Thread: So this is my theory

Originally Posted by Dannon Oneironaut

And, did you finish reading the story? I know that it was long, and in my opinion very badly written. The tense kept changing, and whether he was talking about one person or more than one, but I understood his story, but I didn't think that it was very charismatic. But the moral of the story is that IT IS a hallucination. THE MORAL ACCORDING TO TIBETAN BUDDHIST PHILOSOPHY IS THAT IF YOU BELIEVE THAT IT IS A HELPFUL SPIRIT WITH INFINITE WISDOM THAN YOU ARE DELUDED! So you DO buy it?

Yes, people don't understand the Buddhist scriptures are rarely based on fact lol
It is likely that there was no sand to begin with. It's pointless to argue about the specifics of a Buddhist scripture. It's the overall point that counts.

I remember Alan Watts once talked in one of his lectures about how Buddhists rarely even read the scriptures. Most of the time, they have the books on these little stands and they turn them around and it flips through all the pages of the book in a few seconds. And that's what they do with them lol

I think most people from Western Culture don't understand this way of thinking and they look for hidden meanings or some great insight in a story. The only way to really gain Enlightenment is through actual experience. Although I don't doubt that it is possible just through reading books. But not if you're doing it with the intent of becoming enlightened lol.

Anyway....

Originally Posted by O'nus

- Antidepressants, while not always useful, are sometimes more useful than placebo alone

Agreed.

Originally Posted by O'nus

- Chemicals and neurotransmitters do play a part in depression

Maybe. I'll expand later.

Originally Posted by O'nus

- Psychotherapy is the best means to alleviating any mental disorder

Agreed

Originally Posted by O'nus

- It is sometimes a good idea to interplay psychotherapy with drugs in order to maintain coherence in psychotherapy

Agreed.

Originally Posted by O'nus

In addition, I do not think we severely disagree. I think, in essence, we agree but except on the efficacy of drugs.

Yes I believe so.

Originally Posted by O'nus

Also, I wanted to demonstrate that I do have the significant capability to call upon actual scientific resources for you, as you accused me of being an ignorant hypocrite to science.

I trust this post will alleviate your accusations.

Having scientific studies available to you does not a scientist make.

Originally Posted by O'nus

This is not something that needs proving because it is a method of research.

Well that's not what I meant. What I was saying is that you didn't provide evidence of your claims and you said double-blind studies don't need proving. But you didn't provide any studies.
Also, double-blind studies DO need proving. They need to be replicated at least twice to be considered a pretty solid fact. Because you have to take in to account human error and "funding bias".

Originally Posted by O'nus

"Inhibition of serotonergic raphe neurons is mediated by somatodendritic 5-HT1A autoreceptors, which may be increased in depressed patients. We report an association of the C(-1019)G 5-HT1A promoter polymorphism ....

Yes, all this means is that reduced serotonin causes depressed feelings in... rats, I assume?
Assuming it's the same in humans, which is pretty obvious, less serotonin = depressed is a pretty solid fact. That still doesn't mean that clinical depression is caused by less serotonin. I'll quote two of the studies that you referenced right here.

"The neuroanatomical correlates of depression remain unclear. Functional imaging data have associated depression with abnormal patterns of activity in prefrontal cortex (PFC), including the ventromedial (vmPFC) and dorsolateral (dlPFC) sec...."

This points to damage to the brain as a cause of depression.

"Long-term depression (LTD) at the corticostriatal synapse is postsynaptically induced but presynaptically expressed, the depression being a result of retrograde endocannabinoid signaling that activates presynaptic cannabinoid CB1 receptors and reduces the probability of glutamate release. To stud...."

And this points to endocannabinoids playing a role, reducing glutamate release.

Originally Posted by O'nus

Note: The meta-analysis you sourced is dated 2008. Every single source below is dated earlier than your meta-analysis giving significantly more credibility to their relevancy.

Hmmm, that makes absolutely no sense. Why is it more relevant if it was released earlier? Following that logic, the bible is more relevant today than science.

Originally Posted by O'nus

"The authors provided a very informative commentary on publication bias and antidepressant efficacy. They made clear that the modest advantage of drug over placebo in reported clinical trials is reduced when unreported clinical trials are included in data analysis. The robust placebo response, particularly in less severely depressed subjects, deserves emphasis when considering clinical implications. "

Proving my point.

Originally Posted by O'nus

"We evaluated the effects of a selective serotonin reuptake inhibitor, paroxetine, on tr...."

