upregulate D receptors with ultra low dose Haloperidol

[davea1980]

I had some tolerance for Aderall. I normally crushed these and took 45 mg, one a week on Saturday.
But even i do this once a week, i noticed some tolerance. I dicided to quit for 2 weeks and took 200 microgram Haloperidol, each night for 10 days. After day 10, i stopped for 4 days so all the Haloperidol could left my body. After day 4 i completed my 14 days-off period.

On day 14 i took another 45mg crushed Aderall and the effect was extreme. I took it at 19:00 and felt euphoria till 0:30. Does anybody has experience with this upregulation? or is this placebo-effect? I have read many papers, but most of them were based on patients with Parkinson disease. Thats why they gave lower dosages to them (40 microgram) but healthy people were advised to take 200/250 microgram, when they were depressed.

 

[Keif' Richards]

Dave, please, this is the 3rd or 4th thread you've made in a day regarding your tolerance to Amphetamine. This is all just a quest for a more recreational, powerful experience which is something that we try to steer clear of. As I have mentioned in some of the other threads, we're here primarily to assist people in using drugs in the most safe, responsible manner possible. There is information available online if you're looking to conduct research into your situation, but please, in the future, try to keep your threads tied into the topic of Harm Reduction.

 

[davea1980]

sorry

 

[d1nach]

Haloperidol is some heavy stuff the people ive met who where on would have serious issues stopping it. I mean they would do stuff like punch wire glass windows because they thought someone was talking about them or be totally psychotic. Do you have some type of schizophrenia or bipolar disorder?

If you need haloperidol it could just be just as your prone to psychotic episodes or crazy moods you can be super sensitive to adderall sometimes.

 

[davea1980]

nope. its just for upregulating D receptors.
when taken in a normal dose, it will help againt psychotics and blocks Dopamine receptors, but when taken in ultra low dose it will do the opposite. That called Hormesis effect. Ultra low dose is to low to get therapeutic effect, but high enough to sensitize the receptors ( a professor said that in paper), but was wondering if anybody else tried this also.

 

[keeping]

god haloperidol is a really scary drug. my mate was forcibly injected with it when he ended up in a psyche ward and he was in another world for like a week.
if i where in your situation at the very least i'd find a sedative with less crazy side-effects.

 

[d1nach]

Does he have any data specifically you could use scholar.google.com and pubmed to find papers that measure the change in dopamine receptors from antipsychotics and under what doses durations ect.

He might be a professor but id want hard numbers because your putting your brain on the line and your health and im a professor wouldnt be enough for me.

nope. its just for upregulating D receptors. (1)
when taken in a normal dose, it will help againt psychotics and blocks Dopamine receptors, but when taken in ultra low dose it will do the opposite. (2) That called Hormesis effect. Ultra low dose is to low to get therapeutic effect, but high enough to sensitize the receptors ( a professor said that in paper), (3) but was wondering if anybody else tried this also.

(1) does he have a paper specifically measuring the change in dopamine receptors from antipsychotics?
(2) does he have data to support this antipsychotic in micrograms changes dopamine receptor quantity.
(3) just because hormesis might occur doesnt mean it applies here atless he can prove it.

You might interested in terms autoreceptors, presynaptic receptors, and gcpr.

 

[davea1980]

yep, i printed them. I have them here.
they use 40mcg for patients with Parkinson disease. But 200/250mcg for normal patient with downregulated d receptors or severe deppresion. I didnt safe the link though, because i printed the document.

doctor called Allan Your, from London

 

[davea1980]

i was only able to find the part which refer to the patients with parkinson:
http://www.google.ch/patents/US9192605

but the theorie remains the same. Its for sensitizing the Dpamine receptors. Because Parkinson patients have less of these receptors, the keep the dose extremely low, because only 1-2% of the receptors must be covered. So this method is not specificly for Parkinson treatment, but to sensitize the D receptors.

The only difference is that patients WITHOUT Parkinson, must take a higher dose but STILL a low dose. Like
200 mcg. I am doing this for 2 years now and it seems to work.

Normally i use Dex or Aderall every 2nd week. So i take a break 14 days, i take my drug, and quit another 14 days. But the first 10 days, i take 200mcg Haldol, Tyrosine and Vit B compex. Afterhis day then i quit Haldol for 4 days. Enouh time to let the Haldol vanished from my body and during these 4 days the upregulation started. I experience a mood improvement as well.

As long you can keep the dose ultra low, no harm can be done to your brainies.

i had two persons that i contacted. Both dont know each other. Allan Young and Craig Hudson. Both gave me the same info and dose. Both names were on different papers i read

-----UPDATE-------

a few minutes ago i received a mail from Philip S, from Canada. 200mcg was for mental dificulties like depression. The dose can be lowered to 50mcg, for only the upregulating of the D receptors, take place

this is what i found about this professor, so i take his advise very seriously: ( he is responsing to my email, so i asked him for a paper. hopefully he will sent it )

born February 8, 1934) is a Canadian schizophrenia researcher and neuropharmacologist, known for his research on dopamine receptors. Seeman is a Professor Emeritus at the University of Toronto, where he previously served as the Chair of the Department of Pharmacology.

