2284 replies to this topic

[BigLabRat]

Why do we need stearic acid (or do we even need it). Isn't it made from cottonseed oil and bad for the health?

 

----------------------------------------

 

Where do people get these ideas?

 

Stearic acid is one of the most common of saturated fats. If you think saturated fat is bad for you, your information is from the 1970s.

 

Stearic acid is one of the major fats in beef, in cocoa, in olive oil. It's everywhere. Anyone eating a semi-normal diet consumes quite a bit of it.

 

Yes, it is also found in cottonseed oil--though most stearic acid isn't 'made from' cottonseed oil. Even if it were, once it is converted to high-purity stearic acid, it doesn't matter where it is sourced.

 

In addition, the fear of cottonseed oil is overblown. Yes, there is a toxic compound--a phenol--in cottonseed called 'gossypol'. If you don't want any gossypol in your diet, then you'd better eliminate a lot of other things from your diet, starting with okra and other relatives of hibiscus.

 

Many of the beneficial phytochemicals from plants everyone is urging us to eat are phenols--and a lot of them are poisonous at high doses. So are most things.

[Turnbuckle]

Is Quercetin another candidate for fission enhancement?
The last sentence below sounds scary until you consider all of The info in this thread.

https://www.hindawi....cl/2015/836301/

...
Altogether, our results suggest that in vivo quercetin treatment is associated with a severe mitochondrial dysfunction drastically affecting erythropoiesis and heart mitochondria."

 

 

This may be more the result of dosage. According to that paper--Mice were injected with 50 mg/kg of quercetin for 15 days. Compare that to mice fed up to 25 mg/kg orally, and the results are much different, and it appears that quercetin is useful for biogenesis--

 

Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance.--See Fig 2 where mice fed quercetin at 25mg/kg for 7 days doubled their mtDNA, and half of that was almost as good.

 

The oral dosage must also be derated as oral availability is poor, approximately 16% in the rat--Absolute bioavailability of quercetin was 16% in rats...

 

So that derates 25 mg/kg oral to 4mg/kg if injected, considerably less than the 50mg/kg where a problem was noted. And if you were to take a gram a day, that would be roughly 2mg/kg if you weighed 80 kg and the bioavailability was the same as in rats. So I would use this for fusion/biogenesis only and not for fission.

Edited by Turnbuckle, 10 August 2017 - 04:35 PM.

[Nate-2004]

It isn't just that quercetin has poor bioavailability but oral use does not end up with quercetin in the blood plasma since the liver converts it to its aglycone form which doesn't really show the same promise as its in vitro form.

Edited by Nate-2004, 11 August 2017 - 01:58 PM.

[Turnbuckle]

It isn't just that quercetin has poor bioavailability but oral use does not end up with quercetin in the blood plasma since the liver converts it to its aglycone form which doesn't really show the same promise as its in vitro form.

 

The papers zorba and I linked to were oral and injected in vivo, not in vitro. And quercetin is already the aglycone form. Even if it wasn't and was transformed in the liver, what difference would that make to injected vs oral?

 

 

Quercetin (C15H10O7) is an aglycone, lacking an attached sugar. It is a brilliant citron yellow needle crystal and entirely insoluble in cold water, poorly soluble in hot water, but quite soluble in alcohol and lipids. A quercetin glycoside is formed by attaching a glycosyl group (a sugar such as glucose, rhamnose, or rutinose) as a replacement for one of the OH groups (commonly at position 3). The attached glycosyl group can change the solubility, absorption, and in vivo effects. As a general rule of thumb, the presence of a glycosyl group (quercetin glycoside) results in increased water solubility compared to quercetin aglycone [4,5].

 

A quercetin glycoside is unique by the attached glycosyl group. Generally, the term quercetin should be used to describe the aglycone only; however, the name is occasionally used to refer to quercetin-type molecules, including its glycosides in research and the supplement industry.

 

https://www.ncbi.nlm...les/PMC4808895/

 

 

 

Edited by Turnbuckle, 11 August 2017 - 03:30 PM.

