2255 replies to this topic

[Bryan_S]

Mitochondrial dysfunction in Parkinson's Disease

 

*Appel Alzheimer’s Disease Research Institute, Brain and Mind Research Institute, Weill Cornell Medicine, New York City, New York, USA

 

†Brain and Mind Research Institute, Weill Cornell Medicine, New York City, New York, USA

Received April 3, 2016; revised manuscript received July 4, 2016; accepted July 6, 2016.

 

onlinelibrary.wiley.com/doi/10.1111/jnc.13731/pdf

Edited by Bryan_S, 22 August 2016 - 04:31 PM.

[albedo]

 

Mitochondrial dysfunction in Parkinson's Disease

 

....

 

Very interesting, possibly impacting the PD in the clinic.

 

Connecting the dots …

 

… two wonderful milestones reviews, the 2013’s “The Hallmarks of Aging” (1) and the very recent 2016’s “Metabolic Control of Longevity” (2),  clearly include, in the defined 9 hallmarks of aging, the mitochondrial dysfunctions which increase with aging: “…Part of this deterioration is caused by the above mentioned decrease in NAD+ availability and consequent functional impairment of the deacetylase SIRT1 (Gomes et al., 2013). Indeed, low SIRT1 activity results in the acetylation-dependent inactivation of PGC1a, MYC, and HIF1A, which limits the PGC1a-dependent expression of nuclear genes encoding mitochondrial proteins … (Gomes et al., 2013)…” (2)

 

… and in the paper you reported: “…Activation of PGC-1a is shown to be neuroprotective Many different transgenic mouse models of neurodegenerative diseases. Plioglitazone and benzofibrate which are PPARc agonists are inducers of PGC-1a and mitochondrial biogenesis (Johri et al. 2012). Pioglitazone however was ineffective in a phase II futility trial (NET-PD) FS-ZONE Investigators 2015. Nicotinamide riboside increases SIRT3 which protects against noise-induced hearing loss (Brown et al. 2014)…” (3)

 

See also, from ref. (2):

 

 Metabolic Impact of Hallmarks of Aging.PNG   278.78KB   3 downloads

 

 Metabolic interventions.PNG   143.25KB   3 downloads

 

(1) The Hallmarks of Aging

http://www.cell.com/...8674(13)00645-4

 

(2) Metabolic Control of Longevity

http://www.cell.com/...8674(16)30981-3

 

(3) Mitochondrial dysfunction in Parkinson's Disease

http://onlinelibrary...1/jnc.13731/pdf

[Freebytes]

Seeing articles behind paywalls (especially publicly funded articles) really upsets me. If any of my own tax dollars pay for the research, it should be illegal to put it behind a paywall. Plus, it significantly detracts from research and reproducibility studies. It is a shame that we must have the equivalent of the PirateBay for research papers.

[Nate-2004]

Seeing articles behind paywalls (especially publicly funded articles) really upsets me. If any of my own tax dollars pay for the research, it should be illegal to put it behind a paywall. Plus, it significantly detracts from research and reproducibility studies. It is a shame that we must have the equivalent of the PirateBay for research papers.

 

I completely agree. It's a sick system bent on prestige over quality and reproducibility.

 

 

Mitochondrial dysfunction in Parkinson's Disease

 

 

....

 

Connecting the dots …

 

… two wonderful milestones reviews, the 2013’s “The Hallmarks of Aging” (1) and the very recent 2016’s “Metabolic Control of Longevity” (2),  clearly include, in the defined 9 hallmarks of aging, the mitochondrial dysfunctions which increase with aging: “…Part of this deterioration is caused by the above mentioned decrease in NAD+ availability and consequent functional impairment of the deacetylase SIRT1 (Gomes et al., 2013). Indeed, low SIRT1 activity results in the acetylation-dependent inactivation of PGC1a, MYC, and HIF1A, which limits the PGC1a-dependent expression of nuclear genes encoding mitochondrial proteins … (Gomes et al., 2013)…” (2)

 

… and in the paper you reported: “…Activation of PGC-1a is shown to be neuroprotective Many different transgenic mouse models of neurodegenerative diseases. Plioglitazone and benzofibrate which are PPARc agonists are inducers of PGC-1a and mitochondrial biogenesis (Johri et al. 2012). Pioglitazone however was ineffective in a phase II futility trial (NET-PD) FS-ZONE Investigators 2015. Nicotinamide riboside increases SIRT3 which protects against noise-induced hearing loss (Brown et al. 2014)…” (3)

 

