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Glucosamine promotes longevity by mimicking a low-carb diet

glucosamine

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#1 midas

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Posted 09 April 2014 - 01:58 AM


.. https://www.ethz.ch/...serwartung.html

 

"I would tend to recommend this supplement.” says Michael Ristow, M.D., a professor at ETH Zurich,


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#2 ta5

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Posted 09 April 2014 - 02:48 AM

Great find! Some of the studies were posted in this thread:

http://www.longecity...ndpost&p=602006


Edited by cryonicsculture, 09 April 2014 - 04:51 AM.


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#3 YOLF

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Posted 09 April 2014 - 04:44 AM

Several of the same studies were posted in this thread:

http://www.longecity...ndpost&p=602006

 

 

I think this is the first time trials have shown that it extends lifespans in something with fur on it (mice). I used to take this stuff by the handful. Might have to start getting bulk powder of it. 

 

http://news.yahoo.co...-171630683.html



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#4 hamishm00

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Posted 09 April 2014 - 05:19 AM

What about about the in vitro studies that show glucosamine destroys pancreatic islet cells. I would be careful before loading up on this stuff.
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#5 maxwatt

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Posted 10 April 2014 - 02:46 AM

You can read the full paper published by Nature magazine, online here:

http://www.nature.co...ncomms4563.html

 

The mice received 10 mg per kg by weight glucosamine in their food.  For a person at 2000 calories a day, 30% from fat, scaling by body mass, a gram a day should be the equivalent, .with some to spare

The authors claim a 10 percent increase in life span, but the long-lived mice were not exceptionally long lived for this strain.  Whether glucosamine compensated for a defect in the environment,  or if it would extend the lifespan of optimally raised mice, much less humans, is impossible to say.

 

NATURE COMMUNICATIONS | ARTICLE OPEN

D-Glucosamine supplementation extends life span of nematodes and of ageing mice Sandra Weimer, Josephine Priebs,Doreen Kuhlow,  
  •  

Abstract
D-Glucosamine (GlcN) is a freely available and commonly used dietary supplement potentially promoting cartilage health in humans, which also acts as an inhibitor of glycolysis. Here we show that GlcN, independent of the hexosamine pathway, extends Caenorhabditis elegans life span by impairing glucose metabolism that activates AMP-activated protein kinase (AMPK/AAK-2) and increases mitochondrial biogenesis. Consistent with the concept of mitohormesis, GlcN promotes increased formation of mitochondrial reactive oxygen species (ROS) culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation or impairment of aat-1-expression abolishes GlcN-mediated life span extension in an NRF2/SKN-1-dependent fashion. Unlike other calorie restriction mimetics, such as 2-deoxyglucose, GlcNextends life span of ageing C57BL/6 mice, which show an induction of mitochondrial biogenesis, lowered blood glucose levels, enhanced expression of several murine amino-acid transporters, as well as increased amino-acid catabolism. Taken together, we provide evidence that GlcN extends life span in evolutionary distinct species by mimicking a low-carbohydrate diet.

 


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#6 maxwatt

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Posted 10 April 2014 - 03:07 AM

What about about the in vitro studies that show glucosamine destroys pancreatic islet cells. I would be careful before loading up on this stuff.

 

Do you have a citation?  The papers I am familiar with showing pancreatic cell effects, were all in vitro and at concentrations impossible to be obtained with oral supplementation.  It is possible that the mechanism, at lower concentrations, is what is responsible for the life-prolonging effects noted in Ristow's paper.  I glanced at his paper, and I think they noted a temporary increase in insulin resistance, followed by impaired glucose metabolism leading to mitochondrial biogenesis and protein turnover, duplicating some of the effects of caloric restriction.  They also noted ROS generation was necessary to produce life extension effects.  I need to study the paper a bit to comment further, but this is neither simple nor straight-forward.  The authors also note glucosamine has been taken in quantity for joint pain by many thousands of people for 50 years, and consider it at worse benign as a supplement.  (NB: glucosamine is not effective for joint pain.)

 

More significant, if their result holds, supplementation can be started late in life, the mouse equivalent of 60 years of age.  They claim a 10% extension.  That's as if a 60-year old started a gram a day of glucosamine, he could live to 99 rather than 90 years of age.


