8 ms·

Peptides are a revolution and you don't need to know how they work to know that they work (for various people for various conditions). There is a tension betwee

Peptides are a revolution and you don't need to know how they work to know that they work (for various people for various conditions). There is a tension between empiricism and fundamentalism with much of medical science focusing on fundamentalism. Now with the ability to collect and search large amounts of empirical data and communicate it peer-to-peer people are picking up on a lot of things that work without knowing why they work. I think people are just going to circumvent the fundamentalist and chase after whatever works. I owe my health to early adoption of experimental peptides, I have life long ME/CFS and there is no known treatment for this nor is there any on the horizon. At least they finally have a diagnostic test and know it's not psychosomatic but I could have told them that from day 1. Most doctors are not researchers and have little understanding on statistics instead preferring to rely on discrete classifications and simple decision tress. As someone with hEDS from TNXB I am a walking bag of symptoms and yet not a single doctor could figure it out. I had to research it myself which involved post-doc level textbooks and research journals. I came across the work done by Prof. Khavinson (USSR) and it did appear to me that peptides were incredibly under-explored. Given the poor quality of life with ME/CFS I was willing to take serious risks so previous trials were helpful to give an idea on dosing and lethality, I went through most of the research peptides one by one. I actually waited on semaglutide a bit because I suspected there was a small minority who would have hyper sensitivity and I both expected that to appear in the data, which it did, and I expected to have hypersensitivity, which I did. Others who were less careful ended up with pretty bad gastroenteritis. Semaglutide has been the most effective and with it and a few others I am largely able to lead a normal life. I was getting gray market from the US but now I get it direct from China.

