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The existence of God and the efficacy of prayer

This is the mentality of big pharma. You only have to look at the horrendous damage done by drugs that were on the market and withdrawn that should NEVER have been on the market to begin with. Talk to someone whose mother had been prescribed thalidomide by a doctor as a mild sleeping pill safe even for pregnant women. Around 10 thousands babies worldwide were born with malformed limbs, some were born with no arms or legs or no functional limbs.

The drug was approved and marketed in 1956 and the damage seen within a year but it was not removed from the market until 1962, i.e., another 6 YEARS! But hey gee, they had to test it to make sure that the deformities they saw were caused by the drug. Otherwise they might be accused of confirmation bias, not to mention lost sales while they could get them.

Thalidomide was a case of not knowing what we didn't know. We believed that nothing could pass the placental barrier - clinical trials didn't even consider the effect on the fetus, because we didn't know it was even remotely possible for things ingested by the mother to pass through that barrier. In retrospect, it seems obvious... but prior to that we genuinely didn't know it was something we needed to watch out for.

Identifying thalidomide as the problem, and getting it removed from the market, was further complicated by the chorality of the molecule. I don't recall which is which, so I'll just say that left-handed thalidomide was benign while right-handed thalidomide was highly dangerous. Making it even more complex was the fact that it was only dangerous to fetuses during a very short window of time. There was about a week period where if the mother ingested thalidomide, it would affect development of ears; during another short period it affected limbs, etc. So there was an increase in birth defects, but they weren't all of the same kind, and the exposure was over a surprisingly small window of time, and it was only certain molecular configurations. All of that adds up to make it somewhat difficult to identify what the cause is. All in all, thalidomide was on the market for a relatively short period of time - with a few exceptions, countries pulled it as soon as there was clear evidence linking it to the defects.


ETA: I've probably got some specifics in there a bit off. I'm working from memory, and I'm being lazy. I believe the gist of it is substantially true though.
 
To make sure we're on the same page, here's a list of some of the mutations just in ELM4-ALK lung cancer. ALK lung cancers are only ~5% of adenacarcinoma lung cancers, so we're talking about a subset of a subset of lung cancers only.

https://www.mycancergenome.org/content/disease/lung-cancer/alk/

And at the link, figure 1 lists them.

Are you saying that we should find it strange that all people with EML4-ALK-E14;A20(v7), who account for a tiny percent of all people with cancer, all have the same EML4-ALK-E14;A20(v7) genetic signature? Maybe you could explain why, because I don't find it particularly strange.

Speaking of natural selection, these cancers are treated with targeted drugs, and they mutate in response. Someone who is EML4-ALK-E14;A20(v7) might mutate to any of the other ALKs, or even out of ALK entirely and into EGFR, for example. A rebiopsy after a year or more of treatment will show.

Personally, I think it's obvious you're in way over your head, and rather than being skeptical of cancer research because you understand it so well, you're skeptical because you don't understand it, and don't even realize what you don't know, but might be able to fool vulnerability people by slinging around enough sciency sounding lingo. That's what concerns me.

The link you gave only verifies what I said.
Different cancers have similar genetic alterations, i.e., genetic signatures. So people with lung cancer of the different subtypes all have very similar genetic signatures depending on the subtype.

From the link you gave:
"Lung cancer is comprised of two main histologic subtypes: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Over the past decade, it has become evident that subsets of NSCLC can be further defined at the molecular level by recurrent 'driver' mutations that occur in multiple oncogenes, including AKT1, ALK, BRAF, EGFR, HER2, KRAS, MEK1, MET, NRAS, PIK3CA, RET, and ROS1 "

"Never smokers with adenocarcinoma have the highest incidence of EGFR, HER2, ALK, RET, and ROS1 mutations."


From Wikipedia: "....tumours arise from a single mutated cell, accumulating additional mutations as it progresses. These changes give rise to additional subpopulations...." https://en.wikipedia.org/wiki/Tumour_heterogeneity

Mutations arise spontaneously and are random and only after they arise does natural selection come into the picture.

