Deprenyl - Anti-Aging Drug Proven Effective in Dogs

I cited two. And Deprenyl has been approved since 1989. And the Cleveland Clinic paper is from 2010. That doesn’t qualify as old to me.

This comes from Mayo Clinic:

“When selegiline is taken at doses of 10 mg or less per day for the treatment of Parkinson’s disease, there are no restrictions on food or beverages you eat or drink.”

Also, if you’re following the LEF protocol at daily dosages totaling 10 mg per week, or the most common recommendation of 1 mg per day, you are then taking one seventh or one tenth of a dosage that these sources say are safe to use without food restriction. That’s quite an additional safety margin.

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I wasn’t referring to the Cleveland Clinic paper which does not say there are no chance for possible side effects if you read it very closely so typically patient education and monitoring etc happens to monitor rare side effects, the second cited one that does make this “no side effect” claim was 1998.

I wonder if you read the much more updated FDA drug packet at the very least before taking or suggesting any drug for human use without fully understanding it. This shows that 1998 claim was wrong to assume. It’s a pretty basic step to read the updated fine print as a first step. This one is the 5 mg tablet specifically for PD.

Again, not as simple as you think. Safety margin may be high for 1 mg when applied to tyramine only, but there are still possible risk factors such as a range of drug interactions, not just tyramine.

“In theory, since MAO-A of the gut is not inhibited, patients treated with selegiline at a dose of 10 mg a day should be able to take medications containing pharmacologically active amines and consume tyramine-containing foods without risk of uncontrolled hypertension. Although rare, a few reports of hypertensive reactions have occurred in patients receiving selegiline at the recommended dose, with tyramine-containing foods. In addition, one case of hypertensive crisis has been reported in a patient taking the recommended dose of selegiline and a sympathomimetic medication, ephedrine. The pathophysiology of the ‘cheese reaction’ is complicated and, in addition to its ability to inhibit MAO-B selectively, selegiline’s relative freedom from this reaction has been attributed to an ability to prevent tyramine and other indirect acting sympathomimetics from displacing norepinephrine from adrenergic neurons. However, until the pathophysiology of the ‘cheese reaction’ is more completely understood, it seems prudent to assume that selegiline can ordinarily only be used safely without dietary restrictions at doses where it presumably selectively inhibits MAO-B (e.g., 10 mg/day). In short, attention to the dose dependent nature of selegiline’s selectivity is critical if it is to be used without elaborate restrictions being placed on diet and concomitant drug use although, as noted above, a few cases of hypertensive reactions have been reported at the recommended dose.”

(See WARNING and PRECAUTIONS.)

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Without fully understanding it? I’m not interested in being talked down to by you. Also, if you’re going to keep holding yourself out as a medical doctor and speaking with an air of professional authority, I think you need to provide indentifying information in your profile as other professionals here have done. Otherwise, you should probably amend your username and stop mentioning you’re a medical doctor.

As an analogy, if someone was on a forum complaining about problems they’re having with their residential landlord not making certain repairs, a response from another regular member saying, “If I were you, I’d withhold rent”, would be taken much differently than someone else posting and claiming to be an attorney with username “John Smith, Esq” and saying, “One remedy is to withhold rental payments until requested repairs are made.” And then putting a legal advice disclaimer under their name.

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First, off I didn’t say you didn’t understand because you’re not an MD, nor would I tell someone off just because they are not an MD. I’ve told the same exact things to colleagues. I’m showing you are literally not understanding the issue despite already previously mentioning it twice and not even reading the basics. It’s frustrating.

Second, I don’t need to reveal my full identity publicly due to the sensitive information shared here nor I have any desire for anyone on the internet I don’t fully trust to start harassing me or calling work with any of this. And yes I am real. At least several folks who have been massively messaging me since the day of time think and perhaps know I am. I’m more than happy to use a shared third party to vouch and verify as needed, but I’m not going to share my identity publicly.