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#7 blood

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Posted 10 April 2014 - 05:07 AM

... They also noted ROS generation was necessary to produce life extension effects...

 

I wonder how this would play out in those of us who are taking powerful mitochondrial antioxidants such as C60-OO?


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#8 Kevnzworld

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Posted 10 April 2014 - 07:00 AM

It seems that the MOA of every substance that has increased rodent lifespan is related to glucose metabolism ( other than possibly C60)
" The widely used food supplement glucosamine promotes longevity in ageing mice by approximately 10% due to improved glucose metabolism. "
Acarbose
Green tea extract
Metformin
CR

#9 golgi1

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Posted 16 April 2014 - 04:05 PM

I started taking 2 grams of NAG per day in February, but quickly switched it to 2 grams every other day and, now, I stagger the dose to 2 grams every three days, 2gm/2days/2gm/3days...

 

This last schedule is by far the most effective. Currently, this is all that I take other than ultra LDN (a couple of nanograms) every 2-3 days

 

I initially switched to the 2 day schedule because taking 2 grams every day would cause me to only sleep a few hours each night. I actually didn't feel like I needed more sleep either, but getting only that much sleep is a red flag for me. NAG still causes me to wake up earlier than usual sometimes, but I can now go back to sleep for a full 8 hours most of the time. When I do wake up, I'm not jittery or wired. The effect is one of calm, rested clarity. Although if I do get up after only a few hours, fatigue catches up with me later in the day. I can frequently function on 5-6 hours now, which was before impossible for me. Although, I'll begin to get deeply fatigued at night after a day or two of that.

 

If starting from baseline, it takes a couple of doses for it to really kick in. The overall effect is one of marked anti-inflammation in the brain that continues through the next dose (even three days later). That's the major effect for me, although I'm pretty sure I have some measure of cognitive improvement as well. Although, that improvement could just be the robust anti-inflammation effect keeping me at a level where most healthy people are most of the time.

 

Whatever NAG does, it seems to do it potently and, once the dose is managed, I seem to get mostly benefit with little negative side effect.

 

The pancreatic islet cell warning is new to me, and a worrisome consideration. I wonder if that destructive process could account for increasing negative effects with regular dosing, and thusly my staggered schedule primarily works to mitigate the pancreatic effect (possibly amongst other processes that might lead to side effects). I'm not sure, but if NAG has the potential to negatively affect the pancreas and glucose metabolism, then staggering the dose would make the most sense to mitigate that effect because the body is allowed to regularly recover toward unmolested baseline glucose metabolism. The 2day/3day schedule may keep the brain from being able to predict the dose and adjust, keeping the effect at a consistently more beneficial level. This is just hypothesis.

 

I believe that I did try a lower dose before, but eventually found that 2 grams works best for me. I am overweight at the moment, though. Also, I didn't consistently use the lower dose. I only used it a couple of times.

 

NAG is one of the most potent substances that I've taken, if length of action can be partly equated to potency. Astragalus, which I didn't get along with, was probably the only substance that I can compare it to in terms of length and potency of action. Now that I think about it, NAG may very well likely have a lasting hormetic effect that accounts for its length of action rather than a continued direct action over a period of days. The latter circumstance is unlikely. This hypothesis, if correct, might be an anecdotal endorsement of NAG's action as a calorie restriction mimetic.

 

Last, if NAG was destructive to the pancreas and had a lasting negative effect on glucose metabolism, could the mice have lived an extra 10%? This question is not rhetorical.


Edited by golgi1, 16 April 2014 - 04:24 PM.

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#10 LucidMind

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Posted 17 April 2014 - 07:42 AM

I am assuming that it is glucosamine sulfate, which is the important glucosamine type?



#11 elp

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Posted 19 April 2014 - 09:27 PM

acetyl-l-glucosamine is the most effective at inducing collagen production in the skin...


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#12 medicineman

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Posted 30 April 2014 - 02:20 PM


... They also noted ROS generation was necessary to produce life extension effects...

 
I wonder how this would play out in those of us who are taking powerful mitochondrial antioxidants such as C60-OO?
well, apparently the life extension effects of glucosamine were abolished with the addition of antioxidants.

