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Old 4th November 2016, 8:25 PM   #31
Bold Eagle
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I will still present a hypothesis that high quality molecular intake (gas, liquid, solids) is significantly correlated to longevity.

That is provide high value "building blocks" in the form of clean water, air and food products and you will achieve greater longevity.

Starvation may reduce metabolic activity but if that organism is absorbing medium to poor quality molecules (for example polluted air or water) they will have a reduced longevity potential.

Moreover, if we compared the [faster to the normal consumer (variable: consumption ratio)] in either [poor/moderate vs high quality environments (variable: ecosystems)] I bet there would be a far greater significant correlation in ecosystem vs consumption rate.
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Old 4th November 2016, 11:44 PM   #32
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Quote:
Originally Posted by Bold Eagle View Post
I will still present a hypothesis that high quality molecular intake (gas, liquid, solids) is significantly correlated to longevity.
What is a "quality molecule". Everything is a molecule, there is no such thing as quality when it comes to molecules.

Quote:
Starvation may reduce metabolic activity but if that organism is absorbing medium to poor quality molecules (for example polluted air or water) they will have a reduced longevity potential.
You asked me to provide evidence and I did (you also berated me for no reason). Now it is your turn. Firstly you must define what a "quality molecule" is and how to identify it, secondly you need to reference a study that identifies these "quality molecules" and provides a mechanism as to how they provide longevity.

Quote:
I bet there would be a far greater significant correlation in ecosystem vs consumption rate.
Epidemiology (correlation) is extremely basic science that gives you nothing more than a hint at what you should actually study. It does not prove anything. Once you've identified a correlation you must then identify the actual mechanism upon which it is caused.

So far I've provided a correlation (longevity vs extended/chronic fasting) and also the mechanism upon which it has been shown to work. Eg reduction in IGF-1 causing less cell division coupled with reduced oxidative stress due to slower metabolism. "I bet" doesn't cut it in the science forum, nor do basic epidemiological studies.
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Last edited by Foliage; 4th November 2016 at 11:50 PM.
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Old 5th November 2016, 1:35 AM   #33
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Originally Posted by Foliage View Post
What is a "quality molecule". Everything is a molecule, there is no such thing as quality when it comes to molecules.

You asked me to provide evidence and I did (you also berated me for no reason). Now it is your turn. Firstly you must define what a "quality molecule" is and how to identify it, secondly you need to reference a study that identifies these "quality molecules" and provides a mechanism as to how they provide longevity.

Epidemiology (correlation) is extremely basic science that gives you nothing more than a hint at what you should actually study. It does not prove anything. Once you've identified a correlation you must then identify the actual mechanism upon which it is caused.

So far I've provided a correlation (longevity vs extended/chronic fasting) and also the mechanism upon which it has been shown to work. Eg reduction in IGF-1 causing less cell division coupled with reduced oxidative stress due to slower metabolism. "I bet" doesn't cut it in the science forum, nor do basic epidemiological studies.
You did post links but one fails to load the other hints exactly at my point "nutrient-enriched diets", that is quality molecules.

Quote:
In the experiments now reported the food intake of 12- to 13-month-old mice of two long-lived strains was restricted by using nutrient-enriched diets in accordance with the concept of "undernutrition without malnutrition."
You deserve a better response than this, but if you go to google scholar and try "high-value molecules" (quality) and consider them being absorbed (gas, liquid or solid) and what the outcomes may be (chelating, displacing, etc during the absorption phase - especially considering diffusion) :

http://pubs.acs.org/doi/abs/10.1021/ja310054d (a gas)

http://link.springer.com/article/10....811-013-9983-9 (solid)

I am still searching for the "keyword structure" that could support my hypothetical.

Edit: this looks like a good read;
http://www.sciencedirect.com/science...9286740080567X

Supporting your view;

Quote:
.....physiological experiments that relate the pace of aging to caloric intake;.....

These are damage by reactive oxygen species (ROS) generated by metabolism, genome instability, genetically programmed extension mechanisms, cell death, and systemic aging.
Damn I wasn't meaning to support your argument.......
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Old 10th November 2016, 10:36 PM   #34
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This stuff is really good, been taking it for about 1 month now, about 50 - 100mg Of pharm grade purity 99 percent say 3 days on and 2 days off, and the stuff really has helped with motivation and quality of sleep. From my observations, the elderly that keep active (are motivated to do something with their day) live longer and its known that quality of sleep does improve life, So this shit really works, lols.

Thanks for this thread, Great info.
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Old 10th November 2016, 11:16 PM   #35
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N = 1

Self experimentation is extremely prone to error and placebo effect.
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Old 11th November 2016, 12:40 AM   #36
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Quote:
Originally Posted by sanousie View Post
This stuff is really good, been taking it for about 1 month now, about 50 - 100mg Of pharm grade purity 99 percent say 3 days on and 2 days off, and the stuff really has helped with motivation and quality of sleep. From my observations, the elderly that keep active (are motivated to do something with their day) live longer and its known that quality of sleep does improve life, So this shit really works, lols.
I've been sleeping well too so far.