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From experience being on an maoi for several lengthy periods, I think the dietary restrictions are very overstated. When I was on phenelzine, I pushed the boundaries with all nearly all of the forbidden foods (not including aged meat) and never had a hypertensive crisis. Perhaps there were a few odd occasions where I felt a slightly elevated heart rate. I think the picture became more clear when they did tyramine challenges during the emsam patch trials. Very few of the foods once thought to have tyramine actually do. Anyhow if you want to practice abundant caution with deprenyl you can get around gut mao inhibition with sublingual admin. IIRC the nootropic recommendation is 1mg sublingual to get the approximate effect of 5mg oral, so the drops would be perfect for that. Caveat emptor. Personally I can’t stand how deprenyl makes me feel within 2-3 days of taking 5mg daily. Others describe that as a motivation and mood boost. I just feel agitated.

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Actually, yesterday in another related thread about Deprenyl, I posted an abstract where the researcher recommended 1 mg daily of Deprenyl as an antiaging drug. You then responded and said, “Low-dose Deprenyl is a given, the typical adjunct dose is 1.25 mg per day to start for PD.” I then politely informed you that was only for the pill that dissolves in the mouth, as the typical dosage for regular Deprenyl for treating PD is 5 mg twice daily. You then responded again, claiming the kind that dissolves orally is what you were actually talking about: “Yes, I was referring to ODT 1.25 mg qd as initial dose - also oral tab 5 mg twice daily is not always the case - some docs use half or less to start.” Which makes zero sense as a response to my post about the 1 mg regular Deprenyl paper. You obviously made a mistake and covered it up. And then did you go back and do editing?

You also engage in subtle sophistry and straw man argumentation in your posts and seem to assume that other people aren’t as smart as you so they won’t notice.

I’m not impressed with the idea of another username and possible sock puppet “vouching” for you, not even the owners. You’re the one making the claims. You can support them with identifying info as other doctors and pharmacists and such here, or you can come down to the same level as the rest of us and start sharing your personal opinions and ideas without the air of professional authority. That’s just my opinion. If it isn’t shared by the owners or others here, okay. I’ll just be a dissenting voice.

This will be my last post related to this.

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Nowhere did I suggest a sock puppet, happy to go with admin to vouch and verify NPI and ID privately, and not sure why you’re jumping to an assumption of malice here - where did I use an air of authority or an appeal to authority?

Others don’t necessarily have the same level of general asset protection principles I follow. Heck, I see plenty of colleagues who don’t even buy umbrella insurance at the bare minimum. Nor do others have the sensitive information I have shared previously. For example, psilocybin use. Not quite the type of deal the medical board would take kindly, just to start.

If you don’t like it, so be it. I don’t expect everyone to understand my reasons. I don’t mind if you block me.

Everyone, please try to remember to go easy on the people and focus more just on the science /issue. We are all working on the same or at least similar goals here.

Its also valuable to keep in mind that in texted communications its easy to misinterpret meaning, tone and intent due to lack of facial / visual ques. Try to give everyone the benefit of the doubt, and its better to assume the best of intentions rather than the opposite.

Take what you find helpful in these discussions here, and ignore that which you don’t find helpful. And sometimes, if something that someone says tweaks you the wrong way… Take a break and let it go. Everyone has bad days sometimes.

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Forgive me if I have overlooked it, but has anyone a reason why deprenyl extended the lifespan of older dogs? Does it affect mtor? If not this is a very big deal. Rapamycin is one of very few interventions that helps when started late in life. My dog wants to know how this works.

From the last page (before the references) of the full study.

The mechanism(s) by which L-deprenyl enhances longevity in rodents, dogs, and possibly
people remains undetermined, but one intriguing theory involving a catecholaminergic
> activity enhancing effect has been offered (16, 17). Catecholaminergic (and serotonergic)
activity peaks in rodents during the developmental phase between weaning and sexual
maturity, followed by a steady decline thereafter (17), which correlates with longevity and the
levels of important survival functions such as activity, learning, and sexual performance. Ldeprenyl
enhances the impulse propagation mediated release of catecholamines in the brain
(IS), hence the catecholaminergic neurons work on a higher activity level, which might then
improve performance on the above mentioned functions and prolong life (16).

Direct from the “horse’s mouth”.

