Money is the root of all hype.
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This may be a good source from creatine references.
There is also a sub-section on “Creatine safety profile” that might have some helpful references.
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He is doing a lot of blood tests and scans so he sees what it fits him as a supplement and/or drug.
Customization is the golden standard but it’s expensive!
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Ericross2, I tried carnosine some time ago and noticed no improvements with endurance or high intensity exercise. Recently I tried beta alanine and found no improvements with it, either. I’ve also tried creatine monohydrate several times with no improvements noticed. I tend to try new supplements for a couple of weeks looking for improvements in non-stop lap swimming for endurance and high speed sprints for intensity exercise. I’m not immune to the potential for placebo effect, but I try to be analytical and skeptical when trying a new supplement. I try to eliminate all products that produce little or no results. I am, however, a highly skeptical person. So, it’s possible the products you noted could be useful for you.
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Thanks for the comment, @Jay I haven’t (yet) used any of these. However, if I recall correctly, there may be a “build up” period before anything really happens for at least carnosine and maybe creatine that may be as long as a month or two (depending on dose, and your physiology). So I might guess that two weeks wasn’t enough to see any changes.
Also in both, do they build muscle mass with basic exercise, or with hard work in the gym? —. It sounds like you are pushing yourself hard in the pool but I’d guess you’d have to be working your muscles pretty hard to see a change in two weeks.
I’be been working myself hard at the gym and am see muscle where I’ve never really had any to speak of (for instance, I can now flex my pecs so you can distinguish them, something I’ve never been able to do even when in my 20s and a seriously lean backpacker. So maybe these supplements aren’t really needed. But since I’m 52, I’d love any (safe) help I can get.
Hopefully someone who is actually knowledgeable will correct me if I’ve misspoken.
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Started a thread here - I think @desertshores had a helpful post, but wanted to get down to actually seeing where people were tailoring their own regime. What is your own regime!
It depends on your kidney function. No studies have been done on creatine and people with chronic kidney disease. My own nephrologist advised me against it.
The flushing caused by beta-alanine ingestion is not an inflammatory reaction so I don’t think it increases inflammation. Also you can avoid the flushing effect by taking it with meals and distributing the dose throughout the day.
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The race between NMN and NR is getting a little stale in my opinion. I still advocate for Niacin if you are interested in increasing NAD. Super cheap and the data supports it. Sure there’s the concerns with flushing and liver issues, but the flushing goes away with time (I am on 1000mg/day extended release and experience none) and the liver issues everyone loves to tout have only been evidenced in certain studies. I get my blood tested every 6 months and have seen no variation in my liver enzymes or glucose levels (some reports claim that niacin raises blood glucose). Granted, I am on acarbose and canagliflozin now, but they were normal before that. Not only that, but my cholesterol (which used to be over 200) is at 165 even though I am on supplements that are supposed to raise cholesterol (niacin is legendary and well documented for lowering cholesterol). So, although it may not increase lifespan, I think it will contribute to my health span and I stand by it.
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I had high hopes for Niacin. The flushing never lessened but I really didnt mind as long as it didnt get any worse.
I was at 300mg when I happened to be experimenting with a CGM and noticed that my blood glucose spiked to an intolerable extent whenever I took Niacin. I read that this can occur. I decided that the damage from spiking might offset the benefits so I discontinued it.
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Have you tried the extended release? I get mine on Amazon and haven’t noticed any spikes.
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FWIw
I post this before on another thread;
Work was published around 1949 by William Kaufman, M.D
Titled;
THE COMMON FORM OF JOINT DYSFUNCTION
You can read an online copy at;
The publication addressed more than just “Joint Dysfunction” in my view worth reading.
Use nicicidimide, take 1 gram {yes, 1 gram per hour.{this was Kaufman, protocol]. Take several {that is more than 3g] grams per 24 hours
A very inexpensive way to increase systemic NAD levels.
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I havent tried extended release. There was a reason that I did not,.which unfortunately I dont completely recall.
After my next blood work, if I still need additional benefits I’ll revisit that option.
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Thank you for that. The reason I haven’t used Niacinimide is that it doesn’t have the same cholesterol lowering, triglyceride lowering and HDL raising effects that niacin (nicotinic acid) does. Studies show they both do a good job in raising NAD though.
Reading through the above referenced study again (Niacin Cures Systemic NAD+ Deficiency…) it also looks like it has an effect on MTOR.