Essential Tremor is also a neurodegenerative disease that I have and I haven't seen much of an effect thus far as far as NR is concerned but it could just be preventing further degeneration. Perhaps the 500mg I'm taking daily isn't even nearly enough?  ET though is becoming more accepted as a classification of similar movement disorders resulting from degeneration in different areas of the brain. I think a lot of them classify or diagnose it under the same umbrella because it's a movement disorder that only expresses itself during certain voluntary movements as opposed to Parkinson's which expresses itself at rest. However this study is promising.  Does anybody know what "neuroprotective" means exactly when they say it (other than the obvious)? It seems like a broad term they're using to describe a wide variety of processes that result in the protection of neurons from degeneration.  What I'm hoping for I guess is the regeneration of neurons, which so far I think only stem cells provide?

[Bryan_S]

Nate-2004,

 

Totally different neurological condition but when I crushed my legs in the skydiving accident I developed some peripheral neuropathy in my feet as might be expected. Mainly one foot was just numb all the time and at times it would feel like shooting pains or a dumb bell was just dropped on my foot. But mostly it felt like my toes were being constricted in a vise. After 2 years, 7 months into the NR the feeling in my left foot has returned (no numbness to the touch) and the pain has greatly diminished. I wasn't expecting any improvement and maybe some of the recovery was time dependent anyway. So at least where severed nerves are concerned it takes some time to reverse these conditions if at all and I can't say positively NR did the trick for me. What does grab my interest is the injury was 28-years ago and the pain improvement has been in the last 2-years. Kind of makes you say Hmmm?

 

 

In the hearing loss studies I don't think it reversed old damage just recent hearing injury. It also helped in a preventative capacity where the inflicted injury took place after the NR had been taken. At any rate I was thinking of you when that article was posted and it looks like NR is on the radar for researchers of Parkinson's Disease.

 

http://www.cell.com/...4131(14)00500-2

[wallynext]

Hello I'm very interested in Nicotinamide Riboside, I'm taking 200mg a day, and just found a website full of articles and scientific knowledge regarding NR and DNA repair, what do you think?: www.boostdnarepair.com

[Razor444]

"An MIT Scientist Claims That This Pill Is the Fountain of Youth" (Leonard Guarente)

[Bryan_S]

"An MIT Scientist Claims That This Pill Is the Fountain of Youth" (Leonard Guarente)

 

"Side effects may include an obsession with death, reinforced every morning when you swallow your pill." interesting overview illustrating some of the unseen dynamics, thanks for posting it.

[Bryan_S]

Slowing ageing by design: the rise of NAD+ and sirtuin-activating compounds

http://www.nature.co...rm.2016.93.html

 

Michael S. Bonkowski & David A. Sinclair

AffiliationsCorresponding author

Nature Reviews Molecular Cell Biology (2016) doi:10.1038/nrm.2016.93

Published online 24 August 2016

 

Abstract

"The sirtuins (SIRT1–7) are a family of nicotinamide adenine dinucleotide (NAD⁺)-dependent deacylases with remarkable abilities to prevent diseases and even reverse aspects of ageing. Mice engineered to express additional copies of SIRT1 or SIRT6, or treated with sirtuin-activating compounds (STACs) such as resveratrol and SRT2104 or with NAD⁺ precursors, have improved organ function, physical endurance, disease resistance and longevity. Trials in non-human primates and in humans have indicated that STACs may be safe and effective in treating inflammatory and metabolic disorders, among others. These advances have demonstrated that it is possible to rationally design molecules that can alleviate multiple diseases and possibly extend lifespan in humans."

[Freebytes]

This is a recent study (August) that showed poorer exercise performance in rats subjected to NR treatment.

http://www.ncbi.nlm....pubmed/27489522

"METHODS:

Eighteen Wistar rats were equally divided in two groups that received either saline vehicle or nicotinamide riboside at a dose of 300 mg/kg body weight/day for 21 days via gavage. At the end of the 21-day administration protocol, both groups performed an incremental swimming performance test.

RESULTS:

The nicotinamide riboside group showed a tendency towards worse physical performance by 35 % compared to the control group at the final 10 % load (94 ± 53 s for the nicotinamide riboside group and 145 ± 59 s for the control group; P = 0.071)."

I am suspicious of using 9 rat groups (18 total) versus each other and concluding results from one exercise trial, but it is important to consider studies with negative results as well.

Edited by Freebytes, 24 August 2016 - 05:20 PM.

[Bryan_S]

This is a recent study (August) that showed poorer exercise performance in rats subjected to NR treatment.

