We know the genocides and invasions of countries, but what smaller things have they done?
Do 5ht1a agonists/partial agonists cause permanent up-regulation or down-regulation of receptors? Or any persistent change at all even with discontinuance of the medication? In drugs like Viibryd, Buspar, or Vorioxetene.
They said bupe was a full agonist and that the naloxone in it is what caused the ceiling and blocking effect. And I know thereโs a lot of mis information out there but the fact that itโs being taught to people in trainings by doctors is somewhat alarming..
Or maybe thatโs right and Iโm wrong but in all my research Iโve been taught the opposite
Can someone please help to compare and contrast partial and inverse agonist using the two-state model and how either one can be used to treat disease that is caused by excessive receptor activation of the [named] receptor by an endogenous full agonist .
I have an understanding of what a partial and inverse agonist are with their affinity, efficacy, Emax etc, but is there anything else I am missing and how do either one treat a disease.
Thank you
Does anyone know if there are any studies or individuals who have trialed on themselves, using Nicotine or Dopamine agonists to as a reward system to help cement good habits and drop bad ones?.
(Similar to how treats are used to train dogs)
Since dmt is a serotonergic psychedelic, Iโm thinking it should be okay, right?
Through my research Iโve found a few compounds that are found in other plants besides cannabis which either closely mimic the effect of THC or have been found to attach to the CB1 or 2 receptors either as an agonist or antagonist.
Main two in mind come from Magnolia and Kava, both are CB1 agonists and some also affect CB2. Iโve tried the Kava cannabinoid extract in a drink and it felt just like D8/9. I also tried the highly refined magnolia extract (90% purity) and it was insanely strong for someone with minimal tolerance to THC. Iโm considering using it along with THC-free CBD distillate and terps in place of Delta 8 while Iโm job searching to prevent showing up hot on a pre employment drug test. Also magnolia extracts are legal pretty much everywhere so may be a good alternative to bring along with you on trips to places where cannabis isnโt legal yet. I donโt think the magnolia extract could be vaped in a disty cart but could maybe blend into vape juice.
What do you guys think? Have you tried any of these, and do you think they could be a promising direction to go in for people in places where alt noids and MJ (and even hemp) arenโt legal?
Erinacine E is supposedly a potent KOR agonist and it is thought to be found in the Lions Mane mushroom, albeit only in small quantities.
And I'm wondering how I would go about extracting it? Or if in a high enough dose would Lions Mane produce hallucinogenic effects?
I know this isnt about salvia but it's about another natural KOR agonist so I thought it would be ok to post this.
Is Erinacine E, Collybia and Salvianoids the only known natural KOR agonists?
Would really appreciate your input here on the benefits of PPAR Gamma agonism for; Insulin sensitivity Increasing HDL Lowering LDL Metabolic benefits Inflammation
I have been researching Pioglitazone and considering 15mg daily use.
I appreciate there is some concern over long term epidemiology studies showing an increase risk of bladder cancer, and my questions would be;
This data is in people who are pre diabetic or have type 2 diabetes and therefore one would assume have lifestyle associated factors that are exasperated by any potential issue. In your opinion how does this transfer to people fit and healthy looking to optimise their biology for long term health outcomes?
Is there concern over pro growth factors of daily PPAR agonism?