[Turnbuckle]

More on the value of AMPK activators--

 

Life Extension has a good write-up on AMPK. While LEF is often over the top, in this case I believe their enthusiasm is justified--

AMPK: The Cellular Enzyme That Promotes Longevity And Reduces Fat Storage

 

I've found that the rose hips and gypenosides that promote AMPK for fission (post 272) also normalize my blood pressure, and I'm now using these activators on a daily basis while discontinuing hypertension medications. In addition to BP normalization, I've been able to fast for six days now (losing about 8 pounds so far) with minimal hunger. This is longer than I've ever been able to fast before, and am continuing with it until I lose another 8.

 

AMPK activators are likely good for fusion/biogenesis, as well as for weight loss and hypertension--

 

 

Clearly, these data demonstrate that AMPK is necessary for mitochondrial biogenesis in response to chronic energy deprivation, and it appears likely that pharmacologically activated AMPK conveys its signal to induce mitochondrial biogenesis via the PGC-1α–NRF pathway.

 

The role of AMP-activated protein kinase in mitochondrial biogenesis

 

 

 

 

[Benko]

 

AMPK activators are likely good for fusion/biogenesis, as well as for weight loss 

 

 

 

 

I can vouch for the weight loss. I've lost weight on gynostemma extract and so have about 4 other people I've recommended it to.  

 

Hope this isn't too off topic for your thread.

Edited by Benko, 12 August 2017 - 01:45 AM.

[Fafner55]

Phase 1 Study of Urolithin A Shows Safety and Bioavailability

Following up on the 2016 publication “Urolithin-A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents” (2016) http://www.nature.co...ll/nm.4132.html,

 

“Amazentis SA Announces Successful Phase 1A/1B Study Results in Healthy Elderly Subjects with the Food Metabolite Urolithin A” (2017) http://www.businessw...ase-1A1B-Study 

Phase 1 study of Urolithin A (AMAZ-02) was a single-center, multi-part (single and multiple ascending doses) double-blind, randomized, placebo-controlled study in 60 healthy elderly subjects. Part A of the Phase 1 study involved orally administering single escalating doses (250mg, 500mg, 1000mg, and 2000mg). During Part B, 250mg, 500mg, and 1000mg were selected for 4 weeks of daily oral dosing and their impact on skeletal muscle mitochondrial biomarkers was investigated along with safety and bioavailability. Additional information on the clinical trial design is available on clinicaltrials.gov.

 

All doses were observed to be safe and bioavailable. No serious and no product-related non-serious treatment emergent adverse events were recorded during the conduct of the Phase 1 human study. The impact of Urolithin A on plasma and muscle biomarkers following 4-week multiple ascending dosing were assessed, revealing that Urolithin A intake significantly modulated both gene expression and plasma metabolites linked to mitochondrial and muscle function.

[Turnbuckle]

An addition to the toolbox for biogenesis--

 

Leucine, a branched-chain amino acid--BCAA. BCAAs were already mentioned as promoters of biogenesis, but this paper gets more specific--

 

Leucine Modulates Mitochondrial Biogenesis and SIRT1-AMPK Signaling in C2C12 Myotubes

 

Previous studies from this laboratory demonstrate that dietary leucine protects against high fat diet-induced mitochondrial impairments and stimulates mitochondrial biogenesis and energy partitioning from adipocytes to muscle cells through SIRT1-mediated mechanisms. Moreover, β-hydroxy-β-methyl butyrate (HMB), a metabolite of leucine, has been reported to activate AMPK synergistically with resveratrol in C2C12 myotubes. Therefore, we hypothesize that leucine-induced activation of SIRT1 and AMPK is the central event that links the upregulated mitochondrial biogenesis and fatty acid oxidation in skeletal muscle...Leucine significantly increased mitochondrial content, mitochondrial biogenesis-related genes expression, fatty acid oxidation, SIRT1 activity and gene expression, and AMPK phosphorylation in C2C12 myotubes compared to the controls... Furthermore, leucine treatment for 24 hours resulted in time-dependent increases in cellular NAD+, SIRT1 activity, and p-AMPK level, with SIRT1 activation preceding that of AMPK, indicating that leucine activation of SIRT1, rather than AMPK, is the primary event.