The drugs are supposed to cause spontaneous, random mutations FIRST and only then does natural selection take place. So how do you figure that a random process can lead to similar and predictable results in a large number of people? We are not talking about a few people. Millions worldwide get lung cancer for instance and they all involve random mutations yet they end up with genetic alterations that are similar enough to be called genetic signatures. I think you don't understand what it's about.
 
I am defending a system for obtaining reliable information by eliminating well known sources of error

The truth is that double blinding was introduced to get rid of an ESP problem. In single blinded trials those on the dummy drug NEVER got well only those on the real drug got well. Doctors knew that whatever they give a patient there is ALWAYS a placebo effect . So why didn't those taking the blank get well. The answer is that all the patients were able to perceive what the doctors knew, i.e., what drug they were getting. So they double blinded them to get rid of this problem. And they did because now the placebo effect is seen in BOTH those getting the dummy and the real drug.

As far as cognitive errors are concerned you want to have a look at Ben Goldacre's work. He has made a name for himself exposing the purposeful cognitive bias. To put it in his words half the trial go missing in action. That is they publish what they like in their prestigious medical journals and trash what they don't like. Sometimes even the controlling authorities, let alone the doctors, have a problem trying to get the information.


I have made it clear that I am not dismissing your claims out of hand, but that there is a minimum standard of evidence that must be met before they can be seriously considered. It is the same standard that all such claims must meet, whatever their origin. Get back to me when you have met it.

My work will NEVER get funding because it would crunch the cancer industry. But I don't need their cognitive bias anyway. I am thinking maybe I will write a book, with a title something like "a turning word for cancer". Anyone who is humane and who has cancer would get well if they read it!:D
 
The truth is that double blinding was introduced to get rid of an ESP problem. In single blinded trials those on the dummy drug NEVER got well only those on the real drug got well. Doctors knew that whatever they give a patient there is ALWAYS a placebo effect . So why didn't those taking the blank get well. The answer is that all the patients were able to perceive what the doctors knew, i.e., what drug they were getting. So they double blinded them to get rid of this problem. And they did because now the placebo effect is seen in BOTH those getting the dummy and the real drug.
The placebo effect is indeed seen in both groups, which is why it is necessary to eliminate it (and other sources of error) with a double blind trial, so that any actual effect of the medicine can be identified.

ETA: Just to clarify that the double blinding is to eliminate both the patients' bias and the doctors'. See experimenter effect. Nothing to do with ESP.

As far as cognitive errors are concerned you want to have a look at Ben Goldacre's work.
I have been reading Ben Goldacre's work since he started writing his Guardian column, many many years ago. If you think it offers any support for your bizarre claims and misunderstandings you could not be more wrong.

He has made a name for himself exposing the purposeful cognitive bias. To put it in his words half the trial go missing in action. That is they publish what they like in their prestigious medical journals and trash what they don't like. Sometimes even the controlling authorities, let alone the doctors, have a problem trying to get the information.
He has indeed drawn attention to the deficiencies in many clinical trials and their reporting. If you think that means he would agree to your bizarre misunderstanding of the reason for double blinding, or almost anything else you've claimed, you are, once again, completely wrong.

My work will NEVER get funding because it would crunch the cancer industry. But I don't need their cognitive bias anyway. I am thinking maybe I will write a book, with a title something like "a turning word for cancer". Anyone who is humane and who has cancer would get well if they read it!:D
I'm sure you could make money out of your quackery, many quacks do. To get it taken seriously by real doctors (like Ben Goldacre) you would need to provide objective evidence, something you clearly have no intention of doing.
 
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No discussion of genetic mutations in lung cancer? I'd think that someone who laughs at scientific research on cancer, could explain why the genetic signatures of cancer are wrong.

I went to see one of the upper tier oncologists specializing in ALK+ and EGFR cancers yesterday, and after we talked a bit, he said, "Are you a scientist?" I laughed and said, "no, I'm a historian. But I read the latest papers on ALK."

So I do think an amateur can become knowledgeable, especially if their knowledge is limited to a small field. (I don't know a thing about EGFR, for example, let alone smoker/asbestos/chemical lung cancers, let alone all the others.) To go beyond and prove the research wrong requires even more knowledge, far more than I have.

