I agree! I haven't seen much of an effect expect for maybe a slight sense of clarity in though (less brain fog), however slight is the key word there.
Hey falco, few questions - sorry mate.
LLLT is far more complicated and surpasses my knowledge, What is your thinking towards say Using LLT regularly without supplementing with PQQ or Coq10- just curious as it is extremely expensive stuff when your taking a double dose twice a day.
Id also like to explore more areas of increased mitochondrial function, or atleast things that have a side effect of helping my mitochondria ..... now I understand how dense this forum is with your findings on this area, but time is precious... Any suggestions you would recommend? - I quite enjoyed MK-677, PQQ & have found pregenolone extremely effective with memory.
thinking lithium, any guidance would be appreciated.
p.s I am over sensitive with almost any choline (headache's ) but galanatmine hasn't been that negative with me- just fyi if any one is thinking of using it but worried with this factor.
Thanks, Bluecheer! Good to hear it might be helping a little. My recommendations are definitely on the low end of dosing...especially for ibudilast. 30mg is a common dose and 60mg/day seems to be pretty well tolerated in the studies. If you are only noticing a bit more clarity then that is one route you could try and see if you notice anything different.
LLLT is perfectly fine to use on its own and is actually the heavy hitter in that stack. If you only keep one then it's the one to keep.
If you are cool with using pharmaceuticals then low dose PDE5 inhibition with sildenafil, tadalafil, or vardenafil are good options for mitochondrial function. This combines very well with LLLT and extremely well with ibudilast (PDE4i). I use 2.5 to 5mg max of tadalafil dosed first thing in the morning. 2.5mg per day lasts me 300 days with one purchase (no affiliation). https://www.superior...e.com/tadalafil
There are so many other things for mito function so let me know if you're not interested in PDE5 inhibitors and I'll give you some other suggestions. Tbh, MK-677 (10mg per day) + ibudilast (20mg per day) + tadalafil (2.5 to 5mg per day) + LLLT + pregnenolone is a pretty damn good stack. Ibudilast also mildly inhibits PDE3 so you could even go a little lower with tadalafil. You know the drill. Start low and slowly work your way up.
https://www.ncbi.nlm...pubmed/24042162
J Pharmacol Exp Ther. 2013 Dec;347(3):626-34. doi: 10.1124/jpet.113.208017. Epub 2013 Sep 16.
cGMP-selective phosphodiesterase inhibitors stimulate mitochondrial biogenesis and promote recovery from acute kidney injury.
Abstract
Recent studies demonstrate that mitochondrial dysfunction is a mediator of acute kidney injury (AKI). Consequently, restoration of mitochondrialfunction after AKI may be key to the recovery of renal function. Mitochondrial function can be restored through the generation of new, functional mitochondria in a process called mitochondrial biogenesis (MB). Despite its potential therapeutic significance, very few pharmacological agents have been identified to induce MB. To examine the efficacy of phosphodiesterase (PDE) inhibitors (PDE3: cAMP and cGMP activity; and PDE4: cAMP activity) in stimulating MB, primary cultures of renal proximal tubular cells (RPTCs) were treated with a panel of inhibitors for 24 hours. PDE3, but not PDE4, inhibitors increased the FCCP-uncoupled oxygen consumption rate (OCR), a marker of MB. Exposure of RPTCs to the PDE3 inhibitors, cilostamide and trequinsin, for 24 hours increased peroxisome proliferator-activated receptor γ coactivator-1α, and multiple mitochondrialelectron transport chain genes. Cilostamide and trequinsin also increased mRNA expression of mitochondrial genes and mitochondrial DNA copy number in mice renal cortex. Consistent with these experiments, 8-Br-cGMP increased FCCP-uncoupled OCR and mitochondrial gene expression, whereas 8-Br-cAMP had no effect. The cGMP-specific PDE5 inhibitor sildenafil also induced MB in RPTCs and in vivo in mouse renal cortex. Treatment of mice with sildenafil after folic acid-induced AKI promoted restoration of MB and renal recovery. These data provide strong evidence that specific PDE inhibitors that increase cGMP are inducers of MB in vitro and in vivo, and suggest their potential efficacy in AKI and other diseases characterized by mitochondrial dysfunction and suppressed MB.
https://www.ncbi.nlm.../pubmed/9329386
Study in growth hormone deficient males: "After treatment with 10 mg MK-677, IGF-I concentrations increased 52 +/- 20% (65 +/- 6 to 99 +/- 9 micrograms/L, geometric mean +/- intrasubject SE, P < or = 0.05 vs. baseline), and 24 h mean GH concentrations increased 79 +/- 19% (0.14 +/- 0.01 to 0.26 +/- 0.02 microgram/L, P < or = 0.05 vs. baseline)."
Edited by lostfalco, 18 May 2016 - 11:55 PM.