 

We reviewed that one http://www.longecity...-35#entry784953

 

Comments "questionable on its face."

 

It was not a well funded study and it was done by some graduate students in Greece with very few data points. The study to watch is "Thorne Research Announces Clinical Study to Assess Nicotinamide Riboside on Brain NAD+ in College Football Players" Its already well underway.

[bluemoon]

From the article Bryan_S linked to:

 

Sinclair did say that Basis is “based on solid science” and, if he didn’t have his own NAD booster, he’d “strongly consider” taking it. Was I, then, on safe ground taking it? There was a long pause on Sinclair’s end of the line. “You’re never safe assuming anything,” he said. “The results from studies indicate it should be safe.” And effective? Another pause. “I’d rather not say anything that definitive.”

[albedo]

Looking at the kidneys health, in particular regarding the chronic kidney disease (CKD), I am interested to the potential nicotinamide riboside effects. I wonder if this has been researched well and you might know better.

 

Just as a thought and a research hypothesis ...:

1. ... a bit along the lines of the previous post (1) on the possible NR neuroprotective role (PD, but likely others)…
2. ... due to the effect of NR in promoting the “…peroxisome proliferator-activated receptor-γ coactivator 1 (PGC)-1α expression in the brain…” (2) …
3. ... considering the effect of known blood pressure drugs such as Telmisartan (it is an angiotensin II receptor blockers or ARB) which have been shown to “…effectively lower blood pressure and reduce urinary protein excretion in CKD patients with hypertension (Weinberg 2006). Use of ARBs has also been associated with increased survival among individuals with CKD (Molnar 2014). In addition, long-term use of ARBs does not appear to cause significant side effects in CKD patients (Weinberg 2006; Weinberg 2004)…” (3) ...
4. ... it could be that NR might have an additional path of action, here beneficial for CKD, via the PPAR-gamma activation, similar to Telmisartan, possibly w/o the side effects: “…Telmisartan is a unique ARB; not only does it help reduce blood pressure, but it also activates a nuclear receptor called peroxisome proliferator-activated receptor gamma or PPAR-γ (Yamagishi 2007; Kurtz 2005)…” (3)

I have no time yet to look at all reference quoted and dig more on this, but thought to log it here anyway for research. You might have other pointers to the link between CKD and NR.

1. http://www.longecity...ndpost&p=786921
2. http://www.ncbi.nlm....les/PMC3632303/
3. http://www.lifeexten...-Health/Page-05

 

[tunt01]

 

Looking at the kidneys health, in particular regarding the chronic kidney disease (CKD), I am interested to the potential nicotinamide riboside effects. I wonder if this has been researched well and you might know better.

 

I have no time yet to look at all reference quoted and dig more on this, but thought to log it here anyway for research. You might have other pointers to the link between CKD and NR.

 

 

I have this paper sitting way down on my to-read list.  It's somewhat related to kidney / NAD+ synthesis:

 

PGC1α drives NAD biosynthesis linking oxidative metabolism to renal protection

 

The energetic burden of continuously concentrating solutes against gradients along the tubule may render the kidney especially vulnerable to ischaemia. Acute kidney injury (AKI) affects 3% of all hospitalized patients. Here we show that the mitochondrial biogenesis regulator, PGC1α, is a pivotal determinant of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis.

 

Following renal ischaemia, Pgc1α(-/-) (also known as Ppargc1a(-/-)) mice develop local deficiency of the NAD precursor niacinamide (NAM, also known as nicotinamide), marked fat accumulation, and failure to re-establish normal function. Notably, exogenous NAM improves local NAD levels, fat accumulation, and renal function in post-ischaemic Pgc1α(-/-) mice. Inducible tubular transgenic mice (iNephPGC1α) recapitulate the effects of NAM supplementation, including more local NAD and less fat accumulation with better renal function after ischaemia. PGC1α coordinately upregulates the enzymes that synthesize NAD de novo from amino acids whereas PGC1α deficiency or AKI attenuates the de novo pathway. NAM enhances NAD via the enzyme NAMPT and augments production of the fat breakdown product β-hydroxybutyrate, leading to increased production of prostaglandin PGE2 (ref. 5), a secreted autacoid that maintains renal function. NAM treatment reverses established ischaemic AKI and also prevented AKI in an unrelated toxic model. Inhibition of β-hydroxybutyrate signalling or prostaglandin production similarly abolishes PGC1α-dependent renoprotection. Given the importance of mitochondrial health in ageing and the function of metabolically active organs, the results implicate NAM and NAD as key effectors for achieving PGC1α-dependent stress resistance.

