morgan#1
Member
- Joined
- Dec 3, 2016
- Messages
- 295
Ok I’m trying that.
Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature may not be available in some browsers.
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
I was thinking pyrucet in am and then a small dose of lapodin in pm? Anything to be cautious of regarding taking them at the same time, albeit 12 hours apart
This study shows a an increase in Testosterone of 38% from Etyhlpyruvate with a HED of about 250mg/day for 30days in mice.
They even increased their testosterone (14%) when EP was used with MTX (Methotrexate) which " is an anti-metabolite drug widely used in treatment of neoplastic disorders, rheumatoid arthritis and psoriasis"
This study is from the original thread but I thought it was worth highlighting ,since there are so many study to go through.
Table 3
Comparison of the effect of EP on testosterone level and lipid peroxidation caused by MTX (M±SE)
Group Testosterone (ng/ml)
control 0.42±0.02
MTX 0.19±0.02 a
EP 0.58±0.02 ab
MTX+EP 0.49±0.04 b
Protective Effect of Ethyl Pyruvate on Epididymal Sperm Characteristics, Oxidative Stress and Testosterone Level in Methotrexate Treated Mice
No , it is already the Human equivalent dose. I think it was something like 40/mg/kg/d in mice if I converted that right ...Thanks. The 250mg/kg in mice is equivalent to about 18mg/kg in humans so it should be achievable with 2-3 doses of Pyrucet.
No , it is already the Human equivalent dose. I think it was something like 40/mg/kg/d in mice if I converted that right ...
Yes and applied on testicles could be even better . I have gotten good androgenic results from that, but would adivse everyone to dilute it in Coconut Oil first (!) In order to not start a fire down there (yes it burned)Oh yes, you are right. So, even half a dose of Pyrucet should do!
On websites that sell this stuff and forums like reddit.
I also wanted recommend to read this study from the main thread.
It has some interesting passages like :
Preventive effects of ethyl pyruvate on endotoxin-induced uveitis in rats. - PubMed - NCBI
"Exogenous EP has the potential to augment intracellular pyruvate levels, which enable the cells to protect themselves from reactive oxygen species (ROS)-mediated damage.1–3 However, several studies have shown that EP as an intact ester also has direct pharmacologic effects, which have been recently reviewed by Kao and Fink.4The pharmacologic effects of EP are quite diverse, and include downregulation of the secretion of proinflammatory cytokines, enhanced antitumor immunity, amelioration of redox-mediated damage to cells and tissues, inhibition or promotion of apoptosis based on the circumstances, and support of cellular adenosine triphosphate synthesis. Recently, a number of studies have shown that EP is a robust and potent anti-inflammatory agent in pathologic conditions, such as hemorrhagic shock, sepsis, systemic inflammation, colitis, pancreatitis, and pulmonary fibrosis.5–13 These reports indicate that the anti-inflammatory effects of EP are caused by downregulation of the proinflammatory transcription factor nuclear factor kappa B (NF-κB) and the expression of NF-κB–dependent proinflammatory marker proteins, such as TNF-α, IL-6, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS)"
Also it shows that is doesnt make much of a difference in terms of inflammation if Ethylpyruvate is given 1 hour before or two hours after LPS treatment. What does make a difference seems to be the dosage . At 15mg/kg the results were not sigificant but at at 30mg/kg they were and did not change even with 60mg /kg. Meaning there seems to be a cut of dose (at least in rats) for the anti-inflammatroy and anti-endotoxin effects , which was at around 30mg/kg/day (HED ca.350mg) 1 hour before LPS treatment.
"In addition, EP-rendered protection was also observed in a dose-dependent manner (Figs. 2F, F,2G).2G). The lowest dose of EP (15 mg/kg body weight) partially suppressed the infiltrating cells and protein levels in the AqH and was not statistically significant. However, higher EP dosages (30 and 60 mg/kg body weight) significantly (P < 0.001) suppressed infiltrating cells and protein levels in EIU rat eye AqH (Figs. 2F, F,2G).2G). Our studies also indicate that 30 mg per kg body weight of EP caused significant suppression of EIU, which is almost similar to 60 mg per kg body weight, indicating that in rats, 30 mg per kg body weight of EP is the optimal dose required to significantly prevent LPS-induced ocular inflammation."
