast majority of the NAD” (97)

These mice exhibited normal muscle strength and endurance while young, but deteriorated rapidly as they aged which confirmed Nampt is critical to maintaining NAD+ levels.

As we age, Nampt enzyme activity is lower, resulting in less NAM recycling, less NAD+, more disease and aging (97,101).

NMN and NR SUPPLEMENTS CAN BYPASS NAMPT

NR had been known for decades, but was not thought to be that important until 2004 when Dr. Charles Brenner discovered the enzyme NRK1 can phosphorylate NR directly to NMN, bypassing the Nampt “bottleneck” (100).

This newly discovered “shortcut” in the NAD+ salvage pathway found that NR can be metabolized directly to NMN to boost NAD+ levels more effectively than NAM.

MOST NR IS FIRST METABOLIZED TO NAM

When taken orally as a supplement, most NR does not make it through the digestive system intact, but is broken down to NAM (97,98,99).

Even when taken at very high dosages, NR has not been detected in the bloodstream in any research (97,98,99).

“This evidence indicates that NR is converted to NAM before absorption occurs and that this reaction is the rate-limiting step ” (98)

“NR has been shown be converted to Nam before being absorbed or reaching tissues” (99)

“we were surprised to find that NR exerts only a subtle influence on the steady state concentration of NAD in muscles. Our tracer studies suggest that this is largely attributable to breakdown of orally delivered NR into NAM prior to reaching the muscle. ” (97)

Note:NAM does elevate NAD+, but is on the “wrong” side of the Nampt bottleneck, which limits it’s effectiveness

WHAT WE RECOMMEND


NMN PLUS – THE COMPLETE NAD+ BOOSTER

$46.95

Unlike NR, NMN makes it’s way INTACT through the liver quickly and remains available in the bloodstream for many hours (18,97,98,99)

NMN is the Immediate Precursor to NAD+.

NMN is quickly metabolized into tissues throughout the body, where it bypasses the NAMPT bottleneck and restores NAD+ levels in tissues more effectively than other NAD+ precursors.

Read about the science behind NMN.

OTHER PRECURSORS – MAKING NMN EVEN MORE EFFECTIVE

Boosting NAD+ in the liver is great, but is a small part of the health benefits you get from restoring NAD+ thoughout the body.

All the precursors are effective at boosting NAD+ in the liver, so why waste NMN on that simple task?

  • Niacin (NA) is the fastest, elevating NAD+ to peak levels in liver in 15 minutes (R)
  • Tryptophan is the preferable substrate for NAD+ production in the liver(R)
  • Administration of tryptophan, NA, or NAM to rats showed that tryptophan resulted in the highest hepatic NAD+ concentrations(R)

Including Niacin and Tryptophan help elevate NAD+ levels in the liver to their maximum quickly, sparing NMN to be released into the bloodstream and make its way into tissues throughout the body much more effectively.

Like NR, NAM is also very slow acting, taking 8 hours to reach peak NAD+ levels in the liver when used by itself (16).

We include NAM in NMN Plus to act as a slow release NAD+ booster to ensure levels stay high, and potentially sparing NMN from being utilized for NAD+ metabolism in the liver throughout the day.

According to Dr. Charles Brenner:

“Not every cell is capable of converting each NAD+ precursor to NAD+ at all times…the precursors are differentially utilized in the gut, brain, blood, and organs” (R).

NMN – NICOTINAMIDE MONONUCLEOTIDE

  • THE IMMEDIATE PRECURSOR to NAD+
  • “NMN makes its way through the liver, into muscle, and is metabolized to NAD+ in 30 minutes” (R)
  • Treatment for 1 week with NMN was able to restore NAD+ levels in old mice (22 months) to that of 6 month old mice (R)

NAM – NICOTINAMIDE

  • Converts to NAD+ thru a 2 step salvage pathway(R)
  • Is much slower, taking 8 hours to reach peak NAD+ in humans (R)
  • Has been shown to increase NAD+ level in liver (47%), but was weaker in kidney (2%), heart (20%), blood (43%) or lungs (17%) (R)

NA – NICOTINIC ACID (NIACIN)

  • Elevates NAD+ to peak levels in liver in 15 minutes (R)
  • raised NAD+ in liver (47%), and impressively raised kidney (88%), heart (62%), blood (43%) and lungs (11%) (R)
  • “has been used for primary and secondary coronary heart disease prevention for over 40 years”(R)
  • “NA is one of the most effective means to improve cardiovascular risk factors”(R)
  • Long term human studies show 6.2% and 7.8% reduced All Cause Mortality rate (R)
  • Can cause uncomfortable “flushing” in higher dosages, which limits its usage(R)

TRYPTOPHAN

  • In the liver  tryptophan is the preferable substrate for NAD+ production (R)
  • Administration of tryptophan, NA, or NAM to rats showed that tryptophan resulted in the highest hepatic NAD+ concentrations(R)
  • Shown to be beneficial in several neurological conditions, including insomnia, Parkinson disease, schizophrenia, depression, anxiety, and autism. (R, R)

Click here for pricing and more product info

NOBEL PRIZE WINNING ADVISORS

1000s of articles have teased us with the possibility that taking Niagen could halt or maybe even actually reverse some of the signs of aging. Of course there is a lot of skepticism with such claims.