 

https://www.hindawi....me/2014/239750/

 

 

While this was in vitro, they note--

 

Doubling leucine intake in mice has been found to reverse multiple HFD-induced metabolic abnormalities, including glucose intolerance, hepatic steatosis, and inflammation. These effects are accompanied by corresponding increases in mitochondrial oxidative capacity and mitochondrial content. Since mitochondrial dysfunction and mitochondrial content loss are directly linked to the development of metabolic disorders, increased mitochondrial biogenesis appears to rescue part of these obesity-related abnormalities.

 

 

 

[Nate-2004]

Leucine also activates mTOR and I could swear mTOR inhibition was needed for AMPK activation, or are the two only loosely related?

[Turnbuckle]

Leucine also activates mTOR and I could swear mTOR inhibition was needed for AMPK activation, or are the two only loosely related?

 

 

The results appear to be bimodal according to dosage. According to the same paper--

 

Our data may also reflect dose-dependent effects of leucine treatment. For example, high-dose leucine infusion and supplementation have been shown to induce insulin resistance and glucose intolerance in both human and animal models [38, 39], possibly via activation of mammalian target of rapamycin- (mTOR-) insulin receptor substrate 1 (IRS-1) signaling pathways [40]. In contrast, modest increases in leucine intake, sufficient to induce plasma leucine elevations to ~0.5 mM, significantly reduced obesity-related oxidative and inflammatory stress, resulting in improvement of insulin sensitivity in humans [19]. Similarly, Vaughan et al. found that leucine in the 0.1–0.5 mM range induces a dose-dependent increases of PGC-1α expression, leading to significant elevated mitochondrial density and oxidative capacity in skeletal muscle cells [17]. Consistent with these evidences, we found comparable levels of leucine promoted mitochondrial biogenesis and fatty acid oxidation in C2C12 myotubes.

 

Edited by Turnbuckle, 24 August 2017 - 09:21 PM.

[zorba990]

Based on my experience, adding 10g bcaas, 2g lysine, 1000mg tmg, and 30g whey 1hr post workout enhances recovery and does not inhibit the niacinamide/ribose effects. I still avoid stearic fats, antioxidants, and other fusion inducers like epicatechin and broccoli extracts (except for the sodium butyrate) until 5hrs or more post workout. I have noticed needing extra rest days or else accumulating fatigue is to much for me. Just my n=1

Btw topical niacinamide and ribose makes my skin seem like I put on a ton of moisturizer. No noticeable hair growth yet but no negative effects either.

Edited by zorba990, 26 August 2017 - 12:23 AM.

[nikolay]

My present 7-day protocol for mitochondrial rejuvenation and age regression:

 

Part I—

Day 1: Fission

Day 2: Fusion + biosynthesis

Day 3: Blank

 

Part II—

Day 1: Fission

Day 2: Fusion + biosynthesis

Day 3: Fusion + C60

Day 4: Blank

 

Repeat

 

---------------------------------

Details

---------------------------------

 

Fission—

 

T= -12 hours

Resveratrol (400 mg)

 

T = 0 hours

N+R (2g/5g)

Fisetin (200mg)

Rose hips (1g)

Gypenosides (150mg)

Disodium phosphate (4g)

IP6 (2g)

  

T = 1.5-2 hours

Gym (Exercise Like a Girl)

 

See post 282 for more details

 

---------------------------------

 

Fusion—

 

T = 0

Stearic acid (5-10 g)

 

See: Regulation of mitochondrial morphology and function by Stearoylation of TfR1 — “We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.”

