Depersonalization Support Forum banner
1 - 16 of 16 Posts

·
Registered
Joined
·
161 Posts
Discussion Starter · #1 ·
I may have put this on the wrong section. I am not contributing research but rather asking a question. I apologize to the moderators if this is the wrong category lol.

I've read a post that virtually every case of DPDR has the exact same neurological underpinning. I wonder, how could this be true if some treatments work for some people while others don't? Perhaps I am looking at this too simplistically. Perhaps just because their is a homologous neurological representation of the disorder doesn't explain that the brain will respond to treatments the same way. I don't know.

I am aware that there are no approved medications for treating DPDR. However, I have read countless cases where SSRI's, opiate antagonists, and other pharmaceuticals have drastically improved or even cured the DPDR itself.

I'm inquiring if anyone knows if there is any scientific knowledge on how medication- specifically SSRI's, can treat some cases of DPDR where in other cases it doesn't do anything.
 

·
Registered
Joined
·
436 Posts
I may have put this on the wrong section. I am not contributing research but rather asking a question. I apologize to the moderators if this is the wrong category lol.

I've read a post that virtually every case of DPDR has the exact same neurological underpinning. I wonder, how could this be true if some treatments work for some people while others don't? Perhaps I am looking at this too simplistically. Perhaps just because their is a homologous neurological representation of the disorder doesn't explain that the brain will respond to treatments the same way. I don't know.

I am aware that there are no approved medications for treating DPDR. However, I have read countless cases where SSRI's, opiate antagonists, and other pharmaceuticals have drastically improved or even cured the DPDR itself.

I'm inquiring if anyone knows if there is any scientific knowledge on how medication- specifically SSRI's, can treat some cases of DPDR where in other cases it doesn't do anything.
i think its about the underlying issue and whats causing the dpdr. for example if someone takes a ssri and his dp improves, then (one of) the cause(s) should be depression.

and for those i think who dont benefit from meds, these are the dpdr cases in its primariest form.
 

·
Registered
Joined
·
161 Posts
Discussion Starter · #3 ·
i think its about the underlying issue and whats causing the dpdr. for example if someone takes a ssri and his dp improves, then (one of) the cause(s) should be depression.

and for those i think who dont benefit from meds, these are the dpdr cases in its primariest form.
Right. That definitely makes sense. I guess that would be more or less classified as secondary DP then.
 

·
Registered
Joined
·
294 Posts
I would like to add that anti-depressants can indeed treat depression but are used for many other things as well. My first psychiatrist gave me some SSRI although I told her I did not think I had depression, and she told me the term "anti-depressant" is quite misleading, as they are very efficient to treat anxiety as well, and are prescribed for this purpose too. Anti-depressants are used to treat general anxiety, social anxiety, PTSD, panic disorder as well as non DPDR related disorders like OCD, eating disorders, fibromyalgia, neuropathic pain, some symptoms of narcolepsy and there are indications they can help reducing pain in the case of rhumatoid arthritis.

 

·
Registered
Joined
·
759 Posts
I would like to add that anti-depressants can indeed treat depression but are used for many other things as well. My first psychiatrist gave me some SSRI although I told her I did not think I had depression, and she told me the term "anti-depressant" is quite misleading, as they are very efficient to treat anxiety as well, and are prescribed for this purpose too. Anti-depressants are used to treat general anxiety, social anxiety, PTSD, panic disorder as well as non DPDR related disorders like OCD, eating disorders, fibromyalgia, neuropathic pain, some symptoms of narcolepsy and there are indications they can help reducing pain in the case of rhumatoid arthritis.

I suppose we could interpret these findings in one of two primary ways:

Either serotonin, not water, is the true giver of life;

Or the active ingredient in anti-depressants is the placebo phenomenon.
 

·
Registered
Joined
·
436 Posts
I suppose we could interpret these findings in one of two primary ways:

Either serotonin, not water, is the true giver of life;

Or the active ingredient in anti-depressants is the placebo phenomenon.
xd
 

·
Registered
Joined
·
294 Posts
I suppose we could interpret these findings in one of two primary ways:

Either serotonin, not water, is the true giver of life;

Or the active ingredient in anti-depressants is the placebo phenomenon.
Different medication are used to treat many different symptoms. This is just typical. It's not like there is one precise medicine for each problem and that's all. The body is a very complex machine, and one molecule can play many different roles in the body or in the brain and if you affect this molecule you might have an effect on all of these different functions. And this is why there are side-effects. Take the anti-histamine class of medication for example, among the different effects they have are: blocking some information about balance coming from the ear, they can cause drowsyness and they can prevent allergies. In different antihistamine medication these different effects are more or less prevalent, so anti-histamines that best block those information from the ear are used to prevent motion sickness, but they also cause drowsiness, so very similar medication are used as sleeping pills and so on. Depending what you use them for, you will consider one of these effects the primary effect and the other ones side-effects. Those side effects are not necessarily bad things depending what you need.
This is normal, it always works like that. Take anticholinergics, like scopolamine that is present in the plant datura or belladona. Anticholinergics bloc the activity of acethylcholine, which is a neurotransmitter that has many functions in the body and in the brain. Some people take scopolamine as a recreational drug because it causes hallucinations at high doses (to my understanding it's not really a funny drug though). But there are many side effects like increased heart rate, dilated pupils, which means blurred vision, dry throat, decrease in gastrointestinal secretions and motility (causes constipation), loss of balance... So scopolamine is used for different things: it's applied as droplets in the eyes to dilate pupils for eye examination or surgery, it is also used for motion sickness because of its effect on balance (active principle of the motion sickness pill called dramamine, that some people also take at high doses to have similar effects as datura), it is used to prevent complications from bowel obstruction, make breathing easier for end of life patients who can't swallow or cough well (makes the breathing tract drier), it is also used as an antidote against the effect of some mushrooms, for example, who increase the activity of acethylcholine. So in no way it means it is a miracle medicine, it just means it has many different effects at the same time, that can be considered primary effects or side effects just depending on the reason why you take that medication. It's the same for really a lot of medicines, SSRIs included.
 