To test whether the increase in ROS (Fig. 1i,j) is essential for a GlcN-mediated extension of life span, we repeated the initial life span experiment (Fig. 1b) in the presence of the antioxidants butylated hydroxyl anisole (BHA) and N-acetyl-cystein (NAC), respectively. Although neither BHA (Fig. 2a) nor NAC (Fig. 2b) had a detectable effect on C. elegans life span in the absence of GlcN, the life span-extending capabilities of GlcN were nullified in the presence of BHA or NAC


Edited by medicineman, 30 April 2014 - 02:30 PM.


#13 maxwatt

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Posted 30 April 2014 - 05:24 PM

dose, concentration, timing, tissue partitioning. Moderation in all things, especially antioxidants. abstinence is risky too.

#14 maxwatt

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Posted 30 April 2014 - 08:35 PM

I am assuming that it is glucosamine sulfate, which is the important glucosamine type?

 

No, it is n-acetyl glucosamine.  The sulfate seems to be an anion for stability....

acetylated molecules tend to be more bioavailable than he plain forms, to wit: acetyl salicylic acid aka aspirin versus salicylic acid, or acetylated morphine otherwise known as heroin.

 

Both were Bayer's hot drugs of 1890 or so.



#15 APBT

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Posted 01 May 2014 - 09:30 PM

 

 

... They also noted ROS generation was necessary to produce life extension effects...

 
I wonder how this would play out in those of us who are taking powerful mitochondrial antioxidants such as C60-OO?
well, apparently the life extension effects of glucosamine were abolished with the addition of antioxidants.

To test whether the increase in ROS (Fig. 1i,j) is essential for a GlcN-mediated extension of life span, we repeated the initial life span experiment (Fig. 1b) in the presence of the antioxidants butylated hydroxyl anisole (BHA) and N-acetyl-cystein (NAC), respectively. Although neither BHA (Fig. 2a) nor NAC (Fig. 2b) had a detectable effect on C. elegans life span in the absence of GlcN, the life span-extending capabilities of GlcN were nullified in the presence of BHA or NAC

 

I'm assuming the GlcN and NAC or BHA were co-administered in the quoted study (i.e. given at the same time). 

If that was the case, would timing of GlcN consumption affect efficacy?  That is, take GlcN away from 'heavy' antioxidants and reap the (potential) life-extending benefits.  What is the half-life of GlcN?



#16 APBT

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Posted 01 May 2014 - 09:38 PM

 

The pancreatic islet cell warning is new to me, and a worrisome consideration. I wonder if that destructive process could account for increasing negative effects with regular dosing, and thusly my staggered schedule primarily works to mitigate the pancreatic effect (possibly amongst other processes that might lead to side effects). I'm not sure, but if NAG has the potential to negatively affect the pancreas and glucose metabolism, then staggering the dose would make the most sense to mitigate that effect because the body is allowed to regularly recover toward unmolested baseline glucose metabolism. The 2day/3day schedule may keep the brain from being able to predict the dose and adjust, keeping the effect at a consistently more beneficial level. This is just hypothesis. 

 

Not addressing your exact concern, but.....

 

 

 

http://www.nature.co...ncomms4563.html

GlcN in its endogenously phosphorylated form, GlcN-6-phosphate, is a well-established inhibitor of both hexokinase4 (EC enzyme number 2.7.1.1) and, in particular, its predominant liver-specific functional isoform, glucokinase5 (EC 2.7.1.2), thereby reflecting the initial step within the enzymatic breakdown of glucose to form pyruvate and ATP, which is called glycolysis. Accordingly, short-term administration of high-dose GlcN to model systems678 or humans910 acutely impairs glucosemetabolism that resembles some of the metabolic features of diabetes mellitus. By contrast, chronic GlcN intake has no detectable influence11, or even blood glucose-lowering12 effects in humans. 

 


Edited by APBT, 01 May 2014 - 09:55 PM.


#17 smithx

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Posted 01 May 2014 - 11:44 PM

I have been taking at least 5gm and sometimes up to 20gm of NAG per day, as an auto-immune modulator. I'm happy to provide references if anyone is interested. It seems to help many kinds of autoimmune diseases, including MS and rheumatoid arthritis.