Apparently the suprachiasmatic nucleus timekeeper function is SIRT dependent, so perhaps that explains it.

Quote:
Interestingly, SIRT1 has been shown recently to also control central circadian function in the brain by amplifying expression of BMAL1 (Chang and Guarente 2013). Importantly, SIRT1 levels decline in the SCN of aged mice compared with young controls. This decline is concomitant with the reduction of many of the components of the circadian clock, presumably triggering the degradation of central circadian function with aging (Valentinuzzi et al. 1997). Remarkably, overexpressing SIRT1 in the brain blunts the effects of aging on circadian function, and deletion of SIRT1 compromises function in young animals. SIRT1 deacetylates PGC-1α in neurons to increase activation of BMAL transcription. Thus, a loop of SIRT1, PGC-1α, and NAMPT amplifies the expression of circadian clock proteins and assures proper central circadian function in the SCN (Chang and Guarente 2013). The fact that SIRT1 appears to be the Achilles heel in aging suggests that brain targeted sirtuin drugs may help maintain central circadian function and mitigate health decline.
http://genesdev.cshlp.org/content/27/19/2072.full

Red light reaching the pineal gland via the retina will cause it to release melatonin and I find running f.lux on my computer may also be helping me get better sleep (I don't have a smartphone, but I think it runs on them too). I also have a cool red LED on the back of my bed I'll often turn on, as well as a red lamp in my lounge room lol.

You're right. Placebo or not, it's really good for you.
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Old 18th November 2016, 12:30 AM   #37
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Don’t believe the HYPE about Nicotinamide Riboside

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Nicotinamide Riboside (NR) is a recently discovered form of vitamin B3 that can increase levels of Nicotinamide Adenine Dinucleotide (NAD+) in older individuals back to what they are in youth.
Fishing with that above.....

Damn if you go to google scholar and keyword: Nicotinamide riboside;

Here we can see that a Bogan wrote about it but also clearly defining we need a baseline:
http://www.annualreviews.org/doi/abs....061807.155443

Next...

The NAD+ Precursor Nicotinamide Riboside Enhances Oxidative Metabolism and Protects against High-Fat Diet-Induced Obesity

The high value question is what is most readily available, cost effective and thus high value form?

It needs to be Cochrane Review for greater resolution:
http://www.cochrane.org/search/site/...ide%20riboside

So far only two assessments..............
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Last edited by Bold Eagle; 18th November 2016 at 12:35 AM.
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Old 28th December 2016, 11:58 PM   #38
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Observations at the end of bottle one of NR - 60 x 125mg. Roughly 1 per day:

Sleep appeared to improve
Skating has improved
Mood fine (but I tend to always be pretty baseline fine)
Performing well at work (although with long service leave around the corner I think I am just glowing anyway)
Appetite felt perhaps slightly surpressed but in a good way

As a complete confounding influence, I also tried a mild nootropic called Utopia(n) at the tail end of the NR trial. The effect of that stimulant felt a lot more noticable. As a stimulant, that is not something to take a daily dose of, as NR is being marketed for, but I took one hit one afternoon in which I felt like a skating deity. Taking a second Utopia(n) dose the next day just made me feel like I was hooked on beetlenut, so I haven't had a third try of that one

With a general feeling of improved health, I am considering purchasing a second bottle of NR though. I think I will go for a few weeks without it and see how I feel first.

Last edited by antipody; 29th December 2016 at 12:09 AM.
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Old 20th March 2017, 12:06 PM   #39
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Another article worthy of attention in Feb 17 Science.

Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice

Quote:
By identifying NAD+ decline as a key age-dependent risk factor for glaucoma, Williams et al reveal unprecedented protection by a single molecule against a complex nuerodegenerative disease. How can such a simple manipulation have such profound effects? The NAD+/NADH pair is arguably the central metabolic switch of eukaryotes. In cells with healthy mitochondria, a high local NADH concentration in this organelle will signal an energetically replete state in which the amount of adenosine 5'-triphosphate (ATP) in the cell is high and ATP-generating oxidative phosphorylation in the mitochondria is paused by the relative lack of coupling substrate adenoside diphosphate (ADP). This adaptive NAD+/NADH switch in turn activates anabolic programs. However, when oxidative phosphorylation is impaired, increased NADH concentration is transmitted to the cytosol by efficient shuttles. This represents a chronic reductive stress in which the NAD+ concentration becomes rate limiting for other vital pathways, including DNA repair in the nucleus [induced by poly (ADP-ribose) polymerase 1 (PARP1)] and activation of sirtuins, the NAD+ dependent deacetylases implicated in aging (L. Guarente, Science 352, 1436 (2016)) that also activate the mitochondrial unfolded protein response. Elegant in vitro studies have demonstrated that NAD+ increase allows cultured cells to grow when treated with inhibitors of oxidative phosphorylation that would otherwise arrest cell growth. This clearly demonstrates that NAD+/NADH imbalance, rather than ATP depletion, is the crucial insult consequent to inhibiting oxidative phosphorylation (Garway-Heath et al, Lancet 385, 1295 (2015)). Given that mitochondrial function was not directly addressed by Williams et al, it will be important to determine whether improved oxidative phosphorylation underlies the remarkable effects of NAD+ supplementation.