·
Registered
Joined
·
436 Posts
Different medication are used to treat many different symptoms. This is just typical. It's not like there is one precise medicine for each problem and that's all. The body is a very complex machine, and one molecule can play many different roles in the body or in the brain and if you affect this molecule you might have an effect on all of these different functions. And this is why there are side-effects. Take the anti-histamine class of medication for example, among the different effects they have are: blocking some information about balance coming from the ear, they can cause drowsyness and they can prevent allergies. In different antihistamine medication these different effects are more or less prevalent, so anti-histamines that best block those information from the ear are used to prevent motion sickness, but they also cause drowsiness, so very similar medication are used as sleeping pills and so on. Depending what you use them for, you will consider one of these effects the primary effect and the other ones side-effects. Those side effects are not necessarily bad things depending what you need.
This is normal, it always works like that. Take anticholinergics, like scopolamine that is present in the plant datura or belladona. Anticholinergics bloc the activity of acethylcholine, which is a neurotransmitter that has many functions in the body and in the brain. Some people take scopolamine as a recreational drug because it causes hallucinations at high doses (to my understanding it's not really a funny drug though). But there are many side effects like increased heart rate, dilated pupils, which means blurred vision, dry throat, decrease in gastrointestinal secretions and motility (causes constipation), loss of balance... So scopolamine is used for different things: it's applied as droplets in the eyes to dilate pupils for eye examination or surgery, it is also used for motion sickness because of its effect on balance (active principle of the motion sickness pill called dramamine, that some people also take at high doses to have similar effects as datura), it is used to prevent complications from bowel obstruction, make breathing easier for end of life patients who can't swallow or cough well (makes the breathing tract drier), it is also used as an antidote against the effect of some mushrooms, for example, who increase the activity of acethylcholine. So in no way it means it is a miracle medicine, it just means it has many different effects at the same time, that can be considered primary effects or side effects just depending on the reason why you take that medication. It's the same for really a lot of medicines, SSRIs included.
no the body is not a machine and we human aint as well. scientifical obsessions and wanting evidence for everything could be the root of your dpdr
 
  • Like
Reactions: Aridity

·
Registered
Joined
·
759 Posts
Different medication are used to treat many different symptoms. This is just typical. It's not like there is one precise medicine for each problem and that's all. The body is a very complex machine, and one molecule can play many different roles in the body or in the brain and if you affect this molecule you might have an effect on all of these different functions. And this is why there are side-effects. Take the anti-histamine class of medication for example, among the different effects they have are: blocking some information about balance coming from the ear, they can cause drowsyness and they can prevent allergies. In different antihistamine medication these different effects are more or less prevalent, so anti-histamines that best block those information from the ear are used to prevent motion sickness, but they also cause drowsiness, so very similar medication are used as sleeping pills and so on. Depending what you use them for, you will consider one of these effects the primary effect and the other ones side-effects. Those side effects are not necessarily bad things depending what you need.
This is normal, it always works like that. Take anticholinergics, like scopolamine that is present in the plant datura or belladona. Anticholinergics bloc the activity of acethylcholine, which is a neurotransmitter that has many functions in the body and in the brain. Some people take scopolamine as a recreational drug because it causes hallucinations at high doses (to my understanding it's not really a funny drug though). But there are many side effects like increased heart rate, dilated pupils, which means blurred vision, dry throat, decrease in gastrointestinal secretions and motility (causes constipation), loss of balance... So scopolamine is used for different things: it's applied as droplets in the eyes to dilate pupils for eye examination or surgery, it is also used for motion sickness because of its effect on balance (active principle of the motion sickness pill called dramamine, that some people also take at high doses to have similar effects as datura), it is used to prevent complications from bowel obstruction, make breathing easier for end of life patients who can't swallow or cough well (makes the breathing tract drier), it is also used as an antidote against the effect of some mushrooms, for example, who increase the activity of acethylcholine. So in no way it means it is a miracle medicine, it just means it has many different effects at the same time, that can be considered primary effects or side effects just depending on the reason why you take that medication. It's the same for really a lot of medicines, SSRIs included.
no the body is not a machine and we human aint as well. scientifical obsessions and wanting evidence for everything could be the root of your dpdr
I might have to disagree with both of you on this one, lol.

With respect to what you said, leminaseri, while it is true that the human body is not literally a machine, i think that the metaphor is a rather apt one. The human body, consisting of a materialist structure, is best understood as operating via mechanistic principles, similar to a machine. I also don’t know much about Trith’s story, but I doubt their DPDR is caused or fueled by their interest in science and medicine (sorry about the impersonal pronouns, Trith, I don’t know your gender).

However, the human mind, in my view, is not like a machine, and its functions and operations are best understood according to a different set of principles than those governing the material stuff of the universe. Sure, the mind is contingent on the body, and therefore changes in the body can (and usually do) have an impact on how we perceive our experience. But it’s been rather clear to me that our “minds” work, not according to positive scientific mechanistic principles, but by semantic and teleological ones.

I’m perfectly aware that most drugs have a variety of different effects, which means they are often repackaged and marketed in different ways. The drug Trazodone, for instance, was originally an antidepressant, but because of its extremely soporific effects, it’s mostly used nowadays as a sleep aid (I use it rarely for that purpose when I really really need it). I’m also aware that antidepressants are not just placebos; they do have active ingredients. And it’s certainly possible that their active ingredients work more or less directly on some of those conditions that were mentioned in your earlier post.

But I’ve noticed that many doctors and even scientific researchers don’t seem to understand the difference between signs and symptoms; I often hear them use those terms interchangeably or inappropriately (such as when they talk about the “signs and symptoms” of mental illnesses; there are no signs of mental illness, and most of the time the “symptoms” they mention are metaphorical symptoms). Signs are objective observations about the structure of the body: a rash, for example. Symptoms are complaints a person makes about how his body feels (and metaphorical symptoms are complaints a person makes about his—or someone else’s—existence). Signs are an aspect of body, whereas symptoms are an aspect of mind. Placebos don’t have a significant impact on the body, but they can work wonders for the mind. And all those issues you mentioned that anti-depressants can help improve are either behaviors, thoughts, feelings, or sensations.

