13 replies to this topic

[MikeDC]

The greatest and latest theory in aging is Mitochandria aging theory. Mitochandria disfunction is the main factor in aging.

Decrease of NAD+ In Mitochandria is the main cause of Mitochandria disfunction.

Increasing NAD+ can slow down aging and even reverse aging.
This has been proven in mouse studies and personal experiences from many people taking Nicotinamide Riboside (Niagen).

[MikeDC]

Telomere length reflects sirt1 activity. Increasing sirt1 activity with NAD+ precursors such as Niagen increases telomere length.

https://www.ncbi.nlm...4936455/related

[soulprogrammer]

When we really can achieve immortality? I always told my friends the new borns within 5 years from now would probably all become immortal. Could the scientist speed up the development of not anti-aging drugs but immortality pills? A 70-year old woman can give birth to a new baby who has exactly the same youth looking and functioning as a 18-year old girl's baby. So this mean we can some how reverse a cell from 70-year old woman back to 18-year old. So, the theory is there and immortality is possible (and proven in other plants/animals/insects, except human), so when can we finally find the recipe?

Edited by soulprogrammer, 07 March 2017 - 05:19 AM.

[MikeDC]

Some people think aging is just a switch that can be turned off.
It is not how it works. Little by little our body is damaged. There is not much we can do about that. But we can prevent more serious aging such Mitochandria disfunction by supplementing NAD+ precursors such as Niagen.

Think of our body as a Dam. We can't prevent the small leaks, but we can fill in the big holes such as Mitochandria disfunction.

Edited by MikeDC, 07 March 2017 - 04:00 PM.

[DCBlackwell]

It is not just our genes it is also the genes of the microbes in us and how they interact with our genes.

See

Follow Your Gut: Microbiomes and Aging with Rob Knight - Research on Aging

and the

Stein Institute for Research on Aging

https://healthscienc...es/default.aspx

 

I have genetic variants that slow down my methylation cycle and increase homocysteine, which almost certainly caused my sciatica

(in combination with my changing gut microbiome and my age):

I have two MTHFR and two MTRR heterozygous variants: 

MTHFR rs1801131(uncommon .067% GT(fwd)) http://www.snpedia.c...x.php/rs1801131   and 

MTHFR rs1801133 (common 39%    AG(fwd)) http://www.snpedia.c...x.php/rs1801133 aka C677T(rev), 

MTRR  rs162036  (common 34%    AG(fwd)) http://www.snpedia.c...ex.php/rs162036

MTRR  rs1801394 (common 49%    AG(fwd)) http://www.snpedia.c...x.php/rs1801394

which slow down the Methylation pathway and increase homocysteine (probably also slows down my mitochondra because this pathway feed methyl groups to the mitochondria ).

 

I also have this variant

CTH rs1021737  (uncommon 4%    TT(Fwd)) http://www.snpedia.c...x.php/rs1021737

which slows down my transsulferation pathway and the consumption of homocysteine; another factor increasing my homocysteine levels.

 

I also have common Gene variants effecting my Gastric Intrinsic Factor gene - https://www.ncbi.nlm.nih.gov/gene/2694

FUT2 rs601338 GG http://www.snpedia.c...ex.php/rs601338 secretor

FUT2 rs492602 AA http://www.snpedia.c...ex.php/rs492602 associated with lower B12 and secretor

FUT2 rs602662 GG  19% associated with lower B12

--(Livewello "confusingly" shows A as the minor allele (true for Aggregate 41vs59 but false for EUR 54vs46%)

The concern is the GG which is associated with lower B12 see T.Tanaka 2009 below.

also

ALPL rs4654748 TT 12% (Chr1)http://www.snpedia.c...x.php/rs4654748 assocated with lower?? B6 (Nutrahacker)

Tanaka      https://www.ncbi.nlm...71/pdf/main.pdf T.Tanaka 2009 For ALPL, FUT2(Chr19), and MTHFR studies

                 http://databases.lov...ared/genes/ALPL

 

These FUT2 variants make me susceptible to microbes that apparently attack the stomach or intestinal cells that absorb B12

in combination with my above gene variants and my age.

 

Aging is the combination of many factors, gene variants, metabolic pathways, and our microbes.

 

I am reminded of this quote

"Happy families are all alike; every unhappy family is unhappy in its own way."

and the Anna Karenina Principle

https://en.wikipedia...enina_Principle

which also applies to aging.