Most people have heard of the Dunning-Kruger effect, which "occurs where people fail to adequately assess their level of competence — or specifically, their incompetence — at a task and thus consider themselves much more competent than everyone else. This lack of awareness is attributed to their lower level of competence robbing them of the ability to critically analyse their performance, leading to a significant overestimate of themselves."

I would think that someone, either professional or amateur, who was only a year away from overturning or seriously revising our understanding of oncology and the theory of evolution, would have no problem discussing current oncology papers, that they would soon prove wrong. Unless there was some Dunning-Kruger effect going on, and they skipped right to "consider[ing] themselves much more competent than everyone else," without developing the "ability to critically analyse their performance."

Ouch.

Especially the last two paragraphs.
 
Double blinding was only introduced to try to eliminate placebo but instead it made thing worse. And it is really only relevant to drug trials. It is no some standard to be used in all experiments.

This is false. It is used ubiquitously in drug trials, it might be a requirement in drug trials. But double-blind is also used in tons of other research - any time there is a risk of implicit bias, double-blind is used. It gets used quite a bit in psychological and sociological research, IIRC.

Terminology:

Testable Condition - the characteristic of a specimen that is of interest, and to which a change is expected to occur

Treatment - the action being taken that is expected to cause a change in the specimen

Test Group - the set of specimens with the testable condition
Control Group - the set of specimens who are otherwise believed to be identical to the Test Group, but who lack the testable condition
Test/Control grouping is used to isolate the effect of the treatment on the testable condition. The difference in the change due to the treatment is measured for the Test Group relative to the Control Group. This identifies whether any observed changes in the Test Group are caused by the treatment, or whether there is a chance that they are caused by some other externality

Blind Study - a study in which the specimens do not know whether they are receiving the treatment or not. This is used very frequently whenever the specimens in a study are human - any time there is a risk that knowledge of the treatment may affect the behavior of the specimen.

Double Blind Study - a study in which neither the specimens nor the administrators know whether the specimen is receiving the treatment or not. This is used whenever there is a risk that knowledge of the treatment may affect the behavior of the administrator as well as the specimen.

Here's an example of a study that doesn't involved drugs, but which would benefit from being double blind. This is, of course, invented out of whole cloth. It is intended to illustrate the principles that go in to experiment design, while taking it out of the context of drug trials.

Let's say we have invented a small, hand-held device that emits a small bit of a pheromone compound. The compound can't be smelled by humans or cats, only by dogs. We want to test whether the device can be used to alleviate separation anxiety in dogs.

We start by finding a set of dogs that have the Testable Condition (separation anxiety), as defined by some known destructive behaviors. We then go find a set of dogs that is very similar in terms of breed, age, weight, owner family composition, diet, etc. (anything we can think of that we believe might possibly introduce bias into our results)... but they do NOT have the testable condition. These two groups then will be our Test Group and our Control Group.

The structure of the study is as follows:

Dogs will be paired with their owners, in a room. They'll spend two days living in the room together. At the end of those two days, the owners will begin leaving the rooms for varying lengths of time. Immediately prior to leaving, the owner will press a button on the device releasing the pheromone into the air - this is the Treatment. The behaviors of the dogs will be observed, and we will also take blood samples to test the concentration of specific stress hormones.

Now... there's some concern that the motions of the human could alter the behavior of the dog. If one set of human sis observed to push a button on a device, where another set of humans just leave, the dogs being exposed to the treatment run some risk of developing a classically conditioned response, which we want to avoid. To remove this risk, we'll make the study Blind. We create false devices that still have the button, but which emit a burst of plain air with no pheromone in it. This mitigates the risk of a conditioned reaction to a set of motions, and lets us isolate the impact of the pheromone alone. In application, we'll give half of the Control Group real pheromones, and half of the Test Group just plain air.

But dogs are observant. We're worried that if the owner knows that they're working with the fake, they'll end up giving some subtle indication by body language or facial expression to their dogs. Vice versa of course - if the owners know it's the real thing, they might give indication to the dog as well. Either of those introduces a new factor into the experiment, and we want to avoid that. So we make the study Double Blind. We don't tell the owners whether it's the real pheromone or just a puff of air. Before each owner was given their device, the serial number was taken down. Back in the office, where there's no risk of exposure, is a list of all the serial numbers identifying which contain the pheromone and which do not.

