Jump to content
CrazyBoards.org

Recommended Posts

I came across an interesting article, anti-drug psychiatrist was discussing why the drugs are bad.  I personally think the meds are helpful.

Although he did bring up one point that got me thinking and worried.

Do our brains and our emotions always have the capability to autoregulate?  I mean will it always know how to reach homeostasis?  I wonder this after over a decade of SSRIs and other psych drugs....

What are your thoughts on this guys?

Share this post


Link to post
Share on other sites

I wasn’t diagnosed until 2011. I tried several medications that didn’t work but finally started Wellbutrin in 2014. It worked and then it became less and less effective. My doctor upped my prescription. It worked for a year and then I felt that it just didn’t work at all. I decided last year that I would stop taking everything. It was maybe seven months of pure depression and anxiety. I was a self-hating angry mess and a self-made puddle of tears all the time. I could be happy but then quickly get back into the hole of depression in a few minutes. I’ve been back on Wellbutrin for the last two months at the lowest dosage. I can honestly say that, in my experience, being without medication, even if you exercise and practice yoga, have a loving supportive spouse, a dog, gainful employment; all doesn’t matter if your brain is working against you. I tried going without and was suicidal. 

I don’t know if I answered your question but all I know is my own experience. I’m better on medication. 

Share this post


Link to post
Share on other sites

Flatly, no. Of course not. If they could, there would be no mental illness. Or insomnia, for that matter. It’s an idiotic thing to say.

  • Like 2

Share this post


Link to post
Share on other sites

I'm with Gearhead on this one. MI wouldn't be a problem if this was true. ADs also wouldn't work if they did auto-regulate in the way he describes. They would all stop working just a few months in. The human brain is an amazing thing and it is capable of so much adaptation, but like any part of the body, it can malfunction. I think the person in the article is somewhere between naive and cruel. There are fair questions about the best uses of meds and whether non-med treatments are as accessible as they should be, but to be completely against meds is to say that people should suffer instead of using the medical tools available.

  • Like 2

Share this post


Link to post
Share on other sites

By this logic, before modern psychiatric meds, people’s mental illnesses should have been resolving on their own but asylums were full of people to disprove that.  

  • Like 1

Share this post


Link to post
Share on other sites

With all due respect, Brian, you've gotta be kidding me. I've spent time off meds in earlier years... it got worse, not better.

It's known as the kindling effect. 

Anti-drug psychiatrist? Hope he has a good part-time job elsewhere.

Share this post


Link to post
Share on other sites
On 1/12/2018 at 2:47 PM, Rabbit37 said:

I've spent time off meds in earlier years... it got worse, not better.

Me, too. I wish I'd started on meds much earlier in my mental illness experience. The 10 years without meds meant that my mental health problems had a long time to become entrenched. I had reasons for not pursuing meds in that time and in hindsight those reasons didn't steer me in the right direction, but by doing that I can say that I thoroughly tested the idea that the author is promoting and it made my health worse.

Edited by Ion

Share this post


Link to post
Share on other sites
On 1/11/2018 at 8:23 PM, Gearhead said:

Flatly, no. Of course not. If they could, there would be no mental illness. Or insomnia, for that matter. It’s an idiotic thing to say.

There's not really a gold standard of how everyone is supposed to act...

But my questioning was mostly in regards to severe depressions. There are a lot of treatment-resistant Depressions out there.

If they're "dysregulated" to begin with, how do we figure we're not making it worse with more medications?  Finally reaching a point, making it impossible for our brains to adapt at all or even leading to further psychosis...Something that worries me, among everything else. 

Another thing I've worried myself with, is I take an Anti-Depressant drug, it's highly effective, but after it poops out I'm unable to anything that is effective as this original drug had such a potent and strong anti-depressant effect leaving me in a fog of anxiety and depression indefinitely. 

I'm just thinking outloud, I'm pro-med and have been on them for years, I just worry....a lot so playing devil's advocate here.  I suppose nothing is risk-free at the end of the day.

Any responses interested and appreciated.