dev_l1x_be 7mo ago
Have you tried omega3? There were some improvements I was reading about.
- cjbgkagh 7mo ago
  I have tried everything on just about every list of possible treatments, having been in the fortunate position to have made enough money that I can try things full time and being able to bypass doctors for access to medicine and being able to do my own research.
deinonychus 7mo ago
can you talk about how semaglutide improves ME?
- cjbgkagh 7mo ago
  I don’t know the mechanism, I think ME/CFS is an autoimmune condition and semiglutide appears to help with autoimmune conditions in general. That was my reason for trying it. The improvements snuck up on me after many months as I noticed I was having fewer and fewer bad days.
  - bertylicious 7mo ago
    If you felt improvements with semiglutide only after many months, how long did the other trials last? It sounds like you went through hundreds of trials. Did they all went on for many months? When did you determine that a drug wasn't effective and abort the trial? How come you didn't abort the semiglutide trial earlier?
    - cjbgkagh 7mo ago
      Because I started at such low dose 0.025mg and ramped slowly I didn’t expect to see much of an effect until I got to more normal doses so I was unusually patient with it. Additionally extended water fasting (>5 days) was the only thing helping my headaches so I was focusing on ways to emulate this effect without an unmaintainable amount of fasting. I also had uncontrollable weight gain so I figured that was either related, or if not it would still help to lose weight anyway. Most of the stuff I’ve tried that worked usually has an immediate or overnight effect. Notably Low Dose Naltrexone was overnight, Low Dose Abilify was near immediate. I believe this is due to their immunomodulator properties. So I studied psychopharmacology and focused in on finding weaker ligands than typical as a way to try and safely modulate my immune system. I landed on Modafinil in the morning and Amitryptiline at night, both off label treatments for the probably related dysautonomia. The N of 1 with many overlapping signals and medications was of course very noisy but I treated it like a ML optimization problem. I could tell it was likely beneficial within the first week even with the small dose. I probably could have statistically determined it was working within a few months but I was distracted by work so it took a little longer to be sure.
bertylicious 7mo ago
I'm pretty sure there is no diagnostic test for ME/CFS. What are you referring to? Also I don't understand how semaglutide did help you while you're at the same time part of a minority risk group with a hypersensitivity to it. Isn't that a contradiction?
- deng 7mo ago
  https://link.springer.com/article/10.1186/s12967-025-07203-w https://link.springer.com/article/10.1186/s12967-025-07203-w
  - empiricus 7mo ago
    looks interesting, but has the classic "40 patients".
    - throwaway2037 7mo ago
      What would be enough? 400 patients, 4000, 40k, 400k, 4M?
      - igor47 7mo ago
        Well, reading the study, I'm not sure more patients could rescue it from methodological bias. They assumed the premise basically -- we should find a biomarker, which is kind of what this thread is discussing. Then they went trawling for biomarker in a sea of millions of biomarkers. They did this by training an model that produced the desired result, using a grid search for hyper parameters that even further expanded the available degrees of freedom here beyond what they had from the biology. No pre-registration; There are millions of places where the researchers could have made a different decision -- would they still have gotten a publishable result? Oh plus the authors mostly work for the company whose data they use, which is hoping to sell a diagnostic test. I'm giving you a thorough response because I'm detecting a cavalier anti scientism which I think is sadly becoming more common. This stuff is hard; are you sure you understand it enough to have an informed opinion?
  - 7mo ago
Angostura 7mo ago
> you don't need to know how they work to know that they work Welcome to the powerful world of the placebo
- cjbgkagh 7mo ago
  Placebos would work with anything with a plausible story, since I’ve tried many hundreds of things and only a handful worked I’m highly confident that it’s not a placebo. People with ME/CFS are used to trying things and have them not work so the placebo effect where it exists has usually worn off.
dotancohen 7mo ago
> Peptides are a revolution and you don't need to know how they work to know that they work Perhaps. But knowing the mechanism of how they work sure seems fundamental to ensuring that they are safe to use.
- Amezarak 7mo ago
  I agree with this, but we don't have a good understanding of the mechanisms of how most drugs work, and what else they do. That's why, generally speaking, we require actual observational safety data, and not just a thorough description of the mechanism(s) of a drug. And sometimes we find out years or even decades later we were badly wrong. "Safe" is a very qualified term when it comes to drugs. What actually distinguishes $randompeptide from $approveddrug is the safety data - there are papers all about the proposed mechanisms for most of them.
- cjbgkagh 7mo ago
  If a lot of people take the mediation and die is that evidence that the medication is unsafe? If they live is that evidence that the medication is safe? Either both are true or neither is true. The relative weight of evidence is dependent on priors but it is still evidence.
  - dotancohen 7mo ago
    Your comment reads like someone with no experience in medical trials - neither pharmaceutical nor medical devices. Death is not the only negative outcome. Nor is a procedure that is commonly followed by death necessarily a bad procedure - many cancer treatments for example fall into this category.
    - cjbgkagh 7mo ago
      You’re not understanding the point of the hypothetical, it was to illustrate a scenario in that most people would consider evidential and point out that by definition the opposite outcome must also be evidential even if that outcome was far more likely. It’s to highlight an unintuitive aspect of probability formalized as the bayes ratio. The strength of the evidence is dependent on the priors but it exists. Anecdotal evidence is not zero evidence it is weak evidence and with care a lot of anecdotal evidence can be combined to create stronger forms of evidence. Rounding it down to zero or up to one are both incorrect.
blitzar 7mo ago
> chase after whatever works Crack is really moreish.
stalfie 7mo ago
Non blinded self experimentation is not a useful branch of empiricism. I had an ME/CFS patient that had tried 100s of things and documented the effects thoroughly. She had a quite impressive list. Roughly 30% had had an effect to begin with, but the trend she observed was that it lasted for around a month at most. Placebo was her overall conclusion, but she occasionally got relief anyways so we both agreed that there was no harm in continuing. I'm sure several "peptides" is on her list by now. There is nothing new under the sun, and fad cures for diffuse conditions have come and gone many times before. This is especially the case for conditions involving pain or tiredness, which are extremely sensitive to both placebo and nocebo. What would be revolutionary would be 2-3 double blinded RCTs showing a lasting effect. Which would be great if someone did! But you have to actually bother to do it. And personally I would put money on the outcome being "no effect".