Further it seems to lower nitric oxid amongst other inflammatory mediators :
" EP also prevented the expression of TNF-α and activation of NF-κB in the ciliary bodies and retina of the eye. Moreover, in HNPECs, EP inhibited lipopolysaccharide-induced activation of NF-κB and expression of Cox-2, inducible nitric oxide synthase, and TNF-α."
"EP was also observed to inhibit expression of iNOS and Cox-2 in HNPECs. These results suggest that EP prevents the NF-κB–dependent expression of iNOS and Cox-2 and therefore production of nitric oxide (NO) and prostaglandin (PGE2)"
The study also links to another study/review that seems really interesting and states the following:
The biochemical basis for the anti-inflammatory and cytoprotective actions of ethyl pyruvate and related compounds. - PubMed - NCBI
"Treatment with EP has been shown to improve survival and/or ameliorate organ dysfunction in a wide variety of pre-clinical models of acute illnesses, such as severe sepsis, acute pancreatitis and stroke. Using other animal models, some studies have demonstrated that more prolonged treatment with EP can ameliorate inflammatory bowel disease or slow the rate of growth of malignant tumors. In a clinical trial of patients undergoing cardiac surgery, treatment with EP was shown to be safe, but it failed to improve outcome. The true therapeutic potential of EP and related compounds remains to be elucidated. In this review, some of the biochemical mechanisms, which might be responsible for the pharmacological effects of EP, are discussed."
Some studies from the main thread tell you all by their headline , but other ones like these are real gems !
Understatement of the year. I'm most excited about the significant increase in carbohydrate utilization, as evidenced by the very noticeable increase in hunger. I'm in the process of learning how to dose and adjusting my diet so I get enough carbs without ending up face down in the pasta. But the anti-inflammatory and other effects are also very remarkable and most welcome.It does seem like a very promising chemical.
Understatement of the year. I'm most excited about the significant increase in carbohydrate utilization, as evidenced by the very noticeable increase in hunger. I'm in the process of learning how to dose and adjusting my diet so I get enough carbs without ending up face down in the pasta. But the anti-inflammatory and other effects are also very remarkable and most welcome.
I am very grateful that you uncovered all this in your researches, and that you then made it into a product that I can easily buy and consume. The future now looks both brighter and more certain.
Actually cancer patients have too much intracellular GSH, especially inside the tumor. It does have a role in helping get rid of carcinogens like acetaldehyde, but once a tumor forms GSH is rather harmful.
Glutathione metabolism in cancer progression and treatment resistance
"...Glutathione (GSH) is the most abundant antioxidant found in living organisms and has multiple functions, most of which maintain cellular redox homeostasis. GSH preserves sufficient levels of cysteine and detoxifies xenobiotics while also conferring therapeutic resistance to cancer cells. However, GSH metabolism plays both beneficial and pathogenic roles in a variety of malignancies. It is crucial to the removal and detoxification of carcinogens, and alterations in this pathway can have a profound effect on cell survival. Excess GSH promotes tumor progression, where elevated levels correlate with increased metastasis. In this review, we discuss recent studies that focus on deciphering the role of GSH in tumor initiation and progression as well as mechanisms underlying how GSH imparts treatment resistance to growing cancers. Targeting GSH synthesis/utilization therefore represents a potential means of rendering tumor cells more susceptible to different treatment options such as chemotherapy and radiotherapy."
View attachment 12430
As an advanced prostate cancer patient I have been on androgen deprivation therapy for the last two years. PSA started going up again so now I have started Chemo. I meet with Sam Denmeade at John Hopkins in Maryland to see if I could get on his RESTORE trial. He said my PSA was to high and strongly recommended Chemo to get the PSA down. THIS redox status makes total sense to me now. Unfortunately I have been using various antioxidants thinking they were good for me (believe me a lot of supplements act like antioxidants). Anyone with cancer should stop using all antioxidants immediately. Chemo creates high ROS but the cancer cell creates high GSH. Now using Pyrucet along with Chemo to keep ROS high and GSH low. No oral antioxidant supplementation!
What supplements do you consider antioxidants as my son has a brain tumor .
Dear Obi, that's almost a list on what to get extra in case of cancer. I'm not aware of anyone curing it by avoiding these nutrients (although they must reduce the effect of chemotherapy). As you know, their behavior also depends on the dosage in question.Vit A, Vit E, Vit C, Taurine, Niacinamide, Ubiquinol (CoQ-10), Selenium, Uric Acid, NAC, Glycine, Polyphenols. I am probably missing some others.