 

[d1nach]

"EXAMPLES Example 1 Administration of Low Dose Haloperidol to Rats
The customary dose of haloperidol in treating psychosis in humans is between mg/day and 20 mg/day on a continuing basis. These therapeutic doses are known to occupy between 60% and 70% of dopamine D2 receptors in the human brain, as revealed by positron emission tomography. In the rat, the human dose of 5-20 mg/day of haloperidol corresponds to 0.04-08 mg/kg (S. Kapur, S. C. Vanderspek, B. A. Brownlee, J. N. Nobrega, Antipsychotic dosing in preclinical models is often unrepresentative of the clinical condition: A suggested solution based on in vivo occupancy. J. Pharmacol. Exper. Therap. 305: 625-631, 2003).
However, a surprising finding was that using haloperidol doses in rats of 0.03 mg/kg down to 0.0025 mg/kg, which are much lower than those used clinically, results in levels or proportions of D2High receptors that were moderately elevated by 30% or 40%. Such animals exhibited heightened locomotion and active exploration analogous to increased curiosity and increased well-being in humans. For example, the data in FIG. 1 shows that 0.0025 mg/kg/day of haloperidol (i.p.) in rats elicited a 30-40% increase of D2High receptors between 4 and 5 days. Specifically it was found that 0.0025 mg/kg/day increased D2High by 38% in 5 days, with the animals showing heightened locomotion, active exploration and good grooming.

The data in the FIG. 1 illustrate that a very low dose of haloperidol, 0.005 mg/kg, elevates D2High receptors approximately two-fold over a matter of 3-5 days. On days 3-5 or upon stopping the haloperidol, these rats showed spontaneously increased locomotion and well-being insofar as they groomed themselves more actively as well as being more spontaneously active. These data indicate that low-dose haloperidol has the effect of elevating the levels of D2High receptors in rats and the assay can be used to assess other agents for their ability to elevate D2High levels in animals." (1)

(1) http://www.google.ch/patents/US9192605

Now thats what im talking about. Sounds like my use of sodium channel blockade to sensitize the dopamine receptors.

One important thing here is though i believe he is working with parkinsons so is probably focusing on dopa.i e in the parts of the brain involved in movement not mood.

The use of low dose antipsychotics to increase mood is pretty common.

Have you considered possibly having depression? For example im very addicted to adderall because i ha e severe depression which makes me want it wayyy more than most people.

Maybe you could go to a doctor and try a less potent antipsychotic first.

For example a low dose of seroquel with a ssri under a doctors supervision might be safer as it is fda approved for low mood instead of what sounds to me like self medicating.

 

[davea1980]

its a whole different paper.
this was the only in english.

Im not having a depression. I am trying this 50mcg haldol dose since today.
i must try it out for 14 days and then quit. Thats the method for non-parkinsons.

I am self medicating this only to try this receptor upregulating. I was searching for the right dose bevause many experimentss were with Parkinsons patients. So dosing with healthy people was something different thought. But 50mcg was for healthy people, dr Seeman said.

 

[Scrofula]

Sounds like you forgot an important part to your anecdote, before hitting the google scholar: a control.

I assume you've simply gone off stims for 14 days before? That usually helps with tolerance, and expectations of a brilliant way to get higher made it seem more fun than usual.

But really, it's like saying, "I have four cups of coffee every morning, but lately they just don't feel as strong. I know, not only will I quit for two weeks, I'l actually take sleeping pills each morning, and push myself to get to work, la di dah receptor stuff, and oh shit! that coffee's strong!"

I'd say great if it wasn't a straight from twelve monkeys psych med. Isn't this the one that can cause permanent drooling?

 

[davea1980]

sorry. my english isnt so very good.
what do you ment with permanent dwooling? Will two weeks off, don't do anything against tolerance?

i quit two weeks before, but now the tolrance was back AFTER two weeks break and just one single dose of 55mg. I took Methylfenidaat for 5 years daily and tolrance developed slow, but now it was back after twoo weeks of break and one single dose ( which was great by the way)

but what did you ment ith dwooling?

 

[Scrofula]

Drooling is a common side effect with anti-psychotics.
I'd heard that the drooling can be permanent, or at least, difficulty with saliva or whatever is going on.
I could be getting it confused with the one that causes permanent facial tics.
In any case, those aren't drugs I'm interested in playing around with.

And I don't know what the mechanism would be, but I think tolerance can return much faster if you have experience with a substance before. I could hand wave about epigenetic reasons for that, but I don't know. Experience alone would make it seem like tolerance developed so much faster.

 

[d1nach]

This also assumes that the d2 receptor downregulation is the cause of amphetamine loosing its effects.

Suppose our model of you take a drug it downregulates therefore tolerance therefore if you upregulate it is flawed due to the brain being more complex then we can model how it works. Then this might not produce what we think should happen based on how we think the brain works.

For example, what if one mechanism of tolerance to amphetamine is due to damage to the neurons and how they are connected and coated. Additionally what if strong antipsychotics where also damaging to the connections, coating, and signaling in the areas involved in reward.

Then, both antipsychotics and amphetamine could make you less sensitive the rewarding effects of amphetamine from damage by things like entangling and oxidative stress

 

[Scrofula]

You're also forgetting the tolerance that develops in your NE and HT systems, AND the various GABA and Glutamate pathways. Probably the imidazole receptors too (only heard of them yesterday, involve the sympathetic and NE systems, how imidazole is different from histamine, no idea).

We call it a "rush" with stimulants, but it's not due to just dopamine release. Your heart beats faster because of NE. You feel good because of HT (in the simplest models).

A lot of anti-depressant action is assumed to be because of down-regulation on pre-synaptic autoreceptors. That more long-term effect could easily be a factor in developing tolerance.

Not to mention all the crazy epigenetic modifications going on. Your cells will adapt to the rapid cycling of up- and down-regulation by loosening chromatin, all to preserve that terrible sobriety.