Antidepressants have a notoriously difficult time beating out placebos in clinical trials. Why? Because you can’t invent a drug that will directly change a person’s experience of hopelessness, worthlessness, guilt, or suicide, or make him start acting better. Which isn’t to say that antidepressants don’t play an indirect role in improving those issues (or making them worse) via some of its active properties for many people. How might that work?

I’ve spent a lot of time talking to different people about their experiences with antidepressants, many good, many bad. When it comes to those people who claim ADs made them worse, we all know what their main complaint is, right? That drug made them feel kind of numb and like a zombie. Sure, they might no longer be sulking and moping all over the place, and the heaviness of the depression is less strong, but they also experience less of the emotional experience of life; it all just feels kind of blah (you know, sort of what DPDR can feel like!). But when it comes to those who swear by ADs and claim they saved their lives, when I try to push through the hyperbolic adulation and ask them specifically how they felt differently on ADs, they often say things like “well, the heaviness lifted, I started slowly getting back into life, taking care of myself, even going back to work and socializing. I mean, it kind of felt like it wasn’t really me doing all these things, but whatever, I’m just glad to be out living my life again.” Do you think we are talking about two different effects of ADs—one therapeutic and the other toxic? Or do you think perhaps we are talking about the same or a very similar effect interpreted differently?

The issue I have with psychiatric research is that it is primarily based on working backwards from the fact that the drugs can be effective, and then trying to explain the effectiveness by reference to what the drug does in the body. This is why every modern person “knows” that serotonin imbalances play an important role in depression. But 30 to 40 years ago everybody “knew” that depression was caused by both serotonin and norepinephrine, because the drugs that were common at that time were the SNRIs, the serotonin and norepinephrine reuptake inhibitors. And around 50 years ago, depression was believed to be the result of 3 chemicals: serotonin, norepinephrine, and dopamine, because depression responded to the monoamine-based pharmacological treatments. It would seem as though overtime we’ve narrowed the source of depression to a single chemical. But I think the better explanation for the change in our knowledge probably has something to do with the fact that altering only one chemical in the brain has a lesser side-effect profile and fewer long-term complications than when you chronically mess with 3 chemicals at once.

There is little to no direct empirical evidence that serotonin in the brain is even linked to depressive phenomenology. Direct studies comparing diagnosed depressed people to those not so diagnosed have found either no link whatsoever, or some studies have found a link, but it is a very weak one and also highly variable.
 

·
Registered
Joined
·
294 Posts
I might have to disagree with both of you on this one, lol.

With respect to what you said, leminaseri, while it is true that the human body is not literally a machine, i think that the metaphor is a rather apt one. The human body, consisting of a materialist structure, is best understood as operating via mechanistic principles, similar to a machine. I also don’t know much about Trith’s story, but I doubt their DPDR is caused or fueled by their interest in science and medicine (sorry about the impersonal pronouns, Trith, I don’t know your gender).

However, the human mind, in my view, is not like a machine, and its functions and operations are best understood according to a different set of principles than those governing the material stuff of the universe. Sure, the mind is contingent on the body, and therefore changes in the body can (and usually do) have an impact on how we perceive our experience. But it’s been rather clear to me that our “minds” work, not according to positive scientific mechanistic principles, but by semantic and teleological ones.

I’m perfectly aware that most drugs have a variety of different effects, which means they are often repackaged and marketed in different ways. The drug Trazodone, for instance, was originally an antidepressant, but because of its extremely soporific effects, it’s mostly used nowadays as a sleep aid (I use it rarely for that purpose when I really really need it). I’m also aware that antidepressants are not just placebos; they do have active ingredients. And it’s certainly possible that their active ingredients work more or less directly on some of those conditions that were mentioned in your earlier post.

But I’ve noticed that many doctors and even scientific researchers don’t seem to understand the difference between signs and symptoms; I often hear them use those terms interchangeably or inappropriately (such as when they talk about the “signs and symptoms” of mental illnesses; there are no signs of mental illness, and most of the time the “symptoms” they mention are metaphorical symptoms). Signs are objective observations about the structure of the body: a rash, for example. Symptoms are complaints a person makes about how his body feels (and metaphorical symptoms are complaints a person makes about his—or someone else’s—existence). Signs are an aspect of body, whereas symptoms are an aspect of mind. Placebos don’t have a significant impact on the body, but they can work wonders for the mind. And all those issues you mentioned that anti-depressants can help improve are either behaviors, thoughts, feelings, or sensations.

Antidepressants have a notoriously difficult time beating out placebos in clinical trials. Why? Because you can’t invent a drug that will directly change a person’s experience of hopelessness, worthlessness, guilt, or suicide, or make him start acting better. Which isn’t to say that antidepressants don’t play an indirect role in improving those issues (or making them worse) via some of its active properties for many people. How might that work?

I’ve spent a lot of time talking to different people about their experiences with antidepressants, many good, many bad. When it comes to those people who claim ADs made them worse, we all know what their main complaint is, right? That drug made them feel kind of numb and like a zombie. Sure, they might no longer be sulking and moping all over the place, and the heaviness of the depression is less strong, but they also experience less of the emotional experience of life; it all just feels kind of blah (you know, sort of what DPDR can feel like!). But when it comes to those who swear by ADs and claim they saved their lives, when I try to push through the hyperbolic adulation and ask them specifically how they felt differently on ADs, they often say things like “well, the heaviness lifted, I started slowly getting back into life, taking care of myself, even going back to work and socializing. I mean, it kind of felt like it wasn’t really me doing all these things, but whatever, I’m just glad to be out living my life again.” Do you think we are talking about two different effects of ADs—one therapeutic and the other toxic? Or do you think perhaps we are talking about the same or a very similar effect interpreted differently?