 

My fasting glucose has increased lately, however, so this idea that it may damage islet cells is very worrisome. Does anyone have a reference for this?

 



#18 APBT

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Posted 02 May 2014 - 12:21 AM

http://www.ncbi.nlm....pubmed/11893929

 

Glucosamine-induced beta-cell dysfunction: a possible involvement of glucokinase or glucose-transporter type 2.

Abstract
INTRODUCTION:

The mechanism for beta-cell dysfunction induced by glucosamine has not yet fully been investigated previously.

AIM:

To investigate the effects of glucosamine on insulin release or gene expression related to glucose metabolism in rat islets cultured with glucosamine for 24 hours.

METHODOLOGY:

After islets were cultured with glucosamine or diazoxide, we measured glucose- or arginine-induced insulin release by using radioimmunoassay (RIA) and gene expressions by semiquantitative polymerase/chain reaction.

RESULTS:

Coculture with glucosamine inhibited 27 mmol/L glucose-induced insulin release with no effects on 20 mmol/L arginine-induced insulin release. Coculture with diazoxide did not restore the impaired glucose-induced insulin release. In glucosamine-cultured islets, glucose-transporter type 2 or glucokinase mRNA expression decreased, whereas hexokinase mRNA increased. Phosphofructokinase-A, pyruvate dehydrogenase E1alpha, or pyruvate carboxylase mRNA was not affected by the addition of glucosamine. Pancreatic and duodenal homeobox-1, preproinsulin, or p21 (induced by oxidative stress) mRNA expression did not change, whereas uncoupling protein 2 mRNA, which plays an important role in thermogenesis, decreased in glucosamine-cultured islets.

CONCLUSION:

These data imply that glucosamine impairs glucose-induced insulin release probably through the inhibition of glucose metabolism.

PMID:   11893929   [PubMed - indexed for MEDLINE]
 
 

 


http://www.eje-onlin...id=eje;58/4/558

 

EFFECTS OF GLUCOSAMINE ON THE RESPIRATION OF PANCREATIC ISLET B-CELLS

ABSTRACT

Metabolic effects of D-glucosamine on the pancreatic islet B-cells were evaluated by measurements of the oxygen uptake of isolated and surviving islets. The tissue specimens, which were obtained from obese-hyperglycaemic mice and consisted of more than 90% B-cells, were incubated in Cartesian divers with Krebs-Ringer phosphate medium at +37° C. Addition of glucosamine to the incubation medium caused a significant inhibition of the endogenous islet respiration and an even more pronounced inhibition of the oxygen uptake in the presence of D-glucose. When islets were pre-incubated with glucosamine and subsequently supplied with glucose, there was a relatively slight elevation of the oxygen consumption rate, indicating a partial block of the stimulating effect of glucose on the islet respiration. The results support the view that the diabetogenic effect of glucosamine is caused in part by a direct interference with the glucose utilization in the pancreatic B-cell, resulting in a diminished insulin release.

 

 

 


http://joe.endocrino...t/208/1/41.long

 

Hexosamines stimulate apoptosis by altering SIRT1 action and levels in rodent pancreatic β-cells

  1. Mathieu Lafontaine-Lacasse
  2. Geneviève Doré and 
  3. Frédéric Picard

+Author Affiliations

  1. Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec,Laval University, Y3106 Pavillon Marguerite-d'Youville, 2725 Chemin Ste-Foy, Québec, Québec, Canada G1V 4G5
  1. (Correspondence should be addressed to F Picard; Email:frederic.picard@criucpq.ulaval.ca)
Abstract

The activity and levels of SIRT1, which promotes cell survival in several models, are linked to glucose concentrations and cellular energy metabolism. The present study aimed to determine whether impaired Sirt1 activity is involved in the induction of apoptosis by the nutrient-sensing hexosamine biosynthesis pathway (HBP). Pancreatic Nit-1, Rin-m5F, and Min6 β-cells were acutely treated at different doses and times with glucosamine, which enters and stimulates the HBP. Sirt1 levels were genetically modulated by retroviral infection. Expression levels, cellular localization, and activity of apoptosis-related markers were determined by qPCR, immunoblotting, and co-immunoprecipitation. Glucosamine treatment dose- and time dependently induced cell apoptosis in all cell lines studied. HBP stimulation time dependently modified SIRT1 protein levels, notably in the cytoplasm. This was concomitant with increased E2F1 binding to the c-myc promoter. In both NIT-1 and min6 β-cells, genetic knockdown of Sirt1 expression resulted in higher susceptibility to HBP-stimulated apoptosis, whereas overexpression of Sirt1had the opposite impact. These findings indicate that reduction of SIRT1 levels by hexosamines contributes to β-cell apoptosis. Methods to increase SIRT1 levels or activity could thus prevent the decrease in β-cell mass, notably that observed in type 2 diabetes.