- malfist 7mo ago
  > Non blinded self experimentation is not a useful branch of empiricism. Amen to this. The plural of anecdote is not data. People have been hawking snake oil for centuries, and people have been believing snail oil cured them for centuries.
- jmcqk6 7mo ago
  What do you think about the mis-alignment between goals here? For medical research, the goal is to find general practices that will broadly help, and identify risks with the intervention. Even then, with many interventions, it's understood that they will effect people differently. For individuals, they don't care about variation in communities, or standard medical practices, they are looking for relief for their specific condition. Of course, declaring that just because something worked for one person, it should work for others, is wrong in both camps. I feel like a big part of the disconnect here, and a big reason why people are talking past each other, is that they actually have different goals, and aren't really aware of that difference.
  - stalfie 7mo ago
    Well, to be honest I think the primary disconnect is in epistemological understanding. The OP did not declare peptides to be a personal revolution, he/she seemingly generalised their own experience to be widely applicable. Basic human thought patterns usually lead people to think that anecdotes about their personal experience is valuable for understanding the world, but this is wrong. The scientific revolution basically illustrated the flaw in this premise outside of hypothesis generation. It takes specific education to make human beings truly believe that their anecdotal experiences are mostly irrelevant beyond understanding their immediate circumstances. The proportion of humanity that truly think this way is relatively small. Understanding the world through anecdotes still works okay-ish for a lot of areas, but ascertaining relatively subjective effects of experimental pharmaceuticals is not one of them. But to many people it's non obvious that this is the case. And as a general method of thinking about this issue, it is just the wrong way to go about things. And that's the disconnect, in my opinion. The OP drew a conclusion from a thought pattern that comes easily to human beings, but that is just wrong in this situation. Of course, perhaps this is reinforced by underlying motivations, but that's not what makes people talk past each other. These kinds of discussion are usually driven by so called "deep disagreements" in epistemological understanding, in my experience.
beowulfey 7mo ago
Clinical trials are not looking for fundamental mechanisms, they are there to ensure an effect is strong enough to say a product should be sold for that purpose. Otherwise you end up with snake oil salesmen. Because how can you be sure you are even injecting the thing the sellers claim it is? I would encourage everyone interested in peptides to read about the state of medical science before the establishment of the Pure Food and Drug Act of 1906.
- 5o1ecist 7mo ago
  [dead]
ramraj07 7mo ago
Im sorry for your quality of life problems but calling doctors bad at statistics and then giving anecdotal evidence as proof has to start ringing some logical bells right? You dont even have to take our word. Use an LLM as judge. Paste your comment into chatgpt and see what it says.
- ben_w 7mo ago
  > Paste your comment into chatgpt and see what it says. Isn't one of the bigger problems with ChatGPT that it's much too supportive of whatever the human is talking about?
  - alex_duf 7mo ago
    I guess it depends on how you frame it. "I've just posted this comment, what do you think" vs "Someone online has just posted this comment, what do you think". But it does require to know the bias that LLMs have ahead of testing this.
  - ramraj07 7mo ago
    Thats the point. If even such a sycophantic ai disagrees with your points you have a problem
- 5o1ecist 7mo ago
  [dead]
- aeonik 7mo ago
  I didn't read their whole comment, but I worked in the Internal Research department of a medical school. I did their statistical studies and built software for analysis pipelines. Doctors, at least 15 years ago, were definitely bad at statistics. They were not required to take a statistics course at all. Most programs would require Algebra and Calculus as part of their science reqs. Some would maybe take one basic research course, and they would then become obsessed with p values of 0.05. They did not have a basic understanding of how to interpret research unless they were an auto didactic and went out of their way to improve. It's something my director (a doctor and software engineer), and the Dean complained about relentlessly.
deng 7mo ago
> There is a tension between empiricism and fundamentalism with much of medical science focusing on fundamentalism. This is a deeply unfair statement, and also a false dichotomy. Medical science is of course empiric. What you call "fundamentalism" is that compounds need to undergo a rigorous regiment of empiric testing before they are given to potentially millions of people. And no, it's not just because of Thalidomide. Many, many compounds fail clinical trials because of severe side effects, like liver toxicity, severe immune reactions or heart problems. Then there's of course increased risk of cancer, which can take many years to manifest itself empirically. You argue that you prefer living with these uncertainties rather than ME/CFS, and that's of course entirely understandable, but disparaging the field of medical science as focused on "fundamentalism" because we do not give large patient cohorts untested compounds is polemic. I understand where you are coming from, and I'm sorry that you suffer from this terrible condition, but likewise, you should try to understand the other side.
- ndr 7mo ago
  I think the grandparent meant "fundamentalism" as "mechanistic", and lots of things we can know (as you say using the scientific method) to be useful long before we have a good mechanistic explanation of how they work. Some examples: aspirin (willow bark used for thousands of years, drug synthesized in 1897 and mechanism explained almost 100y later), or general anesthesia used again since mid 1800s and the mechanism is quite still debated. This is not to downplay all the long term, or developmental, risks that using something novel can result in. But we can empirically know something about the effects without having good mechanistic models.
  - deng 7mo ago
    But it is usually not necessary for approval of a compound to be able to describe how it works on a molecular or cellular level. What you need to show are three things: efficacy, safety and quality, so basically: the compound has the intended clinical benefit, has an acceptable safety profile and can be produced with a consistent manufacturing quality. Most compounds fail because of lack of efficacy (roughly half), and roughly a third because of lack of acceptable safety.
deleted 7mo ago
[deleted]
allador 7mo ago
That is so dangerous, buying grey market replicas of pharmaceuticals. Unless you have a research lab built out in your house, you have zero way of knowing what it is that you're actually getting. Whether the dosing matches the claimed dose. Whether there are bacterial growth, or other manufacturing chemical left in by bottom-of-the-barrel chinese manufacturer. I understand your risk profile may be different than others, but when you can get the real thing officially, I'm not sure why anyone would risk this.