The issue I have with psychiatric research is that it is primarily based on working backwards from the fact that the drugs can be effective, and then trying to explain the effectiveness by reference to what the drug does in the body. This is why every modern person “knows” that serotonin imbalances play an important role in depression. But 30 to 40 years ago everybody “knew” that depression was caused by both serotonin and norepinephrine, because the drugs that were common at that time were the SNRIs, the serotonin and norepinephrine reuptake inhibitors. And around 50 years ago, depression was believed to be the result of 3 chemicals: serotonin, norepinephrine, and dopamine, because depression responded to the monoamine-based pharmacological treatments. It would seem as though overtime we’ve narrowed the source of depression to a single chemical. But I think the better explanation for the change in our knowledge probably has something to do with the fact that altering only one chemical in the brain has a lesser side-effect profile and fewer long-term complications than when you chronically mess with 3 chemicals at once.

There is little to no direct empirical evidence that serotonin in the brain is even linked to depressive phenomenology. Direct studies comparing diagnosed depressed people to those not so diagnosed have found either no link whatsoever, or some studies have found a link, but it is a very weak one and also highly variable.
If you know that different drugs can have different purposes then you understand why I said what I said in my previous comment. Leminaseri said that if someone's conditions improves thanks to anti-depressants then it must mean that the problem was caused by depression. So I explained that SSRI's are not only used to treat depression, and that in general many medication have many different effects and can be used for different purposes other than treating one disease (depression in the case of SSRI's). So I was listing the many different pruposes as an example of that. I am saying this because you replied with a sarcastic comment implying that I was praising SSRI's for being a miracle cure to every disease, which really wasn't what I wanted to say with that list. And now we switched to a different topic, which is if they are efficient / if they make sense / why doctors prescribe them. First I hope you understand now the point of that comment I made. If you do, then I have no problem switching to a different topic now.
(and i am a man, thanks for asking!)
 

·
Registered
Joined
·
759 Posts
If you know that different drugs can have different purposes then you understand why I said what I said in my previous comment. Leminaseri said that if someone's conditions improves thanks to anti-depressants then it must mean that the problem was caused by depression. So I explained that SSRI's are not only used to treat depression, and that in general many medication have many different effects and can be used for different purposes other than treating one disease (depression in the case of SSRI's). So I was listing the many different pruposes as an example of that. I am saying this because you replied with a sarcastic comment implying that I was praising SSRI's for being a miracle cure to every disease, which really wasn't what I wanted to say with that list. And now we switched to a different topic, which is if they are efficient / if they make sense / why doctors prescribe them. First I hope you understand now the point of that comment I made. If you do, then I have no problem switching to a different topic now.
(and i am a man, thanks for asking!)
I do understand the point you were trying to make in response to leminaseri’s claim that if antidepressants help a person’s condition then that problem must have been caused by their depression. The point I was trying to make in my “sarcastic” response (which I would argue wasn’t so much sarcastic as it was rhetorical) was that I disagreed with both of you and to offer an alternative hypothesis for how anti-depressants work not only for depression but also for the other conditions you mentioned. I did not mean to imply that you were claiming that anti-depressants were a “miracle cure”—I did see the link you made to the Wikipedia page where you got that information—so I apologize if it came across that way.

That said, having read the entire Wikipedia article on ADs lends support to the claims I was making, I think, especially the part where the writer (surprisingly) acknowledged all the significant problems with clinical trials of ADs, but even with those biases, they still struggle to exceed placebos. But if you don’t mind, I’d like to talk a little bit about what I consider to be the fundamental absurdity about the placebo-controlled trial, and especially how we talk about the placebo.

Because I always hear that if a drug cannot demonstrate itself to be more effective than a placebo, then that means the drug does not work. If I have a problem, whether it be a bad headache, or feeling depressed, or I lack confidence to ask someone on a date, and I take a drug—whether it has an active ingredient or it’s just a sugar pill—and as a direct consequence of that action I experience significant improvement in my problem, that means that that intervention…worked!!!

Here in the United States we allow pharmaceutical companies to advertise directly to the consumer because we are absolute morons on many things. And one commercial advertises for a drug called Rexulti. Rexulti is being marketed as a sort of antidepressant booster, so they are claiming that if you are taking one AD and it’s helping, but you are not as happy as you would like to be, then adding Rexulti to your regimen might help you to become super duper happy!!! And they state in the commercial that clinical trials have shown Rexulti users to experience 62% greater reduction in “depression symptoms” over that of a placebo. Sounds impressive, right? But I would like to ask the manufacturer’s of Rexulti: where did they get that number from? Because 62% is a very specific number, so what were they measuring? Did they watch the participants closely over the course of the trial to calculate how much of their day they spent socializing and engaging in other meaningful activities? Did they count the number of times people smiled or laughed, or how often they were using positive vs negative expressions? Or did they,—as I suspect is probably the case—rely on self-reports and, if so, what does that 62% statistic refer to? Are they saying that 62% more Rexulti users than placebo claimed to experience significant benefits? Or did they actually ask each participant to assign a percentage value to their symptoms of depression? So one person might have said “I experienced a 47% reduction in my feelings of hopelessness.” And other said “well you’re lucky, I only experienced an 11% reduction in my feelings of hopelessness.” And a third said “hehe, sucks to be you guys, because I experienced a whopping 94% reduction in my feelings of hopelessness!” And then when they combined all these results, it was 62% more reduction for the Rexulti group?

Modern man is so idiotically positivistic in his thinking that we believe that if we can just assign a number to any phenomenon—including our own thoughts, feelings, sensations and beliefs—and we can get many other people to do the same, then we can input all those numbers into a computer program and, what comes out the other side of that program? Objective scientific data!

I have a riddle for you: one participant in a clinical trial for an AD at the start of the trial rates his depression as 9/10, and at the end he rates it as 4/10. The second participant rates his at the start as an 8/10, and at the end he rates it as a 5/10. Which of those two participants was more depressed at the beginning of the trial? Which was more depressed at the end of the trial? And which received the greater benefit from the trial? The answer, my friend, is blowing in the wind…the answer is blowing in the wind.