The family in our case being our family of genes and gene variants and the genes of our microbes and our environment especially the food we eat.

 

Here in America the biggest aging factor is our American diet.

EAT YOUR vegetables!  

I know that was one of my problems.

 

 

 

Edited by DCBlackwell, 07 March 2017 - 07:55 PM.

[MikeDC]

individuals have different issues. For a perfect normal person, the decline of NAD+ is a major aging factor that needs to dealt with. Niagen is a perfect solution.

[soulprogrammer]

Some people think aging is just a switch that can be turned off.
It is not how it works. Little by little our body is damaged. There is not much we can do about that. But we can prevent more serious aging such Mitochandria disfunction by supplementing NAD+ precursors such as Niagen.

Think of our body as a Dam. We can't prevent the small leaks, but we can fill in the big holes such as Mitochandria disfunction.

 

What about for example Turritopsis dohrnii, the immortal jellyfish,  it also has what you called body damaged over time, but it somehow able to achieve biological immortality?

 

Think lizard, it can regrow its limbs while human cannot? 

 

"The bristlecone pine is a good example. Some of these North American trees are astonishingly old. They began growing 5000 years ago"

 

5000 years? Wouldn't the tree exposed under sun, environment, bacteria, insects damaged so many years yet it survive until now?

 

I personally believe a gene reprogramming will do the work.  Humans are programmed to get old and died eventually, if we can reprogram our gene to stop growing old, then we will achieve biological immortality. DNA is just a set of program codes. We need to modify our DNA - our program codes such that it stop aging or reverse aging.

 

NR, or Niagen is good and the only supplement for now that seems to work for delaying aging and reversing some of the effects of old age, but it wont stop aging. We need something dramatically different, a different paradigm shift in stopping and reversing aging.

 

 

 

Edited by soulprogrammer, 08 March 2017 - 01:47 AM.

[MikeDC]

You want to reinvent human. Good luck with that. I think it is a miracle already to have discovered NAD+ and Niagen.

[PeaceAndProsperity]

MikeDC are you perchance shilling for a patented product you sell? Are you perchance a seller of this product? Why do you shill for this specific NAD precursor and not any of the other NAD precursors that are much cheaper? I am not accusing you, just curiosity.

[MikeDC]

PeaceAndProsperity:
Are you really that ignorant as you sound?

Take your niacin and be happy.

I am happy taking Niagen. I have no interest to convince you to take Niagen and you don't deserve my attention.

I am posting so people who are smart enough to read and learn can benefit.

Edited by MikeDC, 10 March 2017 - 09:30 PM.

[MikeDC]

Dr. Brenner is the Roy J. Carver Chair and head of biochemistry at the University of Iowa. He's also a founding co-director of the University of Iowa Obesity Initiative. Researchers around the world have validated and added to his research providing evidence of NR's unique properties in neuroprotection, sirtuin activation, protection against weight gain on a high-fat diet, and improvement of blood glucose and insulin sensitivity. Dr. Brenner is one of five Scientific Advisors for CDXC.
The following interview explains the differences in Niacin/Nicotinic Acid/NA, Nicotinamide/NAM and Niagen/NR/Nicotinamide Riboside. I'm breaking the names out because it can get confusing given how similar they are.
Following is my interview with Dr. Charles Brenner, an expert in NAD+ and energy metabolism, a published researcher, and inventor of the NR NAD+ related patents.

Q: Thank you for taking the time to answer some questions. It is greatly appreciated, especially since I take Niagen daily along with many friends and family. Many don't understand the importance of NAD+. Would you be kind enough to take the time to explain it a bit?
Answer (Charles Brenner): NAD+ is the central mediator of metabolism. No cell can survive without it. NAD+ is required for foods to be converted to energy, for the synthesis of hormones, for DNA to be repaired, and for resistance to stresses like reactive oxygen species. NAD+ declines in aging. Our resiliency and metabolism decline in aging. Boosting NAD+ is a way to maintain youthful metabolism and youthful resiliency.
Q: Why are nicotinamide and niacin in our diet at 15 mg/day?
CB: Deficiency of vitamin B3 causes pellagra - almost no one has pellagra anymore. Low doses of nicotinamide and/or niacin prevent this deficiency.
Q: Why do some people take large doses of niacin?

CB: High doses of niacin, meaning 500 mg to 4 grams/day, improve cholesterol (HDL up, LDL down, free fatty acids down). Unfortunately, high dose niacin causes flushing, which limits its use.
High dose nicotinamide is not as commonly used. It doesn't improve cholesterol.
Q: What is the relationship between NR and NAD+?