 

---------------------------------

 

Biogenesis—

 

T = 0 (with Fusion)

Resveratrol (200mg)

PQQ (10mg)

BCAA (10g)

Hydroxytyrosol (25mg)

Epicatechin (500mg)

 

T = 4 hours

PQQ (10mg)

Hydroxytyrosol (25mg)

Epicatechin (500mg)

 

See also post 191

 

---------------------------------

 

C-60 (with Fusion)

 

One teaspoon of an experimental mix of MCT oil with added hydroxytyrosol (HT). See my profile write up, Section 5.

 

Isn't Metformin a good or an even better option to use instead of rosehips and gypenosides for AMPK activation? Shouldn't resveratrol be paired with DHEA for men or replaced by pterostilbene instead?

[Turnbuckle]

 

 

 

Isn't Metformin a good or an even better option to use instead of rosehips and gypenosides for AMPK activation? Shouldn't resveratrol be paired with DHEA for men or replaced by pterostilbene instead?

 

 

 

DHEA to avoid joint pain with resveratrol was mentioned more than once before on this thread, but I did not include it as it isn't directly involved. As for AMPK activators, there are many more than previously listed, and if someone could order them according to effectiveness, that would be great. The following list is from an herbal site--

 

AMPK activators:

 

AICAR (5-Aminoimidazole-4-carboxamide ribonucleotide)

ALA (alpha Lipoic acid)

Burdock (Arctium lappa, a source of arctigenin)

Green tea extract (Camellia sinensis)

Berberine (Coptis chinensis)

Cordyceps militaris

Turmeric (Curcuma longa)

Goat’s rue (Galega officinalis—source plant for Metformin.)

Jiaogulan (Gynostemma pentaphyllum)

Nootkatone (Present in grapefruit peels) 

Panax ginseng

Quercetin

Resveratrol and GSE (grape seed extract)

Acetyl salicylate (extracted from willow bark, Salix alba)

Artemisinin (Artemisia annua)

Fucoidan (Brown Seaweed)

Reishi (Gandoerma Lucidum)

Rhodiola Rosea

Ursolic Acid: AMPK is activated by Ursolic Acid via ceramide producton. Ceramide in turn activates AMPK.

 

Note that rose hips are not listed and the last item on the list seems inconsistent with the first--

 

 

These results suggest that AICAR reduces ceramide synthesis by targeting SPT2 transcription, likely via AMPK activation as AMPK inhibition prevented the AICAR-induced improvements. Given the role of skeletal muscle ceramide in insulin resistance, it is tempting to speculate that interventions that activate AMPK may lead to long-term ceramide reduction and improved metabolic function.

 

https://dmsjournal.b.../1758-5996-4-45

 

 

 

Edited by Turnbuckle, 26 August 2017 - 02:48 AM.

[nikolay]

Turnbuckle, my point was that many of those have multi-faceted action and possible undesired effects and Metformin could achieve that and do more good things (unless you're among that 20% whose digestive tract cannot tolerate it). What I mean for AMPK is that, for example, Jiaogulan is associated with DNA damage [1], which in some cases is desired, but not in all. Rosehips have loads of Vitamin C, and other nutrients, which is not bad but could sabotage what we're trying to achieve. Also, the fewer components we have in the regimen, the better!

 

[1]: https://www.ncbi.nlm...pubmed/20555000

[Andey]

Turnbuckle, my point was that many of those have multi-faceted action and possible undesired effects and Metformin could achieve that and do more good things (unless you're among that 20% whose digestive tract cannot tolerate it). What I mean for AMPK is that, for example, Jiaogulan is associated with DNA damage [1], which in some cases is desired, but not in all. Rosehips have loads of Vitamin C, and other nutrients, which is not bad but could sabotage what we're trying to achieve. Also, the fewer components we have in the regimen, the better!

 

[1]: https://www.ncbi.nlm...pubmed/20555000

 

  Except metformin is also stressing out mitochondria 

https://www.ncbi.nlm...les/PMC4627534/

[Turnbuckle]

Turnbuckle, my point was that many of those have multi-faceted action and possible undesired effects and Metformin could achieve that and do more good things (unless you're among that 20% whose digestive tract cannot tolerate it). What I mean for AMPK is that, for example, Jiaogulan is associated with DNA damage [1], which in some cases is desired, but not in all. Rosehips have loads of Vitamin C, and other nutrients, which is not bad but could sabotage what we're trying to achieve. Also, the fewer components we have in the regimen, the better!