How do I know if an intervention works for me? If after doing it I feel better in the way I was hoping to feel better. I think it would be less objectionable if pharma companies just sold active placebos as treatment for these conditions, rather than trying to make a drug that does bad shit to the body beat out a placebo in a rigged trial so that they can claim that the drug “works.”
 

·
Registered
Joined
·
294 Posts
I do understand the point you were trying to make in response to leminaseri’s claim that if antidepressants help a person’s condition then that problem must have been caused by their depression. The point I was trying to make in my “sarcastic” response (which I would argue wasn’t so much sarcastic as it was rhetorical) was that I disagreed with both of you and to offer an alternative hypothesis for how anti-depressants work not only for depression but also for the other conditions you mentioned. I did not mean to imply that you were claiming that anti-depressants were a “miracle cure”—I did see the link you made to the Wikipedia page where you got that information—so I apologize if it came across that way.

That said, having read the entire Wikipedia article on ADs lends support to the claims I was making, I think, especially the part where the writer (surprisingly) acknowledged all the significant problems with clinical trials of ADs, but even with those biases, they still struggle to exceed placebos. But if you don’t mind, I’d like to talk a little bit about what I consider to be the fundamental absurdity about the placebo-controlled trial, and especially how we talk about the placebo.

Because I always hear that if a drug cannot demonstrate itself to be more effective than a placebo, then that means the drug does not work. If I have a problem, whether it be a bad headache, or feeling depressed, or I lack confidence to ask someone on a date, and I take a drug—whether it has an active ingredient or it’s just a sugar pill—and as a direct consequence of that action I experience significant improvement in my problem, that means that that intervention…worked!!!

Here in the United States we allow pharmaceutical companies to advertise directly to the consumer because we are absolute morons on many things. And one commercial advertises for a drug called Rexulti. Rexulti is being marketed as a sort of antidepressant booster, so they are claiming that if you are taking one AD and it’s helping, but you are not as happy as you would like to be, then adding Rexulti to your regimen might help you to become super duper happy!!! And they state in the commercial that clinical trials have shown Rexulti users to experience 62% greater reduction in “depression symptoms” over that of a placebo. Sounds impressive, right? But I would like to ask the manufacturer’s of Rexulti: where did they get that number from? Because 62% is a very specific number, so what were they measuring? Did they watch the participants closely over the course of the trial to calculate how much of their day they spent socializing and engaging in other meaningful activities? Did they count the number of times people smiled or laughed, or how often they were using positive vs negative expressions? Or did they,—as I suspect is probably the case—rely on self-reports and, if so, what does that 62% statistic refer to? Are they saying that 62% more Rexulti users than placebo claimed to experience significant benefits? Or did they actually ask each participant to assign a percentage value to their symptoms of depression? So one person might have said “I experienced a 47% reduction in my feelings of hopelessness.” And other said “well you’re lucky, I only experienced an 11% reduction in my feelings of hopelessness.” And a third said “hehe, sucks to be you guys, because I experienced a whopping 94% reduction in my feelings of hopelessness!” And then when they combined all these results, it was 62% more reduction for the Rexulti group?

Modern man is so idiotically positivistic in his thinking that we believe that if we can just assign a number to any phenomenon—including our own thoughts, feelings, sensations and beliefs—and we can get many other people to do the same, then we can input all those numbers into a computer program and, what comes out the other side of that program? Objective scientific data!

I have a riddle for you: one participant in a clinical trial for an AD at the start of the trial rates his depression as 9/10, and at the end he rates it as 4/10. The second participant rates his at the start as an 8/10, and at the end he rates it as a 5/10. Which of those two participants was more depressed at the beginning of the trial? Which was more depressed at the end of the trial? And which received the greater benefit from the trial? The answer, my friend, is blowing in the wind…the answer is blowing in the wind.