dev_l1x_be 7mo ago

Have you tried omega3? There were some improvements I was reading about.

cjbgkagh 7mo ago
I have tried everything on just about every list of possible treatments, having been in the fortunate position to have made enough money that I can try things full time and being able to bypass doctors for access to medicine and being able to do my own research.

deinonychus 7mo ago

can you talk about how semaglutide improves ME?

cjbgkagh 7mo ago
I don’t know the mechanism, I think ME/CFS is an autoimmune condition and semiglutide appears to help with autoimmune conditions in general. That was my reason for trying it. The improvements snuck up on me after many months as I noticed I was having fewer and fewer bad days.
- bertylicious 7mo ago
  If you felt improvements with semiglutide only after many months, how long did the other trials last? It sounds like you went through hundreds of trials. Did they all went on for many months? When did you determine that a drug wasn't effective and abort the trial? How come you didn't abort the semiglutide trial earlier?
  - cjbgkagh 7mo ago
    Because I started at such low dose 0.025mg and ramped slowly I didn’t expect to see much of an effect until I got to more normal doses so I was unusually patient with it. Additionally extended water fasting (>5 days) was the only thing helping my headaches so I was focusing on ways to emulate this effect without an unmaintainable amount of fasting. I also had uncontrollable weight gain so I figured that was either related, or if not it would still help to lose weight anyway. Most of the stuff I’ve tried that worked usually has an immediate or overnight effect. Notably Low Dose Naltrexone was overnight, Low Dose Abilify was near immediate. I believe this is due to their immunomodulator properties. So I studied psychopharmacology and focused in on finding weaker ligands than typical as a way to try and safely modulate my immune system. I landed on Modafinil in the morning and Amitryptiline at night, both off label treatments for the probably related dysautonomia. The N of 1 with many overlapping signals and medications was of course very noisy but I treated it like a ML optimization problem. I could tell it was likely beneficial within the first week even with the small dose. I probably could have statistically determined it was working within a few months but I was distracted by work so it took a little longer to be sure.

bertylicious 7mo ago

I'm pretty sure there is no diagnostic test for ME/CFS. What are you referring to? Also I don't understand how semaglutide did help you while you're at the same time part of a minority risk group with a hypersensitivity to it. Isn't that a contradiction?

deng 7mo ago
https://link.springer.com/article/10.1186/s12967-025-07203-w https://link.springer.com/article/10.1186/s12967-025-07203-w
- empiricus 7mo ago
  looks interesting, but has the classic "40 patients".
  - throwaway2037 7mo ago
    What would be enough? 400 patients, 4000, 40k, 400k, 4M?
    - igor47 7mo ago
      Well, reading the study, I'm not sure more patients could rescue it from methodological bias. They assumed the premise basically -- we should find a biomarker, which is kind of what this thread is discussing. Then they went trawling for biomarker in a sea of millions of biomarkers. They did this by training an model that produced the desired result, using a grid search for hyper parameters that even further expanded the available degrees of freedom here beyond what they had from the biology. No pre-registration; There are millions of places where the researchers could have made a different decision -- would they still have gotten a publishable result? Oh plus the authors mostly work for the company whose data they use, which is hoping to sell a diagnostic test. I'm giving you a thorough response because I'm detecting a cavalier anti scientism which I think is sadly becoming more common. This stuff is hard; are you sure you understand it enough to have an informed opinion?
- 7mo ago

Angostura 7mo ago

> you don't need to know how they work to know that they work Welcome to the powerful world of the placebo

cjbgkagh 7mo ago
Placebos would work with anything with a plausible story, since I’ve tried many hundreds of things and only a handful worked I’m highly confident that it’s not a placebo. People with ME/CFS are used to trying things and have them not work so the placebo effect where it exists has usually worn off.

dotancohen 7mo ago

> Peptides are a revolution and you don't need to know how they work to know that they work Perhaps. But knowing the mechanism of how they work sure seems fundamental to ensuring that they are safe to use.