At the end of the experiment, we should be able to compare the qualitative differences in observed behavior as well as the quantitative differences in stress hormone concentration between the Test Group and the Control Group. We compare the behaviors and hormones of the Test and Control groups that got the actual pheromone to the behaviors and hormones of the group that got plain air. To determine that the device works as expected, we need to be able to show a few things. For simplicity, let's assign some letters:

A - Control Group that were given the false treatment
B - Control Group that were given the real treatment
X - Test Group that were given the false treatment
Y - Test Group that were given the real treatment

What we should expect to see is:

That there is no difference in measurements between A and B (the treatment works on the testable condition, not on something else)
That there is a measurable difference between A and X (the testable condition is present and quantifiable)
That there is a measurable difference between X and Y (the treatment produces a measurable effect)

That's how you do solid, rigorous experiment design, in a nutshell. Of course, that whole sample selection process is a *lot* more complicated than I've listed out above, and the care with which the measurements are done is incredibly important. The overall design has to be solid and experts are needed to ensure that there's no bias and no competing factors present. This was a very basic, very simplistic example... but the idea is there.


ETA: Just for clarity, I am an actuary by trade. But I manage my company's Customer Analytics department. We work closely with several market research firms as well as with our internal marketing departments. We regularly design and implement experiment pertaining to shopping behavior, usage behavior, response to calls to action, the impact of a set of experience models on retention, and the effectiveness of various messaging content and creative concepts. My team doesn't do clinical research... but we apply a *lot* of the concepts of experiment design on a regular basis. Among other things ;) So I'm not speaking as an authority, but I am speaking with some degree of experience.
 
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How strange that all people with the same cancers have cancers with the same genetic signatures. :eye-poppi

Okay, I might very well be ignorant of a nuance here... but isn't this tantamount to saying "how strange that all the specimens within the same species have the same genetic signature"? Isn't that genetic signature how we identify them as being the same species to begin with? Likewise, isn't that genetic signature how we identify cancers as being the same type of cancer?

:p Or I could have just said this, which is much more concise and to the point!
Isn't it strange how every mouse on the planet has mouse DNA? I mean... what are the odds?
 
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This is false. It is used ubiquitously in drug trials, it might be a requirement in drug trials. But double-blind is also used in tons of other research - any time there is a risk of implicit bias, double-blind is used. It gets used quite a bit in psychological and sociological research, IIRC.

Terminology:

Testable Condition - the characteristic of a specimen that is of interest, and to which a change is expected to occur

Treatment - the action being taken that is expected to cause a change in the specimen

Test Group - the set of specimens with the testable condition
Control Group - the set of specimens who are otherwise believed to be identical to the Test Group, but who lack the testable condition
Test/Control grouping is used to isolate the effect of the treatment on the testable condition. The difference in the change due to the treatment is measured for the Test Group relative to the Control Group. This identifies whether any observed changes in the Test Group are caused by the treatment, or whether there is a chance that they are caused by some other externality

Blind Study - a study in which the specimens do not know whether they are receiving the treatment or not. This is used very frequently whenever the specimens in a study are human - any time there is a risk that knowledge of the treatment may affect the behavior of the specimen.

Double Blind Study - a study in which neither the specimens nor the administrators know whether the specimen is receiving the treatment or not. This is used whenever there is a risk that knowledge of the treatment may affect the behavior of the administrator as well as the specimen.

Here's an example of a study that doesn't involved drugs, but which would benefit from being double blind. This is, of course, invented out of whole cloth. It is intended to illustrate the principles that go in to experiment design, while taking it out of the context of drug trials.

Let's say we have invented a small, hand-held device that emits a small bit of a pheromone compound. The compound can't be smelled by humans or cats, only by dogs. We want to test whether the device can be used to alleviate separation anxiety in dogs.

We start by finding a set of dogs that have the Testable Condition (separation anxiety), as defined by some known destructive behaviors. We then go find a set of dogs that is very similar in terms of breed, age, weight, owner family composition, diet, etc. (anything we can think of that we believe might possibly introduce bias into our results)... but they do NOT have the testable condition. These two groups then will be our Test Group and our Control Group.