How do I know if an intervention works for me? If after doing it I feel better in the way I was hoping to feel better. I think it would be less objectionable if pharma companies just sold active placebos as treatment for these conditions, rather than trying to make a drug that does bad shit to the body beat out a placebo in a rigged trial so that they can claim that the drug “works.”
Thanks for taking the time to reply.
First thing, I don't trust pharmaceutical companies that much and I trust advertisement even less. There is a common trick that can be played with this "62% greater reduction", which is that technically a reduction that is very small can still be much greater than another small reduction. For example if the placebo gives a reduction of 1% in symptoms, and Rexultin gives a reduction of 1.62% in symptoms, then technically 1.62 is 62% times greater than 1, but at no point there is a reduction of more than 62% of the symptoms, and phrasing it this way can be very misleading. (When people say "I don't like math because it is useless in life", well there is a good counter example for them, if they don't want to get tricked by bad advertisement). I can't find the scientific paper I saw before, but I could not find the 62% number in it. The reduction was more than 1% but it was definitely not 62%, I do think that they have played that trick.
Second, I personally don't see any problem in using numbers or self-reporting but I can explain why. In all the articles I have seen they did not simply ask people to rate their depression from 1 to 100. Typically they use standardized tests, with many questions covering the possible symptoms. The answers themselves are typically based on self-report, but having a standardized test helps to know what you are measuring. Otherwise people could also have important bias if they don't have an extensive knowledge of which of their symptoms are caused by depression and which are not, they would rate themselves differently based on what they think is depression and what it isn't.
Then, people can have resistance using numbers to evaluate a feeling, because they are unique, and feelings are complex and you cannot summarize a complex feeling with an integer between 1 and 10. That being said, one also cannot evaluate the efficacy of a drug by just evaluating one person's complex feeling and describing it before and after, because people are vastly different and we need a lot more statistics and also compare people between each other, or between those who did take the pill and those who had a placebo. So the study needs to be done over many people. And when we increase the number of people we gain some more information but we need to lose some other information. This is just how statistics work. If you want to know the distribution of the heights of people in a population, you need to plot a histogram, which means that people between 173 and 174 cm might be grouped in the same class. So one person isn't 173.3 anymore, they are now "a person between 173 and 174". So you lose information about each person's accurately measured height, but now you can plot a histogram and study its shape, for example. But if you don't regroup people in classes, you just have a long list of values and the information is unintelligible because you can't have the big picture. So to get global information, some individual information must be lost. But it makes less sense to do this in therapy. In therapy the complex nature of the feelings is important, and their intensity can be evaluated using more complex words. So for me these are two very different things. We don't speak in numbers to our therapists.
Another resistance people have is that besides simplification using numbers feels impersonal. But in order to do some statistics one has to use numbers. And the result would be exactly the same if we used simple words like "excellent", "good", "ok", "bad", or "terrible" or if we matched each of these words with a number 1, 2, 3, 4 or 5. The point is not to feel understood by a therapist here, but just to have something that can be compared.
Then of course it makes no sense to say that one experiences 52% of reduction in symptoms. I don't see any way one could evaluate their symptoms so accurately. It also makes no sense to say that "if you take this drug you will experience 52% reduction in symptoms". But that level of accuracy becomes important when we look at larger numbers and it starts to make sense, not as an individual evaluation but as an average. For example it is always weird the first time we hear that the average number of children is something like 2.45. Because no one has 0.45 children. But that level of accuracy becomes important when we want to see if the average number of children is increasing or decreasing with time, or if one country has a significantly different number from another country. Replacing 2.45 with simply 2, on the grounds that 0.45 children don't exist would be a very hard simplification, and this time that simplification would not help to get a bigger picture, contrary to the previous example. Information would simply be lost for nothing.
The, about the placebo effect itself, yes, the placebo is a true effect and I agree that many people even forget that a placebo effect doesn't mean no effect at all. But I think it is fair to force pharmaceutical companies to be honest about what they sell and to not sell any crap on the grounds that it works anyway thanks to placebo. What is nice that the placebo effect has been shown to happen even if the person knows that they have taken a placebo, provided they have been explained what the placebo effect was. So no need to lie to people, like the homeopathy industry does with stories about memory of water, or dynamisation... The other thing is that contextual effects are not just about the pill, but about the relationship with the doctor, the environment, the attitude of the patient towards therapy, many things that the pharmaceutical industry doesn't control when you buy the actual pill.
And then, about self-reporting, I agree, the way people will report on their symptoms depends on people. One person could give one symptom a 3 and another one a 4 depending on their past experiences. But it still works if the data is averaged over a large number of people, so that the amount of over-rating people and under-rating people converges towards something that is representative of the population, so that if someone does the same study again they don't happen to have mostly over-rating people in their study just by chance. And the other thing is exactly the point of using a control group. It doesn't matter if there are ~40% over-rating people in one group of people as long as there is approximately the same amount of over-rating people in the control group. If the results are skewed towards one direction in the test group, then they will be skewed in the same direction in the control group and it will not mess up with the conclusions of the study. If the only difference between the two groups is the presence or absence of the active molecule, then this is the parameter that will be evaluated.
And it is interesting to note that sometimes self-reporting is considered by people as something very unreliable, and sometimes it is considered as the holy grail of evaluations. Some people would say "I don't care what such study says about that, because this is what I (or someone I know) experienced". But as you say, in the end the subjective experience of going better matters. In hospital, pain can be self-reported by patients to check for the efficacy of pain killers and this is what matters for them. When we want a drug to work, we do want that it changes our subjective experience (but sometimes not only).
 

·
Registered
Joined
·
294 Posts
Oh and about the fact that they have a hard time having showing an efficacy greater than a placebo is explained in different ways, and it doesn't mean that they had cheated on their results before and now they cheat less. One possible explanation is that when depression was evaluated before, patients with mostly severe depression were selected, whereas now people who suffer too but to a lesser extent are also taken into account in studies, and it could be that different medication work mostly on severe depression and not so much on milder depression. To my understanding that's just a possible explanation.
 