Niacin Downregulates mTOR Signaling Pathways
We then asked how niacin affected gene expression. The pathway enrichment analysis of RNA sequencing data indicated that serine-glycine-one-carbon pathways (de novo serine biosynthesis, purine degradation, and glutathione metabolism) were among the most significantly changed in PEO (Figure 6A; Table S3 shows individual transcripts). The finding is intriguing, as these pathways were also found to be modified in mitochondrial myopathy mice, as part of the mitochondrial integrated stress response (ISRmt) (Khan et al., 2017, Nikkanen et al., 2016, Tyynismaa et al., 2010, indicating high conservation of the stress responses in species. Compared with controls, PEO muscle showed macrophage and innate immunity pathway activation (“phagosome formation”), less significant after niacin supplementation (Figure 6A; Tables S3–S5). Only five and two of the disease-associated pathways remained significantly changed after 4- and 10-month supplementation, respectively, in patients compared with controls (Tables S4 and S5). The most prominent niacin-related transcriptomic change in PEO patients’ muscle (PEO 10 months on niacin versus PEO baseline) was wide-spread downregulation of mammalian target of rapamycin (mTOR)-dependent cytoplasmic translation, involving a large number of cytoplasmic ribosome subunits as well as translation initiation factor eIF1 (Figure 6B; Table S6). This was intriguing, as the major translation activator mTORC1 was also activated in mitochondrial myopathy mice, in COX-negative, SDH-positive fibers, and rapamycin (mTOR inhibitor) rescued their disease signs (Khan et al., 2017). In patients, niacin activated the peroxisome proliferator-activated receptor signaling pathway, known to induce mitochondrial biogenesis (Figure 6B; Table S6), which we find to occur in our subjects’ muscle. Niacin also led to decreased atherosclerosis signaling including lowered apolipoprotein expression in patients (Figure 6B; Table S6). The healthy control muscles showed only few changes after 4 months of niacin (Figure 6C; Table S7), emphasizing the importance of NAD+ metabolic changes in mitochondrial myopathy.
I had been taking creatine. started having pain in my foot near the toe (but not the toe). Gout had not occurred to me but sister advised me to check uric acid. I didn’t do that but did research and saw that there is a correlation between creatine and uric acid production. Dropped the creatine, started tart cherry, and couple of other things for controlling uric acid and the problem quickly started to correct.
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According to the poster Bicep, extended release is not recommended because of potential damage to the liver. IR, on the other hand, is metabolized quickly and safely. I tried 100-mg tabs of IR, but the flushing was too much for me. The Mayo Clinic and the Cleveland Clinic advise against niacin supplementation.
Understood and, to be clear, I’m not a medical doctor. However, there are a couple of points to consider here:
-The study I referenced above regarding systemic NAD+ Deficiency used extended release with no liver abnormalities.
-I have used extended release 1000 mg/day for years, as has my wife, with no abnormalities in our liver profiles (granted, that’s an N=2, but…) and we have both seen tremendous reduction in our cholesterol, triglycerides and increases in our HDL.
-Usually the studies that show abnormalities are for the SR prescription version, not the ER version.
-IMO, the Mayo Clinic and Cleveland Clinic are like any other institution. They have amazing doctors and cutting edge techniques, but rarely visit old dogma relating to older meds. Rapa is a great example…if I relied on what they said about Rapa I wouldn’t be experimenting with it.
-I would also say, that in the studies that do illustrate liver abnormalities that the patients are taking other meds that compromise liver function.
I’m not arguing with you @Tim I just think we need to relook at current stances on medicine. Peter Attia said in one of his podcasts (I don’t remember which one off the top of my head), “80% of what you learn in med school is wrong and the other 20% is questionable.”
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Thank you for the explanation. I don’t drink, so my liver may survive an introduction to niacin ER. There is some evidence that niacin can improve kidney function, which is a concern of mine. I will ask my nephrologist for her opinion. But she, like many doctors, is inherently conservative. Your point about the clinics is well taken.
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If you decide to start taking Niacin again, go super slow. The way I did it was to do 250 mg for a month, then went to 500 mg for a month, then 750 mg for a month, then 1000 mg starting in month 4. It helped me stabilize the flushing that inevitably happens. After being on it for as long as I have the flushing is minimal. Again, not a doctor, this is just what worked for me.
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