The structure of the study is as follows:

Dogs will be paired with their owners, in a room. They'll spend two days living in the room together. At the end of those two days, the owners will begin leaving the rooms for varying lengths of time. Immediately prior to leaving, the owner will press a button on the device releasing the pheromone into the air - this is the Treatment. The behaviors of the dogs will be observed, and we will also take blood samples to test the concentration of specific stress hormones.

Now... there's some concern that the motions of the human could alter the behavior of the dog. If one set of human sis observed to push a button on a device, where another set of humans just leave, the dogs being exposed to the treatment run some risk of developing a classically conditioned response, which we want to avoid. To remove this risk, we'll make the study Blind. We create false devices that still have the button, but which emit a burst of plain air with no pheromone in it. This mitigates the risk of a conditioned reaction to a set of motions, and lets us isolate the impact of the pheromone alone. In application, we'll give half of the Control Group real pheromones, and half of the Test Group just plain air.

But dogs are observant. We're worried that if the owner knows that they're working with the fake, they'll end up giving some subtle indication by body language or facial expression to their dogs. Vice versa of course - if the owners know it's the real thing, they might give indication to the dog as well. Either of those introduces a new factor into the experiment, and we want to avoid that. So we make the study Double Blind. We don't tell the owners whether it's the real pheromone or just a puff of air. Before each owner was given their device, the serial number was taken down. Back in the office, where there's no risk of exposure, is a list of all the serial numbers identifying which contain the pheromone and which do not.

At the end of the experiment, we should be able to compare the qualitative differences in observed behavior as well as the quantitative differences in stress hormone concentration between the Test Group and the Control Group. We compare the behaviors and hormones of the Test and Control groups that got the actual pheromone to the behaviors and hormones of the group that got plain air. To determine that the device works as expected, we need to be able to show a few things. For simplicity, let's assign some letters:

A - Control Group that were given the false treatment
B - Control Group that were given the real treatment
X - Test Group that were given the false treatment
Y - Test Group that were given the real treatment

What we should expect to see is:

That there is no difference in measurements between A and B (the treatment works on the testable condition, not on something else)
That there is a measurable difference between A and X (the testable condition is present and quantifiable)
That there is a measurable difference between X and Y (the treatment produces a measurable effect)

That's how you do solid, rigorous experiment design, in a nutshell. Of course, that whole sample selection process is a *lot* more complicated than I've listed out above, and the care with which the measurements are done is incredibly important. The overall design has to be solid and experts are needed to ensure that there's no bias and no competing factors present. This was a very basic, very simplistic example... but the idea is there.


ETA: Just for clarity, I am an actuary by trade. But I manage my company's Customer Analytics department. We work closely with several market research firms as well as with our internal marketing departments. We regularly design and implement experiment pertaining to shopping behavior, usage behavior, response to calls to action, the impact of a set of experience models on retention, and the effectiveness of various messaging content and creative concepts. My team doesn't do clinical research... but we apply a *lot* of the concepts of experiment design on a regular basis. Among other things ;) So I'm not speaking as an authority, but I am speaking with some degree of experience.

[Spoilered only for space- excellent post, EC]

Yabbut...ESP! ESP!!!!!!!!!!
 
The drugs are supposed to cause spontaneous, random mutations FIRST and only then does natural selection take place. So how do you figure that a random process can lead to similar and predictable results in a large number of people? We are not talking about a few people. Millions worldwide get lung cancer for instance and they all involve random mutations yet they end up with genetic alterations that are similar enough to be called genetic signatures. I think you don't understand what it's about.

I don't see why it would be strange to find identifiable types of cancer, even if the types eventually number in the thousands, just as there are biological conditions that can be grouped into Parkinson's, ALS, multiple sclerosis, and other types, rather than each person's body breaking down uniquely.

I wonder about your use of the phrase "random process." Do you mean the theory of evolution in its entirety is a random process? That's a common misconception and might lead to a misunderstanding.

From http://evolution.berkeley.edu/evolibrary/article/evo_32

"...natural selection is sometimes interpreted as a random process. This is also a misconception. The genetic variation that occurs in a population because of mutation is random — but selection acts on that variation in a very non-random way: genetic variants that aid survival and reproduction are much more likely to become common than variants that don't. Natural selection is NOT random!"