·
Registered
Joined
·
759 Posts
Thanks for taking the time to reply.
First thing, I don't trust pharmaceutical companies that much and I trust advertisement even less. There is a common trick that can be played with this "62% greater reduction", which is that technically a reduction that is very small can still be much greater than another small reduction. For example if the placebo gives a reduction of 1% in symptoms, and Rexultin gives a reduction of 1.62% in symptoms, then technically 1.62 is 62% times greater than 1, but at no point there is a reduction of more than 62% of the symptoms, and phrasing it this way can be very misleading. (When people say "I don't like math because it is useless in life", well there is a good counter example for them, if they don't want to get tricked by bad advertisement). I can't find the scientific paper I saw before, but I could not find the 62% number in it. The reduction was more than 1% but it was definitely not 62%, I do think that they have played that trick.
Second, I personally don't see any problem in using numbers or self-reporting but I can explain why. In all the articles I have seen they did not simply ask people to rate their depression from 1 to 100. Typically they use standardized tests, with many questions covering the possible symptoms. The answers themselves are typically based on self-report, but having a standardized test helps to know what you are measuring. Otherwise people could also have important bias if they don't have an extensive knowledge of which of their symptoms are caused by depression and which are not, they would rate themselves differently based on what they think is depression and what it isn't.
Then, people can have resistance using numbers to evaluate a feeling, because they are unique, and feelings are complex and you cannot summarize a complex feeling with an integer between 1 and 10. That being said, one also cannot evaluate the efficacy of a drug by just evaluating one person's complex feeling and describing it before and after, because people are vastly different and we need a lot more statistics and also compare people between each other, or between those who did take the pill and those who had a placebo. So the study needs to be done over many people. And when we increase the number of people we gain some more information but we need to lose some other information. This is just how statistics work. If you want to know the distribution of the heights of people in a population, you need to plot a histogram, which means that people between 173 and 174 cm might be grouped in the same class. So one person isn't 173.3 anymore, they are now "a person between 173 and 174". So you lose information about each person's accurately measured height, but now you can plot a histogram and study its shape, for example. But if you don't regroup people in classes, you just have a long list of values and the information is unintelligible because you can't have the big picture. So to get global information, some individual information must be lost. But it makes less sense to do this in therapy. In therapy the complex nature of the feelings is important, and their intensity can be evaluated using more complex words. So for me these are two very different things. We don't speak in numbers to our therapists.
Another resistance people have is that besides simplification using numbers feels impersonal. But in order to do some statistics one has to use numbers. And the result would be exactly the same if we used simple words like "excellent", "good", "ok", "bad", or "terrible" or if we matched each of these words with a number 1, 2, 3, 4 or 5. The point is not to feel understood by a therapist here, but just to have something that can be compared.
Then of course it makes no sense to say that one experiences 52% of reduction in symptoms. I don't see any way one could evaluate their symptoms so accurately. It also makes no sense to say that "if you take this drug you will experience 52% reduction in symptoms". But that level of accuracy becomes important when we look at larger numbers and it starts to make sense, not as an individual evaluation but as an average. For example it is always weird the first time we hear that the average number of children is something like 2.45. Because no one has 0.45 children. But that level of accuracy becomes important when we want to see if the average number of children is increasing or decreasing with time, or if one country has a significantly different number from another country. Replacing 2.45 with simply 2, on the grounds that 0.45 children don't exist would be a very hard simplification, and this time that simplification would not help to get a bigger picture, contrary to the previous example. Information would simply be lost for nothing.
The, about the placebo effect itself, yes, the placebo is a true effect and I agree that many people even forget that a placebo effect doesn't mean no effect at all. But I think it is fair to force pharmaceutical companies to be honest about what they sell and to not sell any crap on the grounds that it works anyway thanks to placebo. What is nice that the placebo effect has been shown to happen even if the person knows that they have taken a placebo, provided they have been explained what the placebo effect was. So no need to lie to people, like the homeopathy industry does with stories about memory of water, or dynamisation... The other thing is that contextual effects are not just about the pill, but about the relationship with the doctor, the environment, the attitude of the patient towards therapy, many things that the pharmaceutical industry doesn't control when you buy the actual pill.
And then, about self-reporting, I agree, the way people will report on their symptoms depends on people. One person could give one symptom a 3 and another one a 4 depending on their past experiences. But it still works if the data is averaged over a large number of people, so that the amount of over-rating people and under-rating people converges towards something that is representative of the population, so that if someone does the same study again they don't happen to have mostly over-rating people in their study just by chance. And the other thing is exactly the point of using a control group. It doesn't matter if there are ~40% over-rating people in one group of people as long as there is approximately the same amount of over-rating people in the control group. If the results are skewed towards one direction in the test group, then they will be skewed in the same direction in the control group and it will not mess up with the conclusions of the study. If the only difference between the two groups is the presence or absence of the active molecule, then this is the parameter that will be evaluated.
And it is interesting to note that sometimes self-reporting is considered by people as something very unreliable, and sometimes it is considered as the holy grail of evaluations. Some people would say "I don't care what such study says about that, because this is what I (or someone I know) experienced". But as you say, in the end the subjective experience of going better matters. In hospital, pain can be self-reported by patients to check for the efficacy of pain killers and this is what matters for them. When we want a drug to work, we do want that it changes our subjective experience (but sometimes not only).
I’m sorry, Trith. I realize you took a lot of time and effort to write this response, but when I read it, I’m reminded of medieval theologians who explained the complex methodology they used to calculate the number of angels in heaven. The fact that something can be quantified or understood “scientifically” does not mean that is the best way to understand it. Your post was very impressive and it said a lot, but at the same time, in my view, it said nothing at all.
 

·
Registered
Joined
·
294 Posts
I’m sorry, Trith. I realize you took a lot of time and effort to write this response, but when I read it, I’m reminded of medieval theologians who explained the complex methodology they used to calculate the number of angels in heaven. The fact that something can be quantified or understood “scientifically” does not mean that is the best way to understand it. Your post was very impressive and it said a lot, but at the same time, in my view, it said nothing at all.
Haha! No problem. In my opinion it all depends on what you want to study. Here the point is not to understand anything, just to find out to the best of our ability if a molecule does have an effect or not. In order to understand something, like why people have depression or why such medication has or doesn't have an effect we need other methods.
But the point of the scientific method is only to verify things to a reasonable extent. It just means "to verify" and discuss the best way to do it, which is what we all do when we want to find If something is true. If there is a certain bias that is possible, we want to find a way to limit it so that the result is not just caused by that bias. Biases are often not easy to understand, and so are the methods that are used to go around them. So for a lot of people these methods might seem detached from reality, obscure and dogmatic and people prefer simplicity. I don't know about you but in my experience that's what a lot of people mean when they say there are other ways than science. But inherently, science is just about verifying. But for me complexity isn't a problem unless complexity is unnecessary. If I asked an architect to build a house it wouldn't be wise to tell him that his math is too complex so I can probably do a better job without using maths.
But what other way are you thinking about that would work better than using that method, using a placebo control? Is it really the method that you disagree with or is it just that you distrust the people who did the study? Because the two are different.
 