CB: NR is one of three vitamin precursors of NAD. NAD is the master regulator of metabolism, which declines in aging. The basic thesis of NR is that NR boosts NAD+ without inhibiting sirtuins (the problem with nicotinamide), without causing flushing (the problem with niacin) and in damaged cells including nerves and muscles. Nicotinamide and niacin can't substitute for NR because they aren't used in all of the same cells and they don't produce the same results. The best example of these compounds not being equivalent is with respect to glycemic control. Nicotinamide and niacin promote insulin insensitivity (which is bad), while NR promotes insulin sensitivity (which staves off type 2 diabetes). So you should not believe anyone who says that the three compounds are equivalent.
Different cells and tissues use different pathways to make NAD. Some cells don't need a vitamin to make NAD and can make NAD by expressing eight different genes that convert the amino acid tryptophan to NAD. It turns out this is the basis for the differences between NR, niacin and nicotinamide and tryptophan. A lot of different cells need NAD. If the genes for a particular NAD precursor are not on, no amount of that precursor can help that cell make NAD.
For example, if any of the eight genes in the tryptophan pathway are not turned on in a particular type of human cell, that cell can't make NAD from any amount of tryptophan. That's part of the reason why tryptophan is such a poor NAD precursor. Tryptophan is an inefficient precursor in some cells and it's simply not an NAD precursor in other cells because the tryptophan pathway genes are off.
Niacin and nicotinamide are both very important compounds in prevention of dietary insufficiency but they cannot substitute for NR as metabolic boosters because there are different genes required to make NAD from these compounds.
Q: The article I asked you to read stated that "All three produce NAD+ in the human body." Please elaborate on this.

CB: There are trillions of cells in the human body of many hundreds of cell types. For example, there are nerve cells, skeletal muscle cells, cardiac cells, several types of pancreatic cells, several types of blood cells, liver cells, etc. What makes a neuron a neuron and not a hepatocyte is the expression of neuronal genes. When we discovered NR as a vitamin, we discovered the NR pathway to NAD. The value proposition of NR depends on the unique ability of NR to maintain and boost NAD in every cell and tissue and, in particular, in tissues undergoing damage and stress.
There are only two steps in the NR pathway to NAD but there are two genes that can do the first step and three genes that can do the second step. The NR pathway never gets turned off. NRK1 is expressed in every cell and tissue, while NRK2 is turned on by cellular damage, particularly in skeletal and cardiac muscle. This means that people supplementing with NR are able to keep NAD levels high in stressed cells that specifically have the NR pathway turned on to deal with cellular stress. Supplementing with niacin and nicotinamide doesn't help because they don't feed into the NR pathway, which is turned on by stresses.
Q: What's the problem with niacin or nicotinamide as a NAD+ precursor?

CB: There are three problems with niacin and two problems with nicotinamide, particularly at high doses.
First, niacin can't be used in lots of tissues because the niacin pathway is not on. The brain and skeletal muscle can't use niacin to boost NAD and these are two of the most important tissues that suffer the ravages of aging. Niacin also causes flushing at high doses and does not efficiently elevate mitochondrial NAD.
The nicotinamide pathway declines in aging, which means you would need ever higher doses to try to maintain your NAD. Second, at high doses, nicotinamide inhibits sirtuins, which is the opposite of NR. NR is a STAC that extends lifespan in model systems.
Q: Can you give me some clarification on model systems?