 


Edited by APBT, 02 May 2014 - 12:22 AM.

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#19 APBT

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Posted 02 May 2014 - 12:45 AM

For those interested in purchasing NAG, Swanson has their branded version on BOGO.  Additionally, today only (1 May), use coupon code: 1DAYONLY for an additional 15% off your entire order sitewide, plus free shipping.  http://www.swansonvi...ucan-750-mg-60-caps



#20 smithx

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Posted 02 May 2014 - 01:07 AM

Thanks APBT.

 

Those are all in vitro studies, but don't sound encouraging.

 

Is there any way to measure whether damage is occurring or has occurred? For example, doing a glucose tolerance test and measuring insulin release?

 

Also, that last study seemed to indicate that increasing SIRT1 might overcome some of the potential negative effects, so perhaps nicotinamide riboside would be helpful.

 

Does anyone else have any thoughts about these pancreatic effects and/or the mitigation thereof?

 



#21 golgi1

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Posted 02 May 2014 - 03:25 AM

I still feel great on NAG, but my dosing schedule has become even more spaced out. I'm not sure if the perceived benefits have become longer-lasting with time or if merely spacing out the dosing contributes to longer-lasting benefits. It's an average of 4-5 days between doses, but that started due to laziness/forgetfulness and not as a response to any effect. Fortuitously, I discovered that the anti-inflammatory and other effects were lasting and even becoming enhanced on a more spaced out schedule. I'm still at 2 grams, but will likely experiment with reducing that dose over a variety of dose schedules (shorter and up to 4-5 days). I may arrive at 2 grams, but it's clear that NAG requires significant dose and frequency experimentation to get right. The most I can say about anything that can be perceived as negative is that, in the first 2-3 days after dosing, I don't often require more than 4-5 hours sleep.


Edited by golgi1, 02 May 2014 - 03:26 AM.


#22 albedo

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Posted 03 May 2014 - 09:51 AM

I was using glucosamine sulfate to help with signs of osteoarthritis (OA) in my knee as it looked the most effective form (e.g. here). I stopped taking it when suspecing some negative effect on my glucose metabolism even if, researching in the literature, the effect is controversial (e.g. a review is here). I subjectively could benefit from using UC-II collagen. For the record, I also dropped taking chondroitin sulfate due to some evidence on increased prostate cancer risk. Sorry if this was a bit off the longevity promotion focus.


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#23 ta5

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Posted 03 May 2014 - 01:41 PM

Arthritis and spinal disc degeneration runs in my family and I want to do all I can to prevent it. I've always been interested in Glucosamine, but never took it. I used to be concerned about it's effect on glucose metabolism, but not so much anymore. My concern now is that it may prevent rebuilding cartilage. That's definitely not an effect that I want. In the references below, I only included part of the abstract to save space. You can read the whole abstracts here.
 
 
 
Spine J. 2013 Dec 18. 
"...under conditions of mechanical stimulation, although inflammatory gene expression was decreased, PGE2 was not. In addition, matrix metalloproteinase-3 gene expression was increased and aggrecan expression decreased, both of which would have a detrimental effect on matrix homeostasis. Consistent with this, measurement of total glycosaminoglycans and new proteoglycan synthesis demonstrated detrimental effects of glucosamine under all conditions tested. These results may in part help to explain the conflicting reports of efficacy, as there is biological plausibility for a therapeutic effect under conditions of predominate inflammation but not under conditions where mechanical loading is present or in which matrix synthesis is needed."
PMID: 24361347 
 