In this case, of course, a mutation that successfully evades the body's ways of stopping cell growth from getting out of control, becomes a cancer. There are apparently many ways for cells to do that, but not an unlimited number. And in many cases, the similarity is helped by the lungs being damaged the same way, by cigarette smoke in one cohort, or by radon gas in another, or by asbestos in another.

From Wikipedia: "....tumours arise from a single mutated cell, accumulating additional mutations as it progresses. These changes give rise to additional subpopulations...." https://en.wikipedia.org/wiki/Tumour_heterogeneity

Mutations arise spontaneously and are random and only after they arise does natural selection come into the picture.

Yes, I'm sure there are many mutations that appear randomly, start reproducing, and get stopped immediately by the body. We don't care about those. It's the non-random process of natural selection that lets some cell mutations reproduce out of control, that causes cancers which we care about and categorize.

The sentence after the one you quoted explains it: "This heterogeneity may give rise to subclones that possess an evolutionary advantage over the others within the tumour environment..."

Here are some more articles talking about how mutations are a random process, but natural selection, and therefore the theory of evolution as a whole, is not a random process.

https://www.newscientist.com/article/dn13698-evolution-myths-evolution-is-random/

https://www.quora.com/Is-evolution-by-natural-selection-a-random-process

http://www.indiana.edu/~oso/evolution/selection.htm

That last link is rather basic, but begins: "Every time that scientists have examined the process of mutation, seeking to learn if there are recognizable patterns, the answer seems to be that mutation is essentially random... How can an apparently random process result in apparently directed evolution? This question is one of the 'logical' problems that many people have with evolution. It is simply counter-intuitive that a random process can give rise to highly-ordered structures, and to adaptation to specific environment."

I wonder if that's the problem you're having with random mutations producing identifiable types of cancer? It's not a new question, and is often asked by those just starting to understand evolution.
 
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So how do you figure that a random process can lead to similar and predictable results

Even aside from the explanation that Pup gave, we can take it up a level in terms of concept.

Just because a thing is random doesn't mean it can't produce predictable results. There may still be some degree of uncertainty, sure, but the bounds of the outcomes can often be predicted with a high degree of certainty. This is one of the main concepts between Chaos Theory... and also what allows us to predict the weather ;). The movement of the actual air molecules are highly complex and random... but there are factors that exert large effects on those molecules, there are patterns within the randomness that allow us to say the high is expected to be 79F tomorrow, with a 5% chance of rain in the afternoon.


ETA: No, I'm wrong. Not Chaos Theory. Just plain old non-deterministic processes. I overcomplicated myself for no good reason!
 
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We've heard a lot about Big Pharma. Now let's have a few words about Big Quackery.


http://rationalwiki.org/wiki/Big_Placebo

The main difference between Big Pharma and Big Placebo is that Big Pharma is regulated, to make sure its products work and contain the substances on the label, while Big Placebo is free to sell more-or-less whatever it wants, label be damned.

Alternative medicine isn't quite the underdog it's usually made out to be. The revenue of the alternative and traditional medicine industry worldwide is estimated to be $60 billion a year,[3] and the supplement industry was worth $20 billion in 2004 in the U.S. alone.[3] For comparison, Big Pharma is worth about $300 billion a year.[4]

Complementary and Alternative Medicine (CAM) companies could improve their image dramatically by proving that their products are effective. It would also make sure that people using CAM get treatments that are better than placebos. Big Placebo clearly has enough money to test them. But they don't test them. Why? Because it would cost money. CAM companies will never prove the efficacy of their products unless they are required to by regulation, because doing so would require spending money (we can't have that, now can we?) and throwing away many profitable placebos.
 
Heck, and I thought I was being clever, coining a term like Big Placebo. Thankee kindly, Pixel42.

Ay god but the world is a weary place at times.
 
This is one of the most offensive posts I have seen on this site.

If the preferred magic approach by kyrani99 doesn't cure someone, it's their fault because they are a toxic individual.

As far as I can tell, the test for a toxic individual is if they don't get cured by kyrani99's magic approach.

A lovely way to apportion blame. Straight out of the Middle Ages.

NO! The corollary is not true.
If a person is toxic they are not treatable by any method in which they must exercise their own authority because they have none. It is mob rule.