I appreciate your input
I took my muscle relaxer by accident and I want to know if my evening plans are a bust
Abstract: >Derivatives of (2-aminopropyl)indole (API) and (2-aminopropyl)benzofuran (APB) are new psychoactive substances which produce stimulant effects in vivo. (2-Aminopropyl)benzo[ฮฒ]thiophene (APBT) is a novel sulfur-based analog of API and APB that has not been pharmacologically characterized. In the current study, we assessed the pharmacological effects of six APBT positional isomers in vitro, and three of these isomers (3-APBT, 5-APBT, and 6-APBT) were subjected to further investigations in vivo. Uptake inhibition and efflux assays in human transporter-transfected HEK293 cells and in rat brain synaptosomes revealed that APBTs inhibit monoamine reuptake and induce transporter-mediated substrate release. Despite being nonselective transporter releasers like MDMA, the APBT compounds failed to produce locomotor stimulation in C57BL/6J mice. Interestingly, 3-APBT, 5-APBT, and 6-APBT were full agonists at 5-HT2 receptor subtypes as determined by calcium mobilization assays and induced the head-twitch response in C57BL/6J mice, suggesting psychedelic-like activity. Compared to their APB counterparts, ABPT compounds demonstrated that replacing the oxygen atom with sulfur results in enhanced releasing potency at the serotonin transporter and more potent and efficacious activity at 5-HT2 receptors, which fundamentally changed the in vitro and in vivo profile of APBT isomers in the present studies. Overall, our data suggest that APBT isomers may exhibit psychedelic and/or entactogenic effects in humans, with minimal psychomotor stimulation. Whether this unique pharmacological profile of APBT isomers translates into potential therapeutic potential, for instance as candidates for drug-assisted psychotherapy, warrants further investigation.
Unfortunately no full text available on sci-hub yet as the paper was just published yesterday.
Full text here, thanks /u/neuropharmnaut.
About a month ago there was a [post here](https://www.reddit.com/r/
... keep reading on reddit โกI have just started doing research to learn as much as I can for someone very close to me who is about to get the DatScan to confirm a possible clinical diagnosis of Parkinsonโs. The neurologist isnโt convinced itโs Parkinsonโs but said itโs the most likely diagnosis at this point.
If the DatScan is positive he wants to start Sinemet to see if symptoms improve. I have concerns about Sinemet due to the fact that up to 50% develop dyskinesia after a couple of years of treatment. He said that this only happens at high doses. I inquired about dopamine agonists instead like bromocriptine or pramipexole and he seems to frown on them due to their own side effects.
Is the dyskinesia from L-dopa / Sinemet reversible if someone stops taking it?
Also wondering if anyone else has tried dopamine agonists rather than Sinemet and had good results?
I'm due for a 6 month booster soon and thinking of starting progesterone. I'm wondering if this will be the best time to start? I am nearly at 17mos & tanner 4ish.
GLP-1 Agonists (also known as Incretin Mimetics) are a class of meds that mimic the actions of GLP-1 (Glucagon-Like Peptide 1), a naturally occurring peptide that can decrease blood sugar levels by increasing insulin secretion.
GLP-1 Agonists are mainly used by people with Type 2 Diabetes, but bodybuilders are starting to use them off-label as well. These drugs aid in cutting by suppressing appetite, which they achieve through:
- The normalization of blood sugar levels.
- The inhibition of stomach emptying and acid secretion.
- A direct action on the brain that causes a feeling of satiety.
These properties along with the fact that GLP-1 Agonists can control blood sugar levels make these meds an excellent addition to a GH secretagogue or HGH cycle.
Other potential benefits of GLP-1 Agonists besides the appetite suppression and anti-diabetic actions are:
- Enhanced memory and cognition.
- Neuroprotection.
- Cardioprotection through vasodilation.
- Renal protection.
In terms of negative side-effects, GLP-1 Agonists are generally safe & well-tolerated, but they can potentially cause stress and anxiety.
They can potentially cause nausea and gastrointestinal issues too, but the most concerning aspect of these medsis that they could potentially exacerbate pancreatic and thyroid c4nc3r.
There are many different GLP-1 Agonists, but the most popular ones are Semaglutide, Dulaglutide and Exenatide. Even though all of them have the same mechanism of action, they vary in strength, half-life and efficacy.
The most popular one among bodybuilders is probably Semaglutide, which has a very long half-life and is also orally bioavailable. More anecdotal data about the effects of GLP-1 Agonists on bodybuilders is necessary.
Anybody thinks it's a good idea using telmisartan, or some other glp1, while doing GH? Also, would you still use a GDA alongside it?
Partial agonists of receptors have partial efficacies compared to neurotransmitters for such receptors. Aripiprazole in an example of a partial agonist.
Chelated minerals could be partial agonists in guts. Where chelated minerals are supplemented enzymes in guts that require such minerals could have decreased activities in guts.