 

 

 

popular article about the paper:

 

Mitochondrial metabolism linked to acute kidney injury PGC1 alpha works through NAD 'aging molecule' to guard against stress; research offers new therapeutic target for acute kidney injury

 

 

Approximately one out of five hospitalized adults and one out of three hospitalized children worldwide experience acute kidney injury, the sudden loss of kidney function. Many different factors, including surgery, chemotherapy or shock, can lead to acute kidney injury, but exactly why the kidneys are so vulnerable to these and other stressors has not been well understood.

Now a research team led by investigators at Beth Israel Deaconess Medical Center (BIDMC) has discovered that mitochondria, the metabolic energy sources essential to the health of kidneys and other organs, also play a key role in kidney injury. The proof-of-concept study, published online today in the journal Nature, demonstrates that a gene called PGC1 alpha provides kidneys with protection by working through nicotinamide adenine dinucleotide (NAD), a molecule involved in metabolism thought to be key to the aging process.

The new findings suggest that manipulation of NAD could lead to a future therapy for acute kidney injury and also raise the possibility that mitochondrial injury and deficiency in NAD might underlie other types of organ damage, including damage that can lead to stroke or heart attack.

....

 

 

 

 

Edited by prophets, 26 August 2016 - 09:34 PM.

[Bryan_S]

The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia

 

Kilmer S McCully of the U.S. Department of Veterans Affairs posted this study.

 

Available online at www.annclinlabsci.org The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia Kilmer S. McCullyPathology and Laboratory Medicine Service, VA Boston Healthcare System, Harvard Medical School, Boston, Massa-chusetts, USA

 

Abstract. The active site of oxidative phosphorylation and adenosine triphosphate (ATP) synthesis in mi-tochondria is proposed to consist of two molecules of thioretinamide bound to cobalamin, forming thio-retinaco, complexed with ozone, oxygen, nicotinamide adenine dinucleotide. and inorganic phosphate, TR2CoO3O2NAD+H2PO4-.  Reduction of the pyridinium nitrogen of the nicotinamide group by an elec-tron from electron transport complexes initiates polymerization of phosphate with adenosine diphosphate, yielding nicotinamide riboside and ATP bound to thioretinaco ozonide oxygen.  A second electron reduces oxygen to hydroperoxyl radical, releasing ATP from the active site.  A proton gradient is created within F1F0 ATPase complexes of mitochondria by reaction of protons with reduced nicotinamide riboside and with hy-droperoxyl radical, yielding reduced nicotinamide riboside and hydroperoxide.  e hyperhomocysteinemia of aging and dementia is attributed to decreased synthesis of adenosyl methionine by thioretinaco ozonide and ATP, causing decreased allosteric activation of cystathionine synthase and decreased allosteric inhibition of methylenetetrahydrofolate reductase and resulting in dysregulation of methionine metabolism.

Edited by Bryan_S, 29 August 2016 - 04:06 PM.

[stefan_001]

The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia

Kilmer S McCully of the U.S. Department of Veterans Affairs posted this study.

Available online at www.annclinlabsci.org The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia Kilmer S. McCullyPathology and Laboratory Medicine Service, VA Boston Healthcare System, Harvard Medical School, Boston, Massa-chusetts, USA

Abstract. The active site of oxidative phosphorylation and adenosine triphosphate (ATP) synthesis in mi-tochondria is proposed to consist of two molecules of thioretinamide bound to cobalamin, forming thio-retinaco, complexed with ozone, oxygen, nicotinamide adenine dinucleotide. and inorganic phosphate, TR2CoO3O2NAD+H2PO4-. Reduction of the pyridinium nitrogen of the nicotinamide group by an elec-tron from electron transport complexes initiates polymerization of phosphate with adenosine diphosphate, yielding nicotinamide riboside and ATP bound to thioretinaco ozonide oxygen. A second electron reduces oxygen to hydroperoxyl radical, releasing ATP from the active site. A proton gradient is created within F1F0 ATPase complexes of mitochondria by reaction of protons with reduced nicotinamide riboside and with hy-droperoxyl radical, yielding reduced nicotinamide riboside and hydroperoxide. e hyperhomocysteinemia of aging and dementia is attributed to decreased synthesis of adenosyl methionine by thioretinaco ozonide and ATP, causing decreased allosteric activation of cystathionine synthase and decreased allosteric inhibition of methylenetetrahydrofolate reductase and resulting in dysregulation of methionine metabolism.