Chromadex has been producing the only commercially available form of Niagen and supplies it to 20 or more different companies that put their own brand name on the bottle and sell to customers.

Elysium Health is only one of these sellers, although they have fairly deep pockets and extensive connections among top researchers in the field.

They have also enlisted 6 Nobel Laurete scientists to serve as advisors to the company, which lends a great deal of credibility.

However, these scientists have had no significant role in researching,creating or testing Basis or either of the ingredients used.

screen-shot-2016-12-01-at-2-21-53-pm

Elysium Health makes a change to the formula for Basis


Basis contracted to buy Nicotinamide Riboside Chloride (often referred to as NR, or the brand name Niagen), and combine it with another off the shelf product from Chromadex, Pterostilbene.

But in June 2016, Elysium got into a contract dispute with Chromadex and later sued Chromadex for abusing the patent process.

Their goal seems to be to invalidate Chromadex patent(s) so they could produce their own version, which appears to be what they are doing now.

Elysium has changed the product information on their website to list “Nicotinamide Riboside”, without the Chloride.  A key patent Chromadex has licensed the rights to involves adding the Chloride to make it more stable.

This new ingredient used by Basis likely has the same effects in the human body, but we don’t really know for sure.

It seems Elysium Health plans to go forward with this revised formula for now, and continue to use previous test results obtained with their prior  formula that used Chromadex Nicotinamide Riboside Chloride.  It will be interesting to see how that strategy holds up going forward.

Elysium Health has some very slick Marketing people

So now they have changed their product to use a slightly different ingredient, but want to smooth it over and not cause customers to worry about it.

Their answer is to portray the change as something they did on purpose – to MAKE THE PRODUCT BETTER.

When a customer questioned the change, this is how they answered on their Facebook page:

Hi Anne–

Thank you for reaching out to us with your questions. I’d be happy to provide additional information for you here!

From the start, Elysium has always been committed to bringing superior, high-quality supplements to market. As part of that effort, we have established a new supply chain, located in the United States, that utilizes a proprietary process to produce Nicotinamide Riboside — the first of its kind for the production of Basis, and this does fully meet the GMP standard as outlined by the FDA. We believe our vertically integrated supply chain benefits our customers as it enables us to better manage manufacturing, packaging, shipment and eventually the expansion of our new product line.
While the specific Basis formulation and the amount of each ingredient have not changed, this new production process has allowed us to take an exceptional product and make it even purer. This reflects our ongoing commitment to being a trusted source for our customers by continually exceeding the highest standards in the industry.

In regard to your question about GMO’s, this does not apply to Basis as we don’t have food products in our ingredients eligible for genetic modification. Basis is produced by nature identical synthesis, meaning that the active molecules are constructed to be nature identical. This process is preferable to attempting to distill down the ingredients from food as the final product is purer than what the bi-product would be via distillation.
If you have other questions or if there is anything we can do to help, my team can be reached directly here or by email at care@elysiumhealth.com or phone at 888-220-6436.

Pretty slick, I thought. No, they didn’t substitute something they just threw together to get around the patent and supply problem – they made something more pure and trustworthy.

I don’t know who is going to with the legal battles between Chromadex and Elysium Health, but I see Elysium as way ahead in the marketing department even if I don’t really trust their honesty.

WHY BASIS – IS IT BETTER THAN OTHER BRANDS?

Why Logo White red You’ll find very little mention of Niagen in the sales and marketing literature about Basis.

Elysium would like you to think that Basis is some exclusive formula created by their founders.

In fact, they purchase Niagen from Chromadex like several other brands.

The research and testing that has generated so much excitement has been done with Nicotinamide Riboside from Chromadex.

There has been no research published to show that Pterostibene makes Niagen work any better.

Conclusion: ALL Niagen comes from Chromadex, there is no proof that Basis is any more effective than other brands of Niagen.

THE COST

dollar sign moneybagBasis is available only thru their website for $60 a bottle, which would last for one month if taking 2 pills per day (250mg of Niagen).

Recent research indicates that the optimum dosage for maximum increase in NAD+ levels is at least 250mg per day, or more.

In fact, the best evidence on recommended dosage will hopefully soon be available from a recently completed study sponsored by Elysium Health themselves.