 

[1]: https://www.ncbi.nlm...pubmed/20555000

 

 

Good points. The link to jiaogulan, however, shows DNA damage to cancer cells and thus anti-cancer activity.

[aconita]

May I ask where you get your epicatechin from?

 

Stearic acid seems really hard to find in EU too....

 

Best choice so far would be cocoa butter... or maybe cocoa liquor: stearic acid AND epicatechins

 

 

 

[Nate-2004]

Yeah there's tons of it for cheap on Amazon in the U.S. You can pretty much get anything on that site. Stearic Acid is the "good kind" of saturated fat?

[ighbal]

Hi all,

 

might be a dumb question, but i'd like to get your advice. I would be interested to try this fission/fusion protocol.

 

I have already the Stearic acid and the Nad+, but i'd like as well to continue with some part of my current stack. In particular Omega, Vit D3 and L-Carnosine.  

 

Having read the full thread, my understanding is that I should rather continue to supplement with these during the fusion periods. If it is wrong, please let me know as I am eager to learn more. 

[stephen_b]

Any thoughts on how low ubiquinol levels might impact the protocol? 

[nikolay]

Here's a more credible source on AMPK activators: http://www.sciencedi...515000891#t0005

[nikolay]

It also looks like ceramides do that, too: https://www.nature.c...nc2010379a.html

[Turnbuckle]

A note on resveratrol for amplifying nampt that I mentioned in post 282. I've now discontinued that, as nampt is a serious promoter of inflammation. Even while taking DHEA, I noted that one knee would become puffy every time I took resveratrol. Nampt is without a doubt the reason some see joint problems with this supplement--

 

 

Nicotinamide phosphoribosyl transferase (NAMPT) is an inflammatory adipocytokine shown to interact in immune modulation in chronic inflammatory diseases, acute respiratory distress syndrome, sepsis, cancer and obesity in adulthood.

https://www.ncbi.nlm...pubmed/28837586

 

Visfatin/Nampt is released by all human OA tissues in a dimeric enzymatically active conformation and mostly by the synovium, which displays Nampt activity. The Nampt activity of visfatin is involved in chondrocyte and osteoblast activation, so targeting this enzymatic activity to disrupt joint tissue interactions may be novel in OA therapy.

https://www.ncbi.nlm...pubmed/24479481

 

Our results show that the expression of NAMPT in Ly6Chigh monocytes promotes many downstream effects involved in inflammatory arthritis and demonstrate the utility of targeting disease-causing genes, such as NAMPT, in Ly6Chigh monocytes for therapeutic intervention in arthritis.

https://www.ncbi.nlm...pubmed/23313810

 

 

 

[Female Scientist]

Does that mean we should avoid pterostilbene as well? I've been taking pterostilbene on fusion days. My recollection is that it's a more bioavailable form of resveratrol?

A note on resveratrol for amplifying nampt that I mentioned in post 282. I've now discontinued that, as nampt is a serious promoter of inflammation. Even while taking DHEA, I noted that one knee would become puffy every time I took resveratrol. Nampt is without a doubt the reason some see joint problems with this supplement--

Nicotinamide phosphoribosyl transferase (NAMPT) is an inflammatory adipocytokine shown to interact in immune modulation in chronic inflammatory diseases, acute respiratory distress syndrome, sepsis, cancer and obesity in adulthood.
https://www.ncbi.nlm...pubmed/28837586

Visfatin/Nampt is released by all human OA tissues in a dimeric enzymatically active conformation and mostly by the synovium, which displays Nampt activity. The Nampt activity of visfatin is involved in chondrocyte and osteoblast activation, so targeting this enzymatic activity to disrupt joint tissue interactions may be novel in OA therapy.
https://www.ncbi.nlm...pubmed/24479481

Our results show that the expression of NAMPT in Ly6Chigh monocytes promotes many downstream effects involved in inflammatory arthritis and demonstrate the utility of targeting disease-causing genes, such as NAMPT, in Ly6Chigh monocytes for therapeutic intervention in arthritis.
https://www.ncbi.nlm...pubmed/23313810

[Turnbuckle]

Does that mean we should avoid pterostilbene as well? I've been taking pterostilbene on fusion days. My recollection is that it's a more bioavailable form of resveratrol?
 