If a person doesn't get well they must be toxic is FALSE.
A person may not get well for many reason but chief reason is because they haven't appreciated that the body is purpose-driven and not a machine.

It is vitally important to realize what the nocebo effect is all about. :thumbsup:
 
Thalidomide was a case of not knowing what we didn't know. We believed that nothing could pass the placental barrier - clinical trials didn't even consider the effect on the fetus, because we didn't know it was even remotely possible for things ingested by the mother to pass through that barrier. In retrospect, it seems obvious... but prior to that we genuinely didn't know it was something we needed to watch out for.

Identifying thalidomide as the problem, and getting it removed from the market, was further complicated by the chorality of the molecule. I don't recall which is which, so I'll just say that left-handed thalidomide was benign while right-handed thalidomide was highly dangerous. Making it even more complex was the fact that it was only dangerous to fetuses during a very short window of time. There was about a week period where if the mother ingested thalidomide, it would affect development of ears; during another short period it affected limbs, etc. So there was an increase in birth defects, but they weren't all of the same kind, and the exposure was over a surprisingly small window of time, and it was only certain molecular configurations. All of that adds up to make it somewhat difficult to identify what the cause is. All in all, thalidomide was on the market for a relatively short period of time - with a few exceptions, countries pulled it as soon as there was clear evidence linking it to the defects.


ETA: I've probably got some specifics in there a bit off. I'm working from memory, and I'm being lazy. I believe the gist of it is substantially true though.

What you have written is true of the science and I think it was an over the counter medication so it was not doctors keeping track. However I still think greed had something to do with it too. They are slow taking harmful drugs off the market in today's world. And there are plenty of drugs still on the market that do more harm than good and most particularly those prescribed by doctors to elderly people.
 
NO! The corollary is not true.
If a person is toxic they are not treatable by any method in which they must exercise their own authority because they have none. It is mob rule.

If a person doesn't get well they must be toxic is FALSE.
A person may not get well for many reason but chief reason is because they haven't appreciated that the body is purpose-driven and not a machine.

It is vitally important to realize what the nocebo effect is all about. :thumbsup:

Still offensively wrong - I hope that nobody ever comes to you for medical advice.

Most people, including me, have lost someone close due to untreatable illnesses. They died because their illness was untreatable at the time, not because of the nocebo effect.
 
Exactly how have you seen this? Which organs in which organisms in which stages of development? Your statement is very broad, can you please be specific?
I was referring to my own organs. :)

From what kind of cancer do you suffer? How was it diagnosed? Did you receive any medical treatment? How do you know you are in remission? How long a remission have you been fortunate enough to benefit from?

I have no cancer, though I would no doubt have cancer stem cells stored in my body. They are immune products, which, like any other immune products are stored in the body.

I was first diagnosed with uterine cancer (1993) and they wanted to remove my uterus within the next few days. I rejected this and left Cairns to go to Sydney for a second opinion. In Sydney I was diagnosed with stage 4 ovarian cancer with metastasis in the uterus, cervix, bowel and both lungs. The doctors threw their hands up in the air and said there is "nothing we can do".

On the trip down to Sydney, which took 5 1/2 weeks I saw many symptoms disappear. For example I was coughing up brownish red phlegm which disappeared by the time I got to Brisbane (2/3 way down). I told my doctors that I believed I was in remission but they did not want to believe it.

I went to a Chinese herbalist who said he could treat me and was confident that the cancer would go away. The cancer did go away by mid 1994 and at the time I did attribute it partly to Chinese herbs but I later realized that while the herbs helped me, the cancer went away because I was in remission when I left Cairns.

In about May 2004 after having become an activist and having seriously upset a lot of people in the toxic sub-culture I was manipulated and then hassled and I did develop esophageal cancer and could no longer swallow solid food. This time I resolved a pressing issue and within a month the cancer was gone. I did not go to any doctors as I knew there were toxic doctors involved and I would not be able to know if the doctor I chose would do me harm and not good.

In November 2004 I was again harassed and this time developed ovarian cancer again. This time I threw caution to the wind and used Vipassana or Insight meditation to investigate what was going on. I allowed the cancer to metastasis to the bowel until it was the size of a golf ball and quite painful if I bent down, especially if sideways and down. I used what I learnt and was able to get my body to move to spontaneously remission. It was gone by end of February 2005.