+ Oishi, Naoki, Kanzaki, Sho, ShindenShinden, Seiichi, Saito, Hideyuki, Inoue, Yashurio, Ogawa, Karou. (2010). Effects of selective serotnonin reuptake inhibitor on treating tinnitus in pateints stratified for presence of depression or anxiety. Audiology and Neurotology, 15(30), 187-193.

Not a double blind study.

Originally Posted by O'nus

"Improvements in placebo groups of antidepressant trials account for a major part of the expected drug effects. We aimed to determine overall effect sizes of placebo and drug effects in antidepressant trials, and to analyze whether the placebo effect in antidepressant trials also occurs for patient self-perception, general psychopathology, and quality of life. Methods: Search terms covered different variants of pharmacotherapy for patients with depressive disorders from January 1980 to December 2005 in the databases Medline/Pubmed, PsycINFO and CENTRAL, a.o. We included RCTs with a placebo group and an antidepressant group in people with depression. Results: We computed within group effect sizes for several outcome variables and integrated them using random-effect models. A total of 96 studies were included. Mean effect size in the placebo group for primary outcome variables was d=1.69 (95% CI=1.54–1.84) compared to 2.50 in the drug group (95% CI=2.30–2.69). There was a major difference between placebo effect sizes assessed with observer ratings (d=1.85, 95% CI=1.69–2.01) versus patient self-perception (d=0.67; 95% CI=0.49–0.85). The effect sizes in placebo groups in 2005 were more than twice as great as those in 1980, but only for observer ratings, not for patient self-ratings. The result was partly due to increased homogeneity of samples of recently published trials. Conclusions: The placebo effect accounted for 68% of the effect in the drug groups. Whereas clinical trials need to control the placebo effect, clinical practice should attempt to use its full power. "

I should discuss here what I think may be the problem. People self report depression. I mean you've probably been through it. Alot of people have done it online even. In the past week have you.... bla bla bla fucking bla.

So people who aren't really depressed could be getting treatment and responding greatly due to placebo effect, which would push the efficacy of placebos up in the trials.

Originally Posted by O'nus

This conclusion, from Donovan, et. al. best surmises the stance on antidepressants, "...the importance of continuation treatment following acute response in all 5 anxiety disorders, however the relative efficacy of continuation antidepressant treatment appears to vary by disorder". While it is no debating that placebo effect does play a role in therapy, it is also evident that antidepressants can significantly help, past placebo, in therapy. It is not the fact that antidepressants are never useful and always placebo.Depression, along with other mental disorders, do have a significant biological cause. In this case, somatodendritic 5-HT1A autoreceptors facilitating serontonal neurotransmitters and antagonists are significantly proven to play a role in depression and anxiety.I encourage anyone to find any contrary evidence, but it must be from a scientific journal.

I don't need to find contrary evidence because nothing tells us that it is definitely serotonin that causes depression or, in this studies case, anxiety disorders.
In fact, significant evidence is showing recently, you already posted one so I won't bother again, that anxiety disorders in particular have more to do with damage to the brain than serotonin.

Tommo, I thought you were saying antidepressants never work. I told you my story just to make the point that I personally know they do on some people, not to provide conclusive proof for the Harvard Medical Review or anything. I agree that some people have forms of depression that antidepressants will not work on. Sometimes it is purely psychological and has to be worked out through psychotherapy. After reading your last post, I don't even know what the Hell we were disagreeing on.

lol me neither.
If I said never it was a mistake. I mean hardly ever. Statistically speaking.
In other words, less people are helped by them than people who aren't.

Originally Posted by O'nus

Originally Posted by Spenner

With proper inner peace you can summon the will to control your levels of emotion and anxiety without drugs and whatnot.

There are many times when even meditation cannot be done.

You go ahead and try telling a paranoid schizophrenic to "calm down and relax".

It doesn't work. Also, you go ahead and go to a mental asylum and tell me how many people are making an effort to "control their levels".

I'll tell you that, from my experience, it is rather low.

~

Of course, but nevertheless it still holds true that with proper inner peace one may gain some form of control over their emotions in that meditative state. People with disorders preventing them from having such "peaceful" mentalities are obviously going to have a hard time doing so.

Originally Posted by Spenner

Of course, but nevertheless it still holds true that with proper inner peace one may gain some form of control over their emotions in that meditative state. People with disorders preventing them from having such "peaceful" mentalities are obviously going to have a hard time doing so.