 

 

 

I don't know if pterostilbene increases nampt, but even if it does, I'm only saying that I've stopped resveratrol as it is causing inflammation, and nampt is likely the reason. Many take it with no apparent problem. 

[ambivalent]

Thanks for this Turnbuckle, this might be an important observation for me. It does appear pterostilbene activates AMPK (I can't paste a link for some reason).

 

I've had real problems with what I believe to be an arthritic knee for over a year - I assume it had just worsened with time but now I see that it has coincided with starting PT (and NR) - my knee has been much better the last few months and I've greatly reduced PT by coincidence; however, just lately I've started to increase it again and have moderate discomfort. Obviously I'm not highly confident it is PT yet, the peak of my knee inflammation coincided with several weeks of very challenging walking but also very high doses of NR+PT, so it was easy to overlook supplements as a cause, but it should be easy to be ascertain at some point (I've also experienced no other joint pain). I've been ramping up NR again and have noticed the sole of my feet pain I first experienced when taking NR, but perhaps it was the PT. Incidentally, I've been taking NR intermittently with N+R for several weeks but  not noticed the joint or sole pain til lately, though NR dosing has increased. So perhaps we could see if there is correlation with PT and the joint pains experienced.

 

I'm not yet convinced that NR is doing the same as N+R as I've not experienced the alertness with N+R as I did with very high doses of NR (nor have I seen accounts of this); however, that was always combined with PT. Oddly I see more commonality in N+R with c60 - strange responses to alcohol consumption including a surprising lack of a hangover but also very active eyebrow growth. I believe this was N+R but I have been taking NR at the same time but I had not correlated it previously with NR again not high confidence but certainly it isn't c60 - I've been off that for several months - usually the c60/eyebrow growth response is quite quick.

 

I am surprised there aren't more anecdotal accounts of N+R (perhaps another thread).

 

If I'm certain in the future of the relationship I will report back. You think the problem with PT is independent of the NR, so not even on fusion days?

 

Many thanks.

 

 

Edited by ambivalent, 05 September 2017 - 02:20 PM.

[Nate-2004]

Trying to catch up on this thread from the beginning, I've been skipping around. I still don't think that NR is cleaved by enzymes before entering the bloodstream. I don't think there's any supporting evidence to conclude that right now, or to conclude that taking nicotinamide + ribose is going to be the same thing. This was an ongoing debate in the curated thread. I don't think I ever saw any proof either way.

 

That said, the glutathione precursors you're talking about are all easily found in most hydrolyzed collagen powders (Great Lakes). It'd probably be more efficient to just take that after a workout assuming it's been 2 or 3 hrs since you last ingested any protein. Problem with glutamic acid though is that it can lead to overstimulation of nerve receptors, which could be a root cause of essential tremor, a condition I've been dealing with since I was 12. Berberine may help with this but only moderately, and possibly in terms of prevention. See my post here for links to all the relevant research on all that I have stated here.

Edited by Nate-2004, 05 September 2017 - 04:36 PM.

[Nate-2004]

 

I've been following a week-long cycle: 2 days fission, 1 day rest, 3 days fusion, 1 day rest. Have completed 2 cycles so far. As per Turnbuckle's suggestion, will in future add 2-4 gm ascorbic acid to fusion protocol.