Amezarak 7mo ago
I agree with this, but we don't have a good understanding of the mechanisms of how most drugs work, and what else they do. That's why, generally speaking, we require actual observational safety data, and not just a thorough description of the mechanism(s) of a drug. And sometimes we find out years or even decades later we were badly wrong. "Safe" is a very qualified term when it comes to drugs. What actually distinguishes $randompeptide from $approveddrug is the safety data - there are papers all about the proposed mechanisms for most of them.
cjbgkagh 7mo ago
If a lot of people take the mediation and die is that evidence that the medication is unsafe? If they live is that evidence that the medication is safe? Either both are true or neither is true. The relative weight of evidence is dependent on priors but it is still evidence.
- dotancohen 7mo ago
  Your comment reads like someone with no experience in medical trials - neither pharmaceutical nor medical devices. Death is not the only negative outcome. Nor is a procedure that is commonly followed by death necessarily a bad procedure - many cancer treatments for example fall into this category.
  - cjbgkagh 7mo ago
    You’re not understanding the point of the hypothetical, it was to illustrate a scenario in that most people would consider evidential and point out that by definition the opposite outcome must also be evidential even if that outcome was far more likely. It’s to highlight an unintuitive aspect of probability formalized as the bayes ratio. The strength of the evidence is dependent on the priors but it exists. Anecdotal evidence is not zero evidence it is weak evidence and with care a lot of anecdotal evidence can be combined to create stronger forms of evidence. Rounding it down to zero or up to one are both incorrect.

blitzar 7mo ago

> chase after whatever works Crack is really moreish.

stalfie 7mo ago

Non blinded self experimentation is not a useful branch of empiricism. I had an ME/CFS patient that had tried 100s of things and documented the effects thoroughly. She had a quite impressive list. Roughly 30% had had an effect to begin with, but the trend she observed was that it lasted for around a month at most. Placebo was her overall conclusion, but she occasionally got relief anyways so we both agreed that there was no harm in continuing. I'm sure several "peptides" is on her list by now. There is nothing new under the sun, and fad cures for diffuse conditions have come and gone many times before. This is especially the case for conditions involving pain or tiredness, which are extremely sensitive to both placebo and nocebo. What would be revolutionary would be 2-3 double blinded RCTs showing a lasting effect. Which would be great if someone did! But you have to actually bother to do it. And personally I would put money on the outcome being "no effect".

malfist 7mo ago
> Non blinded self experimentation is not a useful branch of empiricism. Amen to this. The plural of anecdote is not data. People have been hawking snake oil for centuries, and people have been believing snail oil cured them for centuries.
jmcqk6 7mo ago
What do you think about the mis-alignment between goals here? For medical research, the goal is to find general practices that will broadly help, and identify risks with the intervention. Even then, with many interventions, it's understood that they will effect people differently. For individuals, they don't care about variation in communities, or standard medical practices, they are looking for relief for their specific condition. Of course, declaring that just because something worked for one person, it should work for others, is wrong in both camps. I feel like a big part of the disconnect here, and a big reason why people are talking past each other, is that they actually have different goals, and aren't really aware of that difference.
- stalfie 7mo ago
  Well, to be honest I think the primary disconnect is in epistemological understanding. The OP did not declare peptides to be a personal revolution, he/she seemingly generalised their own experience to be widely applicable. Basic human thought patterns usually lead people to think that anecdotes about their personal experience is valuable for understanding the world, but this is wrong. The scientific revolution basically illustrated the flaw in this premise outside of hypothesis generation. It takes specific education to make human beings truly believe that their anecdotal experiences are mostly irrelevant beyond understanding their immediate circumstances. The proportion of humanity that truly think this way is relatively small. Understanding the world through anecdotes still works okay-ish for a lot of areas, but ascertaining relatively subjective effects of experimental pharmaceuticals is not one of them. But to many people it's non obvious that this is the case. And as a general method of thinking about this issue, it is just the wrong way to go about things. And that's the disconnect, in my opinion. The OP drew a conclusion from a thought pattern that comes easily to human beings, but that is just wrong in this situation. Of course, perhaps this is reinforced by underlying motivations, but that's not what makes people talk past each other. These kinds of discussion are usually driven by so called "deep disagreements" in epistemological understanding, in my experience.