Interesting postulation and proposal. So we should experiment with supplementing retinol and cobalamin next to the NR. Need to re-read again the pape but this may be a feasible experiement to try.

[Female Scientist]

Interesting idea. Is there other info/data from other sources on the need to supplement with cobolamin and retinol (in aging, or just in general), or is this the first we have heard of it in the context of ATP? AND --  If we wanted to supplement as Stefan suggested as a possibility, what would be ideal? Looks like cobolamin is simply vitamin B12, and retinol is the animal-based form of Vitamin A found in liver, egg yolks, and dairy, correct? Or are there other sources? 

 

The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia

Kilmer S McCully of the U.S. Department of Veterans Affairs posted this study.

Available online at www.annclinlabsci.org The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia Kilmer S. McCullyPathology and Laboratory Medicine Service, VA Boston Healthcare System, Harvard Medical School, Boston, Massa-chusetts, USA

Abstract. The active site of oxidative phosphorylation and adenosine triphosphate (ATP) synthesis in mi-tochondria is proposed to consist of two molecules of thioretinamide bound to cobalamin, forming thio-retinaco, complexed with ozone, oxygen, nicotinamide adenine dinucleotide. and inorganic phosphate, TR2CoO3O2NAD+H2PO4-. Reduction of the pyridinium nitrogen of the nicotinamide group by an elec-tron from electron transport complexes initiates polymerization of phosphate with adenosine diphosphate, yielding nicotinamide riboside and ATP bound to thioretinaco ozonide oxygen. A second electron reduces oxygen to hydroperoxyl radical, releasing ATP from the active site. A proton gradient is created within F1F0 ATPase complexes of mitochondria by reaction of protons with reduced nicotinamide riboside and with hy-droperoxyl radical, yielding reduced nicotinamide riboside and hydroperoxide. e hyperhomocysteinemia of aging and dementia is attributed to decreased synthesis of adenosyl methionine by thioretinaco ozonide and ATP, causing decreased allosteric activation of cystathionine synthase and decreased allosteric inhibition of methylenetetrahydrofolate reductase and resulting in dysregulation of methionine metabolism.

Interesting postulation and proposal. So we should experiment with supplementing retinol and cobalamin next to the NR. Need to re-read again the pape but this may be a feasible experiement to try.

 

 

[stefan_001]

I have not seen these linked before. Its  an experimental paper so I think I will try doing this just using common sense = stick to regular serving sizes recommended in the supplements

 

Interesting idea. Is there other info/data from other sources on the need to supplement with cobolamin and retinol (in aging, or just in general), or is this the first we have heard of it in the context of ATP? AND --  If we wanted to supplement as Stefan suggested as a possibility, what would be ideal? Looks like cobolamin is simply vitamin B12, and retinol is the animal-based form of Vitamin A found in liver, egg yolks, and dairy, correct? Or are there other sources? 

 

The Active Site of Oxidative Phosphorylation and the Origin of Hyperhomocysteinemia in Aging and Dementia

Interesting postulation and proposal. So we should experiment with supplementing retinol and cobalamin next to the NR. Need to re-read again the pape but this may be a feasible experiement to try.

 

Edited by stefan_001, 30 August 2016 - 01:28 PM.

[Harkijn]

The science here is way above my head but it seems to me that preventing hyperhomocystenemia should start with a low methionine diet. Elsewhere on these forums the longevity effects of methionine restriction are expounded.

[Bryan_S]

New Study finds Nicotinamide Riboside safe at typical dosages

http://alivebynature...ypical-dosages/

 

These guys a  little late to the show but worth repeating.

 

 

Mouse Research shows Nicotinamide Riboside cures Liver Disease

 

Both just posted today

Edited by Bryan_S, 31 August 2016 - 07:04 PM.

[stefan_001]

New Study finds Nicotinamide Riboside safe at typical dosages

http://alivebynature...ypical-dosages/

 

These guys a  little late to the show but worth repeating.

 

 

Mouse Research shows Nicotinamide Riboside cures Liver Disease

 

Both just posted today

 

 

I have seen earlier. These articles are identical to these. Seems this site is just copying the articles from here:

 

http://www.timelessl...side-published/

 

http://www.timelessl...cancer-in-mice/

[midas]

Maybe someone here has better access to this.....

 

http://www.readcube....038/nrm.2016.93

 

http://www.nature.co...016.93.html....

"Published on-line 24 August 2016"

Edited by midas, 31 August 2016 - 09:28 PM.