 

My new schedule will look like this:

 

Day 1, & 2: Fission - 2 gm nicotinamide + 5 gm ribose, exercise 1 hour later

Day 3 Rest

Day 4, 5, & 6: Fusion - 5-10 gm stearic acid + 2-4 gm ascorbic acid + 20 gm PQQ + 2 caps BroccoMax

Day 7 Rest

 

A basic question I have is how long should this protocol be followed. Should it be considered a short-term intervention or a long-term process? Also, would you need to adjust the protocol after you have completed X number of cycles? As for now, I have committed to one month (4 cycles), but I would appreciate any thoughtful input.

 

 

I've been doing this for about ten weeks and so far I'm quite happy with the results in the gym. I'm of social security age now and I'm getting the results I got twenty years ago with about one tenth the effort. And that's what I intended from the beginning--to take control of natural mito processes and accelerate them. I expect to use this another couple of months or until I get where I want to be, and then use it intermittently as required. So far I'd say that this beats C60 by a good measure. C60 does improve mito function immediately (particularly if you have damaged mitochondria) and better mito function improves cellular health. But C60 doesn't do QC on mitochondria like this does, so this is more likely to produce true and long lasting age reversal.

 

 

Sorry, quoting an older post, but doesn't this mean only 2 days of exercise a week? It takes about 4 days at the gym for me to just combat depression, maintain muscle mass and not get fat. What's wrong with just alternating days? i.e.

 

1. Fission

2. Fusion

3. Fission

4. Fusion

5. Fission

6. Fusion

7. Fission

 

That's 4 days of exercise per week. For me, every time I go to the gym I use the sauna for 20 mins, but on one of those exercise days, instead of actual exercise I just sit in the sauna for 20 mins, break for 15 and sit in the sauna again for another 20. This supposedly doubles GH according to one study, produces the heat shock proteins I want and also, sauna is proving to have very similar benefits to that of exercise like boosting BDNF (anti-depressant).

 

So why not just alternate days?

 

Ever since I learned that anti-oxidants before a workout will negate the benefits of a workout, I started saving them all to take later in the day after I have worked out and even then I alternate days with some of them. Now I'm considering this fission/fusion protocol but I'm just wondering about this need for breaks and so many days of fusion.

Edited by Nate-2004, 06 September 2017 - 03:58 AM.

[Nate-2004]

Another link on glutamate toxicity. Someone clicked unsure on that post. Be careful with boosting glutamate or glutathione. As someone with ET, it's been implicated numerous times. I'm not sure if that's what they were unsure about or if it was my comment on NR. We're still waiting on more evidence from recent trials so my opinion on that is just an opinion, nothing more until more facts come to light. I'm also unsure about NR.

[BigLabRat]

I've had real problems with what I believe to be an arthritic knee for over a year - I assume it had just worsened with time but now I see that it has coincided with starting PT (and NR) - my knee has been much better the last few months and I've greatly reduced PT by coincidence; however, just lately I've started to increase it again and have moderate discomfort. Obviously I'm not highly confident it is PT yet, the peak of my knee inflammation coincided with several weeks of very challenging walking but also very high doses of NR+PT, so it was easy to overlook supplements as a cause, but it should be easy to be ascertain at some point (I've also experienced no other joint pain). I've been ramping up NR again and have noticed the sole of my feet pain I first experienced when taking NR, but perhaps it was the PT. Incidentally, I've been taking NR intermittently with N+R for several weeks but  not noticed the joint or sole pain til lately, though NR dosing has increased. So perhaps we could see if there is correlation with PT and the joint pains experienced.

 

 

A number of people on the NR personal experience thread have reported joint pain--and appear to associate it with NR.

 

When I look at the pathways involved, nampt is the enzyme that converts nicotinamide to NMN.

 

==================================

 

If you are successful in upping your NAD+, you will generate NADP, and the NADP will be converted into a number of subsidiary chemicals--including nicotinamide (the so-called 'salvage pathway').[See attached diagram.}

 

This could easily lead to higher nampt production in at least some people, and greater inflammation. Too much NAD+ on a continual basis might have consequences, even without pterostilberine.

 

One of the nice things about Turnbuckle's protocol is that it is cyclic, rather than simply swamping the body with the same supplement day-after-day.