beowulfey 7mo ago

Clinical trials are not looking for fundamental mechanisms, they are there to ensure an effect is strong enough to say a product should be sold for that purpose. Otherwise you end up with snake oil salesmen. Because how can you be sure you are even injecting the thing the sellers claim it is? I would encourage everyone interested in peptides to read about the state of medical science before the establishment of the Pure Food and Drug Act of 1906.

5o1ecist 7mo ago
[dead]

ramraj07 7mo ago

Im sorry for your quality of life problems but calling doctors bad at statistics and then giving anecdotal evidence as proof has to start ringing some logical bells right? You dont even have to take our word. Use an LLM as judge. Paste your comment into chatgpt and see what it says.

ben_w 7mo ago
> Paste your comment into chatgpt and see what it says. Isn't one of the bigger problems with ChatGPT that it's much too supportive of whatever the human is talking about?
- alex_duf 7mo ago
  I guess it depends on how you frame it. "I've just posted this comment, what do you think" vs "Someone online has just posted this comment, what do you think". But it does require to know the bias that LLMs have ahead of testing this.
- ramraj07 7mo ago
  Thats the point. If even such a sycophantic ai disagrees with your points you have a problem
5o1ecist 7mo ago
[dead]
aeonik 7mo ago
I didn't read their whole comment, but I worked in the Internal Research department of a medical school. I did their statistical studies and built software for analysis pipelines. Doctors, at least 15 years ago, were definitely bad at statistics. They were not required to take a statistics course at all. Most programs would require Algebra and Calculus as part of their science reqs. Some would maybe take one basic research course, and they would then become obsessed with p values of 0.05. They did not have a basic understanding of how to interpret research unless they were an auto didactic and went out of their way to improve. It's something my director (a doctor and software engineer), and the Dean complained about relentlessly.

deng 7mo ago

> There is a tension between empiricism and fundamentalism with much of medical science focusing on fundamentalism. This is a deeply unfair statement, and also a false dichotomy. Medical science is of course empiric. What you call "fundamentalism" is that compounds need to undergo a rigorous regiment of empiric testing before they are given to potentially millions of people. And no, it's not just because of Thalidomide. Many, many compounds fail clinical trials because of severe side effects, like liver toxicity, severe immune reactions or heart problems. Then there's of course increased risk of cancer, which can take many years to manifest itself empirically. You argue that you prefer living with these uncertainties rather than ME/CFS, and that's of course entirely understandable, but disparaging the field of medical science as focused on "fundamentalism" because we do not give large patient cohorts untested compounds is polemic. I understand where you are coming from, and I'm sorry that you suffer from this terrible condition, but likewise, you should try to understand the other side.

ndr 7mo ago
I think the grandparent meant "fundamentalism" as "mechanistic", and lots of things we can know (as you say using the scientific method) to be useful long before we have a good mechanistic explanation of how they work. Some examples: aspirin (willow bark used for thousands of years, drug synthesized in 1897 and mechanism explained almost 100y later), or general anesthesia used again since mid 1800s and the mechanism is quite still debated. This is not to downplay all the long term, or developmental, risks that using something novel can result in. But we can empirically know something about the effects without having good mechanistic models.
- deng 7mo ago
  But it is usually not necessary for approval of a compound to be able to describe how it works on a molecular or cellular level. What you need to show are three things: efficacy, safety and quality, so basically: the compound has the intended clinical benefit, has an acceptable safety profile and can be produced with a consistent manufacturing quality. Most compounds fail because of lack of efficacy (roughly half), and roughly a third because of lack of acceptable safety.

deleted 7mo ago

[deleted]

allador 7mo ago

That is so dangerous, buying grey market replicas of pharmaceuticals. Unless you have a research lab built out in your house, you have zero way of knowing what it is that you're actually getting. Whether the dosing matches the claimed dose. Whether there are bacterial growth, or other manufacturing chemical left in by bottom-of-the-barrel chinese manufacturer. I understand your risk profile may be different than others, but when you can get the real thing officially, I'm not sure why anyone would risk this.