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Page 5 of the study shows the table of the dogs, with the causes of death of those who did not survive after six months trial length.

The placebo dogs died of:

  1. congestive heart failure
  2. congestive heart failure
  3. mammary gland carcinoma
  4. chronic renal failure
  5. mammary gland carcinoma
  6. anaplastic mammary carcinoma
  7. pulmonary carcinoma
  8. lymphoma
  9. mammary adenocarcinoma
  10. chronic renal failure
  11. neurofibrosarcoma, duodenum

CVD and cancer. Isn’t rapamycin claimed to be cardioprotective and cancer-protective? Do the rapamycin ingesting members need deprenyl?

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“If you wait until you are ready, it is almost certainly too late.” ~ Seth Godin

As shamelessly posted numerous times. From Blagosklonny’s “Rapamycin for longevity: opinion article”

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My point is, if deperenyl only helps in avoiding CVD and cancer, it seems to be duplicative of what is addressed by rapamycin. With regard to catecholaminergic activation, I am looking for other substances with similar mechanisms of action.

It seems, given that they likely act via different pathways (but I just found that there may be some overlap, but in opposite directions…

Findings showed that selegiline increased the level and expression of PI3K, AKT and mTOR as well as decreased the proportion of dark neurons in the CA1 area of the pyramidal layer of the hippocampus. We concluded that selegiline, partially at least, through increases the expression of PI3K, AKT and mTOR as well as decreases the percent of dark neurons in the hippocampus could improve the memory impairment following the ischemia in rats.

But if they are operating on significantly different pathways then they likely impact CVD and cancer in different ways, so thety could be complimentary. All hypothetical right now…

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curt504, While reading through this topic a second time your comments got my attention. You’ve been taking deprenyl for 10 years and you can work like a 40 year old although you’re in your late 60s. However, you note no discernable benefits from deprenyl or rapamycin. Well, do you mind telling why you started deprenyl 10 years ago? And, do you mind listing all of the supplements you take? You must be doing something right and I want to know more. Thanks.

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Hi Jay, Nice hearing from you. You remember that so called millionaire’s protocol? Long, lots of stuff… Basically I take ALL that. LOL!! I have a swallowing problem so I run all pills through a blend jet, morning and night. Alot of anti inflamatories; curcumin + olive oil 2 T in morning and a splash at night to help the absorbsion of evening curcurmine. Ginger extract, baswalia AND 30 others following that Moderator’s post of that millionair guy. He was about 40yrold.

Dryprenyl was tipped by Dr Deen (??) of FL 15 yr ago and he seemed to be a 1 trick pony Dr. I also take LDN, low dose naltrexon. Buy 50mg pills from India, disolve in 4oz + 1 T of water. Then take 1T per night = 5mg dose. LDN is inflamation quieting… I can’t offer any efficacy comments re dyprenyl or anythig else when one takes like me literally a kitchen sink. I can’t imagine it all is useful. My wife nags and has a point.

And the rapa + sinolitics; Dasinitib + Fisetin (been discredited) + quercetin + berberine + grape seed. No logic, just Dr Green said 20mg rapa every 2 weeks so thats my approx protocol per compliance issues. I do the grapfriuit absorbion protocol only with pink GF concentrate, 1/4 can per rapa dose 2 hr prior to rapa.

The forum has been fantastic. But they don’t cover nootrophics (brain) much. I take a stack; piracetum + oxycetum + Alpha-GPC+bacopa (very important/useful)… etc

Who knows the cost of my pee. :-\ LOL

Not sure all this is helpful. But I’m glad to share. Wishing you the best, curt

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Deprenyl is a MAO-B inhibitor which has been used for the treatment/“slowing down” of Parkinson’s disease for years. Also people in Europe were taking it as an anti-ageing medication on a once a week basis. In 2006 another medication from the same group - Azilect was approved by FDA for the treatment of Parkinson’s disease in my opinion not as effective.
It is interesting that it was used on a once a week basis the same way we take Rapamycin!

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Did anyone reach out to the ITP guys?

I would definitely recommend Deprenyl to the ITP guys. It is very well tolerated medication with a long safety record.

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