[lumia]

Maybe someone here has better access to this.....

 

http://www.readcube....038/nrm.2016.93

 

http://www.nature.co...016.93.html....

"Published on-line 24 August 2016"

 

This is a review, though. It's Sinclair, but still a review, so I'd rather just post the abstract.

Slowing ageing by design: the rise of NAD⁺ and sirtuin-activating compounds

• Michael S. Bonkowski
• & David A. Sinclair

 

 

 

Abstract

 

The sirtuins (SIRT1–7) are a family of nicotinamide adenine dinucleotide (NAD⁺)-dependent deacylases with remarkable abilities to prevent diseases and even reverse aspects of ageing. Mice engineered to express additional copies of SIRT1 or SIRT6, or treated with sirtuin-activating compounds (STACs) such as resveratrol and SRT2104 or with NAD⁺ precursors, have improved organ function, physical endurance, disease resistance and longevity. Trials in non-human primates and in humans have indicated that STACs may be safe and effective in treating inflammatory and metabolic disorders, among others. These advances have demonstrated that it is possible to rationally design molecules that can alleviate multiple diseases and possibly extend lifespan in humans.

[APBT]

Maybe someone here has better access to this.....

 

http://www.readcube....038/nrm.2016.93

 

http://www.nature.co...016.93.html....

"Published on-line 24 August 2016"

 

FULL TEXT:

Attached Files

•  SLOWING AGEING BY DESIGN.pdf   1.51MB   33 downloads

[Bryan_S]

Thanks guys.

 

The Nature link had failed, this should be correct http://www.nature.co...rm.2016.93.html

 

Thanks for the post PDF post APBT.

[Nate-2004]

I would be interested in seeing some more extensive study with NR on women in their later 30's and 40's specifically around fertility, success around pregnancy and giving birth, breastfeeding, as well as recovery and longer term effects that follow her and the child through developmental years.

Edited by Nate-2004, 01 September 2016 - 02:51 AM.

[Female Scientist]

I would be interested in seeing some more extensive study with NR on women in their later 30's and 40's specifically around fertility, success around pregnancy and giving birth, breastfeeding, as well as recovery and longer term effects that follow her and the child through developmental years.

Me too. As a woman in that general age range (actually 48 already, yikes) I am keenly aware of such issues -- especially after having multiple IVFs as well as natural conception to eventually have 4 kiddos, my last at age 41, and with the scientific background to understand how the hormone cycle starts to get disrupted with age. So I am very tuned in to hormonal issues around aging, and I definitely see some reversal in that area personally after being on NR since February of this year. The bad news is that women are usually the last to be studied in new medications and I assume supplements, hopefully that will change, but for sure the area around female fertility, aging, and NR seems ripe for study!

[Bryan_S]

I would be interested in seeing some more extensive study with NR on women in their later 30's and 40's specifically around fertility, success around pregnancy and giving birth, breastfeeding, as well as recovery and longer term effects that follow her and the child through developmental years.

 

On that topic I think the study on nicotinamide riboside and senescence might have some bearing. It wouldn't surprise me if it could extend fertility and or germ cell viability and animal studies should be able to indicate that.

NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice.

 

Going to bed

[stefan_001]

 

I would be interested in seeing some more extensive study with NR on women in their later 30's and 40's specifically around fertility, success around pregnancy and giving birth, breastfeeding, as well as recovery and longer term effects that follow her and the child through developmental years.

Me too. As a woman in that general age range (actually 48 already, yikes) I am keenly aware of such issues -- especially after having multiple IVFs as well as natural conception to eventually have 4 kiddos, my last at age 41, and with the scientific background to understand how the hormone cycle starts to get disrupted with age. So I am very tuned in to hormonal issues around aging, and I definitely see some reversal in that area personally after being on NR since February of this year. The bad news is that women are usually the last to be studied in new medications and I assume supplements, hopefully that will change, but for sure the area around female fertility, aging, and NR seems ripe for study!

 

 

Hello, that's a very interesting observation and I have been wondering about this too. What science has classified as a natural process, the disruption of the hormone cycle, may be nothing else than the body starting to drift out of operating range. Like others from a male perspective I believe the body is also somewhat reverting to a younger hormone balance. I have searched for studies of impact on female's before but have not found anything too relevant unfortunately

[bluemoon]

I just saw that Chromadex's stock price has slid to near the sudden drop off point in June before rebounding. I couldn't find any recent news so does anyone know if this is related to a report on NR?