This study of 120 elderly patients tested blood NAD+ levels of 250mg and 500mg of Elysium Health Basis vs placebo.

Once this study is published we’ll have a lot better idea if one bottle per month is sufficient

IS IT WORTH THE EXTRA COST?

If you know that Basis is Niagen + Pterostilbene, and start searching for “Niagen”, you quickly realize you can get the same thing for 1/2 the cost or less elsewhere.

Screenshot 2016-01-25 15.21.18

Conclusion: Since ALL Niagen comes from Chromadex, there is no difference in the quality among brands

What does Basis do?

The field of Anti-Aging supplements is littered with scams and hoax products that are supposed to miraculously stop the aging process.

It is for that exact reason that Elysium Health DOES NOT market Basis specifically as an anti-aging pill.

Rather, they focus on some specific areas that their pill may help with such as:

— DNA repair
— Energy production
— Cellular detoxification
— Protein function

Basis – Conclusion

  • Niagen plus Pterostilbene (similar to Resveratrol)
  • Pre-eminent antiaging researcher as cofounder of company
  • 6 Nobel laureate scientists on advisory board
  • By far the most expensive Niagen on the market
  • One bottle a month may not be enough for optimum results

 

WHAT WE RECOMMEND


NMN PLUS – THE COMPLETE NAD+ BOOSTER

$46.95

Unlike NR, NMN makes it’s way INTACT through the liver quickly and remains available in the bloodstream for many hours (18,97,98,99)

NMN is the Immediate Precursor to NAD+.

NMN is quickly metabolized into tissues throughout the body, where it bypasses the NAMPT bottleneck and restores NAD+ levels in tissues more effectively than other NAD+ precursors.

Read about the science behind NMN.

OTHER PRECURSORS – MAKING NMN EVEN MORE EFFECTIVE

Boosting NAD+ in the liver is great, but is a small part of the health benefits you get from restoring NAD+ thoughout the body.

All the precursors are effective at boosting NAD+ in the liver, so why waste NMN on that simple task?

  • Niacin (NA) is the fastest, elevating NAD+ to peak levels in liver in 15 minutes (R)
  • Tryptophan is the preferable substrate for NAD+ production in the liver(R)
  • Administration of tryptophan, NA, or NAM to rats showed that tryptophan resulted in the highest hepatic NAD+ concentrations(R)

Including Niacin and Tryptophan help elevate NAD+ levels in the liver to their maximum quickly, sparing NMN to be released into the bloodstream and make its way into tissues throughout the body much more effectively.

Like NR, NAM is also very slow acting, taking 8 hours to reach peak NAD+ levels in the liver when used by itself (16).

We include NAM in NMN Plus to act as a slow release NAD+ booster to ensure levels stay high, and potentially sparing NMN from being utilized for NAD+ metabolism in the liver throughout the day.

According to Dr. Charles Brenner:

“Not every cell is capable of converting each NAD+ precursor to NAD+ at all times…the precursors are differentially utilized in the gut, brain, blood, and organs” (R).

NMN – NICOTINAMIDE MONONUCLEOTIDE

  • THE IMMEDIATE PRECURSOR to NAD+
  • “NMN makes its way through the liver, into muscle, and is metabolized to NAD+ in 30 minutes” (R)
  • Treatment for 1 week with NMN was able to restore NAD+ levels in old mice (22 months) to that of 6 month old mice (R)

NAM – NICOTINAMIDE

  • Converts to NAD+ thru a 2 step salvage pathway(R)
  • Is much slower, taking 8 hours to reach peak NAD+ in humans (R)
  • Has been shown to increase NAD+ level in liver (47%), but was weaker in kidney (2%), heart (20%), blood (43%) or lungs (17%) (R)

NA – NICOTINIC ACID (NIACIN)

  • Elevates NAD+ to peak levels in liver in 15 minutes (R)
  • raised NAD+ in liver (47%), and impressively raised kidney (88%), heart (62%), blood (43%) and lungs (11%) (R)
  • “has been used for primary and secondary coronary heart disease prevention for over 40 years”(R)
  • “NA is one of the most effective means to improve cardiovascular risk factors”(R)
  • Long term human studies show 6.2% and 7.8% reduced All Cause Mortality rate (R)
  • Can cause uncomfortable “flushing” in higher dosages, which limits its usage(R)

TRYPTOPHAN

  • In the liver  tryptophan is the preferable substrate for NAD+ production (R)
  • Administration of tryptophan, NA, or NAM to rats showed that tryptophan resulted in the highest hepatic NAD+ concentrations(R)
  • Shown to be beneficial in several neurological conditions, including insomnia, Parkinson disease, schizophrenia, depression, anxiety, and autism. (R, R)

Click here for pricing and more product info

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 and insulin resistance (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)