Edited by BrianOCD

Share this post


Link to post
Share on other sites

@BrianOCD it might be better to look at it a different way. There's a lot of evidence in favor of the influence that genetics has on our mental illnesses and how they progress. Even the brains of people with mental illness self-regulate. This can be seen in PET scans with and without the presence of pharmaceutical agents. After all it's a critical organ, if it wasn't capable of homeostasis, I would imagine we could die lol. However, genetics provide instructions for our body to use to achieving that "equilibrium". As you can imagine, if the instructions are wrong or if they're missing a step, finding this happy medium might be difficult. Each gene has multiple SNPs that dictate the function of that gene and sometimes they contradict each other. And sometimes one gene can compensate for the dysunction of another.

For example, here's a review of my genetics that I did with my pdoc and how he explained it to me. I have a genetic mutation for very low levels of MAO-A which leads to higher levels of serotonin in the brain (among other neurotransmitters). Additionally, I have 3 separate "short" allele SNPs for the serotonin transporter (SERT/SLC6A4). So not only do I poorly break down serotonin, but I also remove serotonin from the synapse more slowly (reuptake). However, my HTR1A gene (5HT1A) is overexpressed (rs6295), meaning that I have more of those receptors in the brain. This has been shown to reduce serotonin firing that would lead to lower serotonin in the synapse, thus compensating for my other deficiencies.

Share this post


Link to post
Share on other sites
6 hours ago, browri said:

@BrianOCD it might be better to look at it a different way. There's a lot of evidence in favor of the influence that genetics has on our mental illnesses and how they progress. Even the brains of people with mental illness self-regulate. This can be seen in PET scans with and without the presence of pharmaceutical agents. After all it's a critical organ, if it wasn't capable of homeostasis, I would imagine we could die lol. However, genetics provide instructions for our body to use to achieving that "equilibrium". As you can imagine, if the instructions are wrong or if they're missing a step, finding this happy medium might be difficult. Each gene has multiple SNPs that dictate the function of that gene and sometimes they contradict each other. And sometimes one gene can compensate for the dysunction of another.

For example, here's a review of my genetics that I did with my pdoc and how he explained it to me. I have a genetic mutation for very low levels of MAO-A which leads to higher levels of serotonin in the brain (among other neurotransmitters). Additionally, I have 3 separate "short" allele SNPs for the serotonin transporter (SERT/SLC6A4). So not only do I poorly break down serotonin, but I also remove serotonin from the synapse more slowly (reuptake). However, my HTR1A gene (5HT1A) is overexpressed (rs6295), meaning that I have more of those receptors in the brain. This has been shown to reduce serotonin firing that would lead to lower serotonin in the synapse, thus compensating for my other deficiencies.

So what about the psych drugs we take?  Do they hit us at the DNA at all or will our brains sort things out regardless of the drugs we take?

When I say "sort things out" I mean for the individual, not necessarily a golden normal or anything...

Share this post


Link to post
Share on other sites

Check out some of the studies on the effects of antidepressants on BDNF.

If auto-regulation was a thing, there wouldn't be the association between MDD and impaired neuronal plasticity.

"Previous human postmortem studies showed decreased BDNF expression or CREB immunoreactivity in the brains of participants with major depression who had not been treated with antidepressants, but those who were treated with antidepressant drugs had increased BDNF expression and CREB in the brain"

The Roles of BDNF in the Pathophysiology of Major Depression and in Antidepressant Treatment

Anecdotally, I sure as shit didn't get any better, being off meds for nearly 15 years. Of course the meds I was on..questionable if they even really worked.

  • Like 1

Share this post


Link to post
Share on other sites
9 hours ago, BrianOCD said:

So what about the psych drugs we take?  Do they hit us at the DNA at all or will our brains sort things out regardless of the drugs we take?

When I say "sort things out" I mean for the individual, not necessarily a golden normal or anything...

Some medications do cause critical modifications to our gene expression. A lot of these studies were done on fluoxetine which causes quite a few changes. Part of the hypothesis of antidepressant delay is not only that serotonin receptors take time to desensitize but that other changes are occurring in gene expression that do take time as well. Some changes in gene expression we already talk about all the time on these boards, the changes in liver enzymes (the P450 isoenzyme CYP system). Drugs that induce or inhibit liver enzymes are often doing this at the genetic level by increasing or decreasing gene expression. I use a sight called SelfDecode to review my own genome and this is what it has for venlafaxine (with references ;))