·
Registered
Joined
·
759 Posts
Haha! No problem. In my opinion it all depends on what you want to study. Here the point is not to understand anything, just to find out to the best of our ability if a molecule does have an effect or not. In order to understand something, like why people have depression or why such medication has or doesn't have an effect we need other methods.
But the point of the scientific method is only to verify things to a reasonable extent. It just means "to verify" and discuss the best way to do it, which is what we all do when we want to find If something is true. If there is a certain bias that is possible, we want to find a way to limit it so that the result is not just caused by that bias. Biases are often not easy to understand, and so are the methods that are used to go around them. So for a lot of people these methods might seem detached from reality, obscure and dogmatic and people prefer simplicity. I don't know about you but in my experience that's what a lot of people mean when they say there are other ways than science. But inherently, science is just about verifying. But for me complexity isn't a problem unless complexity is unnecessary. If I asked an architect to build a house it wouldn't be wise to tell him that his math is too complex so I can probably do a better job without using maths.
But what other way are you thinking about that would work better than using that method, using a placebo control? Is it really the method that you disagree with or is it just that you distrust the people who did the study? Because the two are different.
Excellent questions, and I appreciate you bringing them up. You’ve probably noticed in a lot of my posts I often express a strong skepticism about science. But it isn’t so much the biases and personal judgments of scientists that I have a problem with (though I do believe that we too often fail to acknowledge them), and it’s certainly not a fear of complex math and statistics that frustrates me (math used to be my favorite academic subject growing up, and I was pretty good at it too). It’s also not the scientific method per se that I take issue with. My biggest complaint about modern man is that we have adopted the proposition that science equals truth, and so we tend to either only accept scientific knowledge, or at least we elevate those knowledges that are scientific above all other forms of understanding.

Because science is not only about observation, experimentation, and performing complex mathematical calculations, it is also a language, that is, a form of discourse. Scientists, like the rest of us, interpret their observations through the medium of language, and I’ve noticed that scientists seem to be either unaware or minimize the significance of the role that language plays in their work. The discourse of science is what philosophers often refer to as “positivism.” Science understands all manner of things in terms of materialist entities, mechanistic forces, cause-and-effect deterministic relationships. This manner of talking about things appears to be the best way to understand much of the natural world, e.g., the structure and motion of the planets. But it is my belief that our attempts to understand humans and their behavior through that discourse has been an utter disaster: epistemologically, morally, and spiritually.

So the issue that I take with the placebo-controlled trial has nothing to do with the fact that the math is too complicated for my poor brain to handle, even though it is. But einstein’s equations on relativity are also over my head, but I do accept that that is a valid and meaningful way to describe and understand his observations. My issue with psychiatry has to do with how we are constructing these problems, like depression. If we construct depression as a disease “just like diabetes,” then we will talk about its manifestations in terms of “signs and symptoms,” it’s etiology in terms of “pathogenesis,” and whatever makes it go away as “treatment. But that is not the best way to understand depression, in my view. Depression is the label that we attach to the affective experience we have as the result of a loss or lacking of something of value to us. Yes, that experience is often accompanied by uncomfortable sensations, changes in perception, appetite or sleep changes, but that’s just because depression, like all our mood states, is simultaneously a thought-and-feeling. All any medication can do directly for that experience is either numb a person to the “feeling” aspect, or just damage them so they are simply unaware of what they were even depressed about in the first place.

This is how I understand human beings to work. We have our structures, which are determined through a combination of our genetics and environmental factors. That structure then determines how we experience ourselves at a very basic level. Then, we use language, whether it be a primitive language like infants and toddlers and other animals use, or whether it be a complex highly symbolic language like those of modern adult humans, to interpret our experiences of ourselves and the world around us. Finally, we act in the world in pursuit of whatever valuable or meaningful goals we might have. The concept of “physical illness” deals with those first two domains, whereas the concept of “mental illnees” deals with the latter two. But when we fail to understand this, and we try to understand language and behavior in terms of materialist structures, we end up with less than ideal results, and often we just make problems worse.

This is the central issue I’ve been grappling with from my own experience, and I know many on this site ask themselves the same question: is my experience DPDR the consequence of some organic problem that then influences my thinking to become more abstract, anxious, and existential? Or am I engaging in abstract, anxious, existential rumination which is creating this wall between me and the external world around me? With modern science’s insistence of a monistic view of man, I feel frustrated that I’m unlikely ever to get a coherent answer to that question.

I see a huge problem with the way our society looks at science. Here in the US now with the issue of abortion on everyone’s mind, I’ve often heard people claim that “abortion is murder; science proves it.” Other people have argued that science proves the opposite. But science has not and cannot “prove” either position, because murder is not a scientific concept, it is a moral and legal concept. Whether or not abortion is murder is not a question for scientists to answer, we use a different kind of discourse to make those determinations.

In response to our conflict with Critical Race Theory being a model for public education, I’ve heard many people say “well, if CRT is not truth, then why hasn’t science disproved it?” Umm…because CRT is not science, it is a completely different epistemological system that interprets and understands it’s subject matter very differently than science does. Whether or not it is a good system that we wish to use in public education is a different question (which I’m not going to get into here), but the answer depends not on what science says about it, but it depends on what goals we want to try to achieve with our education system.

When modern people are asked “what is beauty,” the most common response I get is that “beauty is symmetry.” Why is beauty symmetry? Because symmetry is the only aspect of what we generally consider to be beautiful for which science has come up with an answer. And while I think science’s explanation is moderately convincing, I strongly disagree that “beauty is symmetry.” Many people find asymmetry to be beautiful, especially in people. Because people with asymmetrical features stand out from the rest of the cookie-cutter crowd, they might be viewed very arresting, interesting, special, and therefore beautiful. Beauty is not a part of the discourse of science either, it is a question of aesthetics.

In summary, the way that I come to knowledge and understanding is not based on the latest scientific study, or what scientists have to say. My understand depends on whichever explanation can consistently, accurately, and meaningfully serve as a representation of empirical reality, or whatever it’s subject matter happens to be, and also whichever one works the best when we use it. Often, that is positivist science. But much of the time it is not. If there needs to be a lot of complex math involved in order to demonstrate that some drug “works” better than a placebo, then I assume that drug is probably mostly a placebo. When it comes to pain management, marijuana can be very helpful in reducing a person’s experience of pain. But I didn’t need any placebo-controlled study to know that. I know that marijuana is a dissociative, somewhat distancing him from his experience of his own body, thereby resulting in a reduction in pain. But because we are uncomfortable with making people high for medicine, we have tried to extract the “high producing” properties from the “pain reducing” properties in developing CBD oil and the like. But I find all that to be rather silly. Marijuana relieves pain mostly because it makes a person high.
 
1 - 16 of 16 Posts
Top