What occurs in guts affects bodies systematically. Chelated minerals, where such chelated minerals are partial agonists in guts could have adverse affects systematically. Tests on blood and/or tests on plasma of mineral levels could be normal, however, dysregulations of enzymes that require minerals are at headwaters of various medical difficulties that individuals are having.
Layperson understanding:
Strattera is an NRI.
Norepinephrine is associated with vigilance and alertness.
However patients commonly report fatigue as a side effect.
Why would this be?
I was curious if someone here is on this type of treatment or knows the effectiveness of it. My endocrinologist talked about this and testosterone injections. Most cases I read of people with the syndrome end up with testosterone in a variety of ways, and I canโt find a lot of stuff on these โgnrh agonistsโ. Itโs the first time Iโll go on any type of therapy so I donโt really know whatโs the most optimal.
Thanks for reading
it doesn't feel sedating except at very high doses. It feels almost like a hypomanic state. The dopaminogenic effect seem the strongest to me.
I enjoy myrrh (the tree resin) which contains compounds that selectively activate delta-opioid receptors. Myrrh taken orally can be comforting in a similar way to kratom, though much milder.
Kratom also activates these delta receptors (DOR), along with the more euphoric mu receptors (MOR). Myrrh is uplifting in a similar way to kratom but without directly activating the mu receptors and its DOR activation enhances the brain's natural MOR signaling. Myrrh itself can produce a mild mood lift with analgesia that is subtle but perceptible. It doesn't pack a punch like kratom, but it also produces a gentle warm euphoria that is quite unique.
Myrrh treats many ailments and is a wonderful medicine, a sort of panacea that even improves mood and heals the stomach. Myrrh should be useful for quitting kratom as it can be used to activate the delta opioid receptors for some comfort while giving the mu receptors time to recover. It can ease the transition away from kratom in a similar way that kratom is used to "step down" from prescription opioids. It's great to have another opioidergic tree that can smooth the tapering process, ease withdrawals, allow for MOR recovery, and its use may be continued even after one is finished tapering off of kratom.
Myrrh is produced into capsules for oral supplementation, and also raw chunks of the myrrh gum resin which can be eaten whole (but they must be broken down so that you don't choke on a jagged piece of resin). I prefer capsules containing the myrrh gum resin over capsules containing a myrrh extract (which may not contain the full spectrum of compounds).
My psychiatrist is prescribing pramiprexole dihydrochloride (sorry if there is a spelling mistake there) and wondering what folks think of this? What would be potential concerns or things to watch out for?
I won't enter in too much details in order to not waste too much time with something that's not the focus of this post.
Ths long lasting blissful afterglow is, most likely, due to the strong sigma-1 agonism. I can't find any other disso with such a profile.
Thinking about 3-Me. But apparently, there is still no study about the binding profile, or at least I can't find any.
Holy shit. I am also desperately summoning the user that have the awesome blog and posted things about his research regarding arylcyclohexylamine SARS (which I can't remember his username rn lmao)
So I'm restarting the gym again today for the first time since they closed from covid in March 2019. I've decided it's probably wise to not jump straight back into what I was doing previously to avoid injury from imbalances I've almost certainly picked up in the past year and a half. My plan is to have the first 2 weeks be a bit more general, 2 muscle groups per work out, about 8-12 sets on each so I can get an idea of weights etc. My main question is for this period would I be better served using agonist approach (back&biceps, chest&triceps etc) or antagonist approach (biceps&chest, triceps&back). I'm anticipating quite a bit of DOMS which is making me lean towards an agonist approach but conversely I may not get a good idea of initial weight numbers for each muscle group without doing an antagonist approach. Any input is greatly appreciated
Can someone please help to compare and contrast partial and inverse agonist using the two-state model and how either one can be used to treat disease that is caused by excessive receptor activation of the [named] receptor by an endogenous full agonist .
I have an understanding of what a partial and inverse agonist are with their affinity, efficacy, Emax etc, but is there anything else I am missing and how do either one treat a disease.
Thank you