Spine (Phila Pa 1976). 2013 Jan 15. 
"...The MRI index and NP area of injured discs of glucosamine treated animals with annular puncture was found to be lower than that of degenerated discs from rabbits not supplemented with glucosamine. Consistent with this, decreased glycosaminoglycan was demonstrated in glucosamine fed animals, as determined by both histological and GAG content. Gene expression was consistent with a detrimental effect on matrix. Conclusions. These data demonstrate that the net effect on matrix in an animal model in vivo, as measured by gene expression, MRI, histology, and total proteoglycan is anti-anabolic. This raises concern over this commonly used supplement, and future research is needed to establish the clinical relevance of these findings."
PMID: 23324939
 
Osteoarthritis Cartilage. 2007 Nov;15(11)
"...GlcN-S and GlcN-HCl had no effect. Under anabolic condition 5mM GlcN-S and GlcN-HCl significantly reduced total GAG content. ...GlcN-S and GlcN-HCl, but not GlcN-Ac, reduce anabolic and catabolic processes. For anabolic processes this was demonstrated by decreased ECM synthesis, for catabolic processes by protection against IL-1beta mediated ECM breakdown. This might be due to interference of GlcN with Gluc utilization. We suggest that the claimed structure modifying effects of GlcN are more likely based on protection against ECM degradation than new ECM production."
PMID: 17543549 
 
Osteoarthritis Cartilage. 2006 Mar;14(3)
"...Addition of 5mM GlcN led to significant down-regulation of aggrecan (2.65-7.73-fold) and collagen type II (7.75-22.17-fold) gene expression, indicating inhibited anabolic activity. ...The effects of GlcN on gene expression in a human osteoarthritic explant model suggest that enzymatic breakdown of the extra-cellular matrix might be reduced by the addition of 5mM GlcN. Additionally, restoration of already damaged cartilage is not to be expected, because gene expression of anabolic genes is also down-regulated. We suggest that chondroprotective properties of GlcN in vivo may be based on inhibiting further degradation due to catabolic activities, rather than on the ability to rebuild cartilage."
PMID: 16300972 
 

Edited by ta5, 03 May 2014 - 01:44 PM.


#24 YOLF

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Posted 20 May 2014 - 03:02 AM

I am assuming that it is glucosamine sulfate, which is the important glucosamine type?

 

 

acetyl-l-glucosamine is the most effective at inducing collagen production in the skin...

So which form was used in the study? I don't see any reference to it, but I see that the sulfate form won't affect blood sugar on a bulk powder site.



#25 albedo

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Posted 22 May 2014 - 04:35 PM

Cryonicsculture, I could not find it either, maybe a good question to the authors :-)

 

Does it fundamentally matter? Could it be also the HCL form?

 

In the original study:

http://www.nature.co...63.html#methods

 

they mention "All chemicals were obtained from Sigma-Aldrich (Munich, Germany) unless stated otherwise" and the CAS reference 3416-24-8

 

When you search in the company's database:

http://www.sigmaaldr...ng=en&region=GB

 

you hit first on Glucosamine hydrochloride with reference CAS 66-84-2 which looks same as 3416-24-8 (http://de.wikipedia....wiki/Glucosamin).

 

My apologies to the chemists out there if this does not make sense :-)


Edited by albedo, 22 May 2014 - 04:41 PM.


#26 niner

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Posted 23 May 2014 - 08:34 PM

Glucosamine is just a protonated amino sugar with a positive charge, and it needs a negative counterion in order to form a crystal.  I don't think there would be much difference between sulfate or chloride- they should both dissociate in solution.


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#27 Darryl

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Posted 23 May 2014 - 08:55 PM

Another study:

 

Kantor, E. D., Lampe, J. W., Navarro, S. L., Song, X., Milne, G. L., & White, E. (2014). Associations Between Glucosamine and Chondroitin Supplement Use and Biomarkers of Systemic Inflammation. The Journal of Alternative and Complementary Medicine.