CB: Basically, we are talking about yeast, flies, worms and rodents - systems in which scientists have total control over the genetics, environment and diet and can carefully look at results. In yeast, nicotinamide shortens lifespan. NR extends yeast lifespan even when they are on a high sugar diet.
In mice and people, both nicotinamide and niacin can induce insulin resistance, which is a precursor to diabetes. NR promotes insulin sensitivity and resistance to diabetic neuropathy. The previous blog on Seeking Alpha suggested that people could take either nicotinamide or niacin to get the same benefits of NR. That's just utterly inconsistent with facts. NR is a STAC - to my knowledge the only bona fide one in the marketplace - I don't count resveratrol because that has been pretty much debunked. Nicotinamide is a sirtuin inhibitor and niacin can't contribute to brain or muscle NAD.
Q: The previous article did some calculations about the efficiency of NR versus nicotinamide and niacin, justifying why the individual wanted to take particular amounts of low cost vitamins in place of NR. You were the senior author of the clinical study. Were those calculations correct?
CB: No. The Seeking Alpha blogger did a calculation of how much more nicotinamide or niacin in order to have the activity of NR in a mouse's liver. The paper is here.
It's well known that niacin and nicotinamide work in liver. The problem again is niacin can't be used by muscle or brain and that damaged tissues induce the NR pathway in order to maintain function. Niacin isn't used by all tissues and high dose nicotinamide inhibits sirtuins. His premise was false because it was based on liver data. He's not going to get any benefit to damaged nerves or muscle so his idea is simply invalid.
NR is the only NAD-boosting compound that elevates metabolism, protects damaged nerves, extends lifespan in mice and other model systems, and increases insulin sensitivity. Inexpensive NAD precursors are not STACs and cannot substitute for NR. We are dealing with an aging population with a high incidence of chronic diseases that involve inflammation, insulin insensitivity, neuropathy and heart diseases, all of which can potentially be addressed uniquely by NR. You can be assured that there is no other NAD precursor that can do what NR does.
Having Dr. Brenner take the time to explain a bit more about Niagen was very helpful. It's clear that its benefits can't be duplicated by the other B vitamins.
Published research is demonstrating NR is an effective NAD+ precursor in slowing or stopping neuronal cell death associated with NAD+ depletion. Not only does Niagen appear to be an anti-aging ingredient, there is research being published showing neuroprotection. Following are some highlights.
Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection:
Additional studies with nicotinamide riboside in models of Alzheimer's disease indicate bioavailability to brain and protective effects, likely by stimulation of brain NAD synthesis.
Dr. Jeffrey Milbrandt published a study titled SARM1 activation triggers axon degeneration locally via NAD+ destruction. This study clearly shows the harm when NAD+ is low.
Along the same lines as the study Dr. Milbrandt published is one titled "Neuronal death induced by misfolded prion protein is due to NAD+ depletion and can be relieved in-vitro and in-vivo by NAD+ replenishment":
We propose the development of NAD(+) replenishment strategies for neuroprotection in prion diseases and possibly other protein misfolding neurodegenerative diseases.
Of the ongoing and upcoming human clinical trials of NR, several of them deal with neuroprotection. Thorne Research and the Mayo Clinic are running a trial dealing with concussion. Kansas University will be running an Alzheimer's Disease trial. UT Health Science Center in Texas will run one dealing with Mild Cognitive Impairment. These will be interesting trials to watch.

[PeaceAndProsperity]

Good explanation but as I said before we have yet to see any rejuvenation in humans from this NR compound.

 

Lots of false statements are also made, since niacin is superior in some aspects to NR. Practically the only superiority of NR is in respect to NAD, but it has yet to show any rejuvenating effects. This might put into question whether declining NAD levels are what causes aging to occur in the first place and even how much NAD matters for anti-aging purposes.

[soulprogrammer]

"in respect to NAD, but it has yet to show any rejuvenating effects".

 

Isn't that the Sinclair's research shown the old mice's egg rejuvenate to become like young mice's egg after feeding the mice for 3 weeks. There is a video that show the picture of the egg before and after NMN treatment. The picture clearly shows that boosting NAD+ rejuvenate the old mice's egg. You can watch the video from youtube if you haven't.

 

However, there is still no research that proves it will rejuvenate human cells indeed. Well, if there is a solid proof that show NAD+ rejuvenate human cells, I believe everyone here will all taking NR already.  So, perhaps those who want to wait can wait for solid evidence. Those who want try, are free to try. These human clinical trials will probably takes years for publication.

 

The bottom line, evidence shows it is working in mice, thus it "might" work in human too. If it doesn't work in human, nothing to lose just some of your money burn.

Edited by soulprogrammer, 11 March 2017 - 03:05 AM.

[MikeDC]

Multiple human clinical trials have shown that Niagen is the most effective NAD+ precursor.
There have been more than 50,000 studies on NAD+ and many on human subjects.
NAD+ works the same way between humans and mouse. Actually there are many addiction
Treatment clinics that have successfully used NMN to treat addiction with great results.
NMN is another NAD+ precursor that is effectively the same as Niagen since it is converted
To Nicotinamide Riboside before entering the cell.
Not to mention the 300,000 people who are using Niagen already. Many are getting younger,
Or have more energy, or cured their ataxia SCA1.