Gene Interaction Organism
CYP2D6 Affects metabolic processing Humans (R, R)
CAT Decreases activity , Decreases reaction , Increases reaction Rats (R)
KCNJ3 Affects activity , Affects cotreatment Mice (R)
CYP3A4  Increases metabolic processing (R)
PLXND1   Affects cotreatment , Decreases expression Fish (R)
ARC Increases expression Rats (R, R)
HTR7 Affects cotreatment , Decreases expression Fish (R)
EFNA5   Affects cotreatment , Increases expression Fish (R)
ROBO2   Affects cotreatment , Decreases expression Fish (R)
KCNJ5 Affects activity , Affects cotreatment Mice (R)
HTR4   Affects cotreatment , Decreases expression Fish (R)
HTR1A  Affects cotreatment , Decreases expression Fish (R)
HTR2C Affects cotreatment , Decreases expression Fish (R)
EFNA3 Affects cotreatment , Increases expression Fish (R)
SLC6A4 Affects response to substance Humans (R)
KCNJ5 Affects activity , Affects cotreatment Mice (R)
ABCB1  Increases expression Humans (R)
HTR4   Affects cotreatment , Decreases expression Fish (R)
ARC Increases expression Rats (R, R)
EFNA3 Affects cotreatment , Increases expression Fish (R)
ACP5 Decreases expression Humans (R)
PREX2 Decreases expression Humans (R)
LMO7 Decreases expression Humans (R)
KCNH2   Decreases activity Humans (R)
ARHGAP10 Increases expression Humans (R)
NR3C2 Decreases expression Rats (R)
MAPK1  Increases phosphorylation Rats (R)
SOD1 Increases expression Rats (R)
SERPINI1 Increases expression Rats (R)
TMEM261  Increases expression Humans (R)
BRINP3 Increases expression Humans (R)
SYT4   Increases expression Humans (R)
LIPG  Increases expression Humans (R)
ANKRD55  Increases expression Humans (R)
BDNF   Increases expression Rats (R)
SALL1 Increases expression Humans (R)
TRIM13 Decreases expression Humans (R)
NASP  Increases expression Humans (R)
MAPK3 Increases phosphorylation Rats (R)
ABCC1   Increases expression Humans (R)
AKT1  Increases expression Rats (R)
NSUN2 Decreases expression Humans (R)
CTNNB1  Increases expression Rats (R)
NR3C1 Decreases expression Rats (R)
RING1  Increases expression Humans (R)
PRL  Increases expression Humans (R)
UBE2Q1 Decreases expression Humans (R)

Who really knows at this point if all these actions actually have an impact on mood, but for all that venlafaxine does and how effective it can be for some people, a lot of this may be important. Feel free to check out these various genes to see what they do. The HTR ones are important because those genes encode the serotonin receptors. In this case, venlafaxine reduces the expression of 5HT7, 5HT4, 5HT1A, and 5HT2C. Most importantly is the reduced expression of 5HT1A which would result in fewer of these receptors. In studies, reduced expression of this gene was associated with increased serotonin firing and higher levels of serotonin in the synapse, assuming normal function of the SERT. However many of these other ones could play a critical role based on what we are just now learning about the role other neurotransmitters besides serotonin play in the role of depression, like the glutamate system. Venlafaxine increases expression of the ARC gene which is associated with consolidation of synaptic plasticity, but it also regulates synaptic activity of AMPA receptors, which accept glutamate. Also, as @argh indicates below, brain-derived neurotrophic factor (BDNF) plays a major role in many different psychiatric disorders including depression. Venlafaxine has been shown to up-regulate this gene.

8 hours ago, argh said:

Check out some of the studies on the effects of antidepressants on BDNF.

If auto-regulation was a thing, there wouldn't be the association between MDD and impaired neuronal plasticity.

The human brain does auto-regulate through a wide variety of processes. However, as I have indicated, in people with psychiatric disorders, these instructions for self-regulation may be "faulty" in that certain functions like BDNF may be overexpressed or underexpressed, leading to a lack of balance between different genes and the underlying functions that they encode. So while the brain is in fact regulating itself based on the instructions it has, the instructions themselves are bad instructions leading to poor regulation. And as you indicated, this translates into lack of neuronal plasticity and in some cases markers for neurotoxicity can be seen especially in the presence of an overactive glutamatergic system.

 

  • Like 1

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now


×