 

Study participants included 217 men and women age 50–75 years living in the Seattle metropolitan area. Use of glucosamine and chondroitin supplements was ascertained by home interview/supplement inventory. Inflammation was assessed by using blood and urine collected at the time of home interview. Measures of systemic inflammation included plasma high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, soluble TNF receptors I and II, and urinary prostaglandin E2-metabolite (PGE-M). Multivariate-adjusted linear regression was used to evaluate the associations between supplement use and biomarkers of inflammation. High users (14 or more pills/week) of chondroitin had 36% lower hsCRP (ratio, 0.64; 95% confidence interval [CI], 0.39–1.04; p for trend=.03) and 27% lower PGE-M (ratio, 0.73; 95% CI, 0.5–0.98; p for trend=.07) than nonusers. Compared with nonusers, high users of glucosamine had 28% lower hsCRP (ratio, 0.72; 95% CI, 0.47–1.08; p for trend=.09) and 24% lower PGE-M (ratio, 0.76; 95% CI, 0.59–0.97; p for trend=0.10). Use of glucosamine and chondroitin supplements was not associated with the other markers of inflammation.

 


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#28 APBT

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Posted 23 May 2014 - 11:32 PM

I've written one of the study authors for confirmation, but have yet to receive a reply; if I do I will post it in this thread. 

In the meantime, the form of Glucosamine used in the study was GlcN.  This is Glucosamine D-sulfate.  Molecular Formula: C6H13NO5   Molecular Weight: 179.17112

Note, it is not GlcNAc (NAG), this is specifically stated, see the quote from the study below (my bold blue).  Although, it appears NAG works too, using a different pathway.

 

 

 

Under 'DISCUSSION' http://www.nature.co...tml#/discussion

Unlike for DOG and most other life span-extending compounds, extensive published evidence indicates that GlcN is safe for human use even at high doses, making it readily available for interventions to extend human healthspan particularly because, on an observational and uncontrolled basis, it has been repeatedly suggested that supplementation with GlcN may decrease overall mortality in humans49, 50.

Note added in proof: While this publication was in the press, Denzel and co-workers published findings on the role of N-acetyl-glucosamine (GlcNAc) supplementation in C. elegans lifespan extension, suggesting a different mechanism. This appears to depend on the hexosamine pathway which, however, is unlike to contribute to the phenotype observed in our study (Fig. 5 andSupplementary Fig. 4a�c), indicating that GlcN and GlcNAc promote longevity independently51.

 



#29 albedo

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Posted 24 May 2014 - 08:41 AM

Glucosamine is just a protonated amino sugar with a positive charge, and it needs a negative counterion in order to form a crystal.  I don't think there would be much difference between sulfate or chloride- they should both dissociate in solution.

Thank you! I knew there was a chemist or someone knowledgeable in chemistry out there to clarify the discussion.

 



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#30 Phoenicis

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Posted 13 June 2014 - 09:35 PM

A recent review in antiaging firewalls -

 

I actually really appreciate NAC as well, I think it would make the most sense to take NAC in the mornings and glucosamine in the evenings. While antoxidants like NAC might interfere with GlcN's LE, it may still be useful for taking care of excess pollutants during the day time. Nicotinic acid and maybe NR throughout the day should improve NAD+ levels and avoid reduced SIRT1 from GlcN. Taking the GlcN in the evening, when we have the least amount of antioxidants left over, might work best. What say you?

 

 

 

 

... They also noted ROS generation was necessary to produce life extension effects...

 
I wonder how this would play out in those of us who are taking powerful mitochondrial antioxidants such as C60-OO?
well, apparently the life extension effects of glucosamine were abolished with the addition of antioxidants.

To test whether the increase in ROS (Fig. 1i,j) is essential for a GlcN-mediated extension of life span, we repeated the initial life span experiment (Fig. 1b) in the presence of the antioxidants butylated hydroxyl anisole (BHA) and N-acetyl-cystein (NAC), respectively. Although neither BHA (Fig. 2a) nor NAC (Fig. 2b) had a detectable effect on C. elegans life span in the absence of GlcN, the life span-extending capabilities of GlcN were nullified in the presence of BHA or NAC

 

I'm assuming the GlcN and NAC or BHA were co-administered in the quoted study (i.e. given at the same time). 

If that was the case, would timing of GlcN consumption affect efficacy?  That is, take GlcN away from 'heavy' antioxidants and reap the (potential) life-extending benefits.  What is the half-life of GlcN?

 

 


Edited by Phoenicis, 13 June 2014 - 09:37 PM.






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