This was the thinking of a group of scientists in the 60's or 70's, I can't remember, who gave LSD to patients with schizophrenia in their insane asylum (that's what they were called then, not being derogatory lol). This helped them to work through things that came up during the trip with the psychiatrists.

Could be a possible route for people who can't even begin to meditate.

Originally Posted by LostKiddo

1) People that are schizofrenic and also other types of "crazy", if u will, people can see stuff and hear stuff that isn't there.

2) This happens through brain "malfunction".

3) Humans are known to use aproximately 9-11 % of their brain, the "crazy" people are known to use a little more.

4) Through training, it would be possible to see/hear/experience things that aren't there, but you would be able to induce the illusion. (Awake)


Statement 4 = True or false ? please comment, i'm curious about the oppinions.

Yes i simplified the whole thing because i'm sure you guys all know what I mean and stuff and i don't need to write an essay for you people to make you understand what i mean and all ...

NO NO NO NO FUCKING NO.
This is an old wives tale. It has been proven otherwise multiple times. Besides, what does the other part do?? Just sit there taking up space?? If so, no matter what part of your brain was taken out, as long as it wasn't that specific 9-11%, they would live. However, this is not the case. I'm bored of proving a point now, so ask me any questions you want.

Originally Posted by tommo

Having scientific studies available to you does not a scientist make.

I was not trying to assert that I am a scientist but that I do acknowledge and utilize science. Mostly, in response to your prejudice comment about psychologists.

I think you're a good debater and have a decent attitude. I would think you've become one of my new favourite persons to debate, except for the fact that you've demonstrated such prejudice.

Well that's not what I meant. What I was saying is that you didn't provide evidence of your claims and you said double-blind studies don't need proving. But you didn't provide any studies.
Also, double-blind studies DO need proving. They need to be replicated at least twice to be considered a pretty solid fact. Because you have to take in to account human error and "funding bias".

You mis-understand - I mean that the method of what double-blind studying is does not need proving in of it self.

It's like asking me to prove that science works by using science. I just meant that double-blind studies, as in the methods they use, do not need proving as to why they work; just justification.

Yes, all this means is that reduced serotonin causes depressed feelings in... rats, I assume?
Assuming it's the same in humans, which is pretty obvious, less serotonin = depressed is a pretty solid fact. That still doesn't mean that clinical depression is caused by less serotonin. I'll quote two of the studies that you referenced right here.

This points to damage to the brain as a cause of depression.

And this points to endocannabinoids playing a role, reducing glutamate release.

The facts do show a significant neurological association for depression. Also, with brain damage, it can cause depression.

Remember that the best ways to find out if something is a neurological function is to create a lesion.

Hmmm, that makes absolutely no sense. Why is it more relevant if it was released earlier? Following that logic, the bible is more relevant today than science.

You mis-understand; I mean that it is earlier to our current date. If you read the dates, you might have understood more. My sources, in response to yours, were all dated from 2009 or 2010. Please pay attention.

Proving my point.

Not a double blind study.

Not all of them had to be double-blind studies.

Also, it was the most current publishing I could find.

I should discuss here what I think may be the problem. People self report depression. I mean you've probably been through it. Alot of people have done it online even. In the past week have you.... bla bla bla fucking bla.

So people who aren't really depressed could be getting treatment and responding greatly due to placebo effect, which would push the efficacy of placebos up in the trials.

This argument could also be used the other way around;

Many people get depression but do not always report it and just let it go.

The truth is that most depression is healed spontaneously on their own, not with therapy. This may also account for the apparent "placebo effect" and what actually is just the naturally self healing.

I don't need to find contrary evidence because nothing tells us that it is definitely serotonin that causes depression or, in this studies case, anxiety disorders.

Of course there is no definitive evidence for it. The fact is that there are different kinds of depression and that neurology significantly plays a role in them.

If you can name one thing that causes all depression, one certain factor, then we would have something unique. The truth is that there are always multiple factors playing into depression. Biology is one of them.

In fact, significant evidence is showing recently, you already posted one so I won't bother again, that anxiety disorders in particular have more to do with damage to the brain than serotonin.

I think you're taking that out of context to argue for your side...? The point was that you can take brain damage victims and observe how their brain damage affects their behaviour. It is like cutting a part of the brain and saying, "Let's see what happens" and recording the behaviour.

What do you think...?

~