Between 2006 to 2010 I was hassled many more times and developed various cancers, ovarian, bowel, pancreatic in the islet cells/beta cells, skin and bone (twice). I used these occasion to make further investigations before deliberately moving my body to spontaneous remission.

Then they tried several others which I was able to prevent. These included attempt on my heart, optic nerve, brain, lungs, stomach, esophagus and bone.


By what method did you find the changes in gene expression in these cancer cells? How did you distinguish the cancer cells from non cancerous stem cells? Did you use in situ hybridization, or perhaps PCR and direct sequencing? What kind of cancer cells were these? What kind of stem cells did they become?

None of the above. The method I used in all cases was Vipassana. This is a meditative technique I had mastered many years earlier under instructions from a Burmese Buddhist master. I am not good enough to see at the molecular level very well. I can see some. But I could see the cells and most structures of the cell including inside the nucleus and DNA as a whole.

I found that only particular types of cells in tissues became involved. They divided into two asymmetrical daughter cells. I knew from my university studies that only stem cells do this. They did at times divide symmetrically. I also noticed that a lot of the cells in the vicinity were not like the cancer cells and not like the surrounding cells. I later found, having focused on an area of inflammation that these were immune system cells.

I also followed some cancer cells enter the blood stream and they did not go there alone. They were accompanied by immune system cells and appeared to be able to follow the immune system cells. There was no doubt the immune system was aiding the cancer cells.


Please tell me you did not determine the changes in gene expression and the change from cancer to stem cells by. "insight meditation"! How can insight meditation tell you what is going on at the cellular level? Is this just another way to say you imagined it all?


...by insight meditation?

ABSOLUTELY! :D

how did you identify the new versus the old cells? What sort of cellular tagging protocol did you use?

Before investigating what caused a remission you will need to establish what kind of cancer you had.

I didn't need to identify the new cells, but they were obvious as they were in the place where the cancer had been and there was a lot more cells than should be, ie still a mass of cells but healthy cells. However all one needs to do in a mental prescription is to affirm that the body keep the newer cells in favor of the old during the apoptosis process that clears away the mass. The body does the job.

Of course a person knows what cancer they have. However it is superfluous in deliberately effecting spontaneous remission.
 
The above probably the wins the prize for the most seriously (and dangerously) deluded thing I think I've ever seen anyone write on any forum like this.

If you really believe things like the above then frankly there is no possibility at all of anyone having any kind of reasoned intelligent conversation with you.


postscript - since I wrote the above (as a quick draft a couple of days ago), I notice that Kyrani has persisted with assertions about how sick people can cure themselves simply by having a faith-belief in something (where the "something" seems to be a religious god). Obviously beliefs like that are lethally dangerous. Though they are of course not usual in religions like Christianity and Islam.

In fact such beliefs are really an essential foundation of the faith. Where for example you are persuaded to believe that God is the final arbiter of whatever happens to you - if you get sick and die then that was God's wish (or if you recover and live, then that too was God's wish). Millions of Christians still believe that even today in 2016.

That's an obvious example of why religions become so dangerous. And anyone could give numerous examples of how that same basic belief becomes a lethal danger that pervades absolutely everything from belief in faith healing, to belief in demonic possession and churches that still encourage exorcism, to Popes declaring certain people to be "Saints" claiming that they performed miracles confirmed by science, etc etc. ... all the way up to group's like the Taliban, Isis and Al Qaeda murdering thousands of people all around the world where they actually believe (and insist) that their religious wars are commanded by God in their holy books ... but astonishingly, they do not actually believe their victims are really dead! Instead what they believe as irrefutable god-given fact, is that their victims are all judged by Allah, so that Allah decides whether the victim was rightly killed, in which case he or she is sent to everlasting hell ... or if the murder was a mistake and the victim was innocent, then Allah will grant them a place in paradise instead (apparently vastly better than being alive on Earth) .... the person who just had his head chopped off is not really dead! ... he's just being sent to Allah for final proper religious judgement in the after-life! Are these people religiously dangerous? .... rhetorical question.

You are trying to misrepresent what I have said.
 

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