Another suprising finding by WIlliams et al is that the higher dose of dietary nicotinamide not only reversed the ageing phenotype in the retina and protected retinal ganglion cells when eye pressure was increased, but also decreased eye pressure in the glaucoma mouse model. NAD+ supplementation thus targets the two major risk factors that predispose to retinal ganglion cell dysfunction and degeneration in glaucoma.

Last edited by antipody; 20th March 2017 at 12:13 PM.
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Old 24th March 2017, 3:39 PM   #40
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And another...

http://science.sciencemag.org/content/355/6331/1312

Quote:
DNA repair is essential for life, yet its efficiency declines with age for reasons that are unclear. Numerous proteins possess Nudix homology domains (NHDs) that have no known function. We show that NHDs are NAD+ (oxidized form of nicotinamide adenine dinucleotide) binding domains that regulate protein-protein interactions. The binding of NAD+ to the NHD domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate–ribose) polymerase], a critical DNA repair protein. As mice age and NAD+ concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD+. Thus, NAD+ directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.
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Old 24th March 2017, 6:16 PM   #41
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Saw something interesting mentioned today on ABC with human trials intended in a few months.

DNA repair discovery could lead to drugs to reverse ageing, fight cancer and help space travel

Quote:
"For most of the 20th century we knew that our [cells' ability to repair DNA gets worse over time] and we get old and it's the main reason we get cancer," Harvard and UNSW professor David Sinclair said.

"So what we've discovered is the reason why."

Published in the journal Science, the international team identified how a vitamin called NAD+ was regulating the interactions that control DNA repair.

The scientists said experiments showed that when mice were given an NAD+ booster called NMN, their cells were better at repairing DNA damage caused by radiation exposure and ageing.
Critical step in DNA repair, cellular aging pinpointed
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Old 24th March 2017, 6:38 PM   #42
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Just my 2c.

My only source here is Michael Mosley and his 5:2 diet book and his series on BBC; Horizon. From memory, what we know is that people who fast or have calorie restricted diets produce less IGF (Insulin Growth Factor) which is associated with less cancer and cell damage in a person's body. The theory is your body spends less time replicating and creating new cells and more time repairing what it has.
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Old 24th March 2017, 6:42 PM   #43
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Just my 2c.

My only source here is Michael Mosley and his 5:2 diet book and his series on BBC; Horizon. From memory, what we know is that people who fast or have calorie restricted diets produce less IGF (Insulin Growth Factor) which is associated with less cancer and cell damage in a person's body. The theory is your body spends less time replicating and creating new cells and more time repairing what it has.
Actually for anyone who has ever looked at the 5:2 diet and it's overall benefits to your health.. this looks interesting :

Fasting Mimicking Diet (FMD
http://www.telegraph.co.uk/wellbeing...st-diet-wrong/

In his study, reported this week in the journal Cell Metabolism, old mice placed on cycles of a four-day low-calorie diet had reduced visceral belly fat, and increased numbers of progenitor and stem cells in several organs — including the brain, where neural regeneration was boosted, as was memory."

"...Decreasing meal frequency is pretty painless and by reducing meal frequency we naturally reduce inflammation (the hallmark of modern chronic disease) in our bodies.’’

Last edited by «¥» Plump-DJ®; 24th March 2017 at 7:19 PM.
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Old 27th March 2017, 2:58 PM   #44
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Quote:
Originally Posted by «¥» Plump-DJ® View Post
Actually for anyone who has ever looked at the 5:2 diet and it's overall benefits to your health.. this looks interesting :

Fasting Mimicking Diet (FMD
http://www.telegraph.co.uk/wellbeing...st-diet-wrong/

In his study, reported this week in the journal Cell Metabolism, old mice placed on cycles of a four-day low-calorie diet had reduced visceral belly fat, and increased numbers of progenitor and stem cells in several organs — including the brain, where neural regeneration was boosted, as was memory."

"...Decreasing meal frequency is pretty painless and by reducing meal frequency we naturally reduce inflammation (the hallmark of modern chronic disease) in our bodies.’’
There link to a talk earlier in this thread, about the interaction between metabolism, diet and cancer. Well worth listening to.

Another study in last week's Science update suggests pancreatic function is improved by fasting...


http://science.sciencemag.org/conten...et_cid=1233308

Quote:
Starvation stresses an animal and can cause tissue loss. Regeneration after refeeding seems to mimic developmental activation of cells and replenishes depleted tissues. Cheng et al. tested the effects on mice of a low-calorie (low in carbohydrates and protein) but high-fat diet that resembles the metabolic effects of fasting but is easier for humans to tolerate. In models of type 1 and type 2 diabetes, mice on this diet showed improved insulin secretion and glucose homeostasis. The diet promoted signaling and transcriptional changes reminiscent of those that occur during the development of pancreatic endocrine cells. The findings raise the possibility of reprogramming endogenous cells in the pancreas to restore function lost in diabetes.
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