Jump to content

The Depression Gene


Lilu
 Share

Recommended Posts

I don't know if this is old news to you guys, but I found this explanation for depression quite convicing.
 
Here's a lecture given by Professor Sapolsky, at Stamford University, on the evidence of genetic predisposition to depression.  He's very clear and easy to understand.
 
Last 5 min of Lecture by famed professor at Stanford University, Robert Sapolsky on Depression and Genetics. Scientists have identified the Gene responsible for depression by studying thousands of children for 20 years.
 
http://www.youtube.com/watch?v=E3YP5HJU-q4
 
I love how he talks and how he explains things. Professor Sapolsky states:
 
"There's nothing out there like Depression. Depression is absolutely crippling. Depression is incredibly pervasive.... Basically depression is like the worst disease you can get....It is devasting. It is wildly common....15% of us will get it at some point in our lifetimes. Currently, World Health Organization says that depression is the 4th leading cause of disability around the world."
 
The theory states that people with this particular mutation in the brain, respond much more severely to stress than people without the mutation.  And that with each occurrence of a stressful even the likelihood of depression grows significantly.  People with the mutation (something about a short alele) are about 33% more likely to develop depression.  In other words, the combination of the genetic mutation AND stress, is what trigger the depression.
 
Now I realize that there are whole bunch of articles on the web saying that the Depression Gene theory has been disproven, but I can't help but think that it really makes sense.  Especially given the evidence in my life.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

  • Moderator Emeritus

I would hate to base any scientific conclusions on a YouTube presentation.  Has Professor Sapolsky published his findings in a format where they can be evaluated scientifically?

 

I tend to think that attitudes and behavior are passed down to children by example more so than by genetics.  Both my parents were worriers and my father, in particular, seemed to believe that every little thing that went wrong was a catastrophe.  As an only child, I could hardly help but learn to be this way myself.

 

One thing my long and painful withdrawal has done for me is to teach me that a lot of things are not worth being anxious or sad, and that the future is going to be what it will be regardless of my efforts to control it.  If I could cope with withdrawal--and I did--I can cope with most tough situations.

Psychotropic drug history: Pristiq 50 mg. (mid-September 2010 through February 2011), Remeron (mid-September 2010 through January 2011), Lexapro 10 mg. (mid-February 2011 through mid-December 2011), Lorazepam (Ativan) 1 mg. as needed mid-September 2010 through early March 2012

"Never attribute to malice that which is adequately explained by stupidity." -Hanlon's Razor


Introduction: http://survivingantidepressants.org/index.php?/topic/1588-introducing-jemima/

 

Success Story: http://survivingantidepressants.org/index.php?/topic/6263-success-jemima-survives-lexapro-and-dr-dickhead-too/

Please note that I am not a medical professional and my advice is based on personal experience, reading, and anecdotal information posted by other sufferers.

 

Link to comment
Share on other sites

I am third-generation for mental illness in my family, and it seems 20% of my grandmother's descendants are just more fragile. It skips all around....my grandmother, dad, and I are the only direct "line." But I still think it is a susceptibility, not a given. But we definitely struggle much harder to process life than the 80%.

1st round Prozac 1989/90, clear depression symptoms. 2nd round Prozac started 1999 when admitted to dr. I was tired. Prozac pooped out, switch to Cymbalta 3/2006. Diagnosed with bipolar disorder due to mania 6/2006--then I was taken abruptly off Cymbalta and didn't know I had SSRI withdrawal. Lots of meds for my intractable "bipolar" symptoms.

Zyprexa started about 9/06, mostly 5mg. Tapered 4/12 through12/29/12

Wellbutrin. XL 300 mg started 1/07, tapered 1/18/13 through 7/8/13

Oxazepam mostly continuously since 6/06, 30mg since 12/12, tapered 1.17.14 through 8.26.15

11/06 Lithium 600mg twice daily, 2.2.14 400mg TID DIY liquid, 2.12.14 1150mg, 3.2.14 1100mg, 3.18.14 1075mg, 4/14 updose to 1100mg, 6.1.14 900 mg capsules 7.8.14 810mg, 8.17.14 725mg, 8.24.24 700mg...10.22.14 487.5mg, 3.9.15 475mg, 4.1.15 462.5mg 4.21.15 450mg 8.11.15 375mg, 11.28.15 362.5mg, back to 375mg four days later, 3.4.16 updose to 475 (too much going on to risk trouble)

9/4/13 Toprol-XL 25mg daily for sudden hypertension, tapered 11.12.13 through 5.3.14, last 10 days or so switched to atenolol

7.4.14 Started Walsh Protocol

56 years old

Link to comment
Share on other sites

I would hate to base any scientific conclusions on a YouTube presentation.  Has Professor Sapolsky published his findings in a format where they can be evaluated scientifically?

 

I tend to think that attitudes and behavior are passed down to children by example more so than by genetics.  Both my parents were worriers and my father, in particular, seemed to believe that every little thing that went wrong was a catastrophe.  As an only child, I could hardly help but learn to be this way myself.

 

One thing my long and painful withdrawal has done for me is to teach me that a lot of things are not worth being anxious or sad, and that the future is going to be what it will be regardless of my efforts to control it.  If I could cope with withdrawal--and I did--I can cope with most tough situations.

 

Dr. Sapolsky is teaching students about research already done. You can read about the study here: 

Getting the Short End of the Allele  (http://news.sciencemag.org/sciencenow/2003/07/18-03.html)

The study is based on data from 847 New Zealanders the scientists have been following for more than 2 decades. The researchers counted stressful life events, such as romantic disasters and job crises, occurring between the ages of 21 and 26 and asked subjects whether, at age 26, they had been depressed in the past year. For those whose lives had gone smoothly, the probability of depression was the same regardless of their 5-HTT alleles. But adverse experiences had more negative effects among people with one s allele and more still for those with two s alleles. For the latter (17% of the group), the probability of a major depression rose to 43% among those who had been through four or more stressful experiences--more than double the risk for those with two l's. Furthermore, among the 73 subjects who had been severely abused as children, the two-s subjects ran a 63% risk of a major depressive episode after the age of 18. In contrast, abused subjects with two l's had the same average risk (30%) as the no-abuse group.

 

The study shows that genes related to psychiatric ills don't operate all by themselves, Weinberger adds, but help determine “how one deals with the environment."

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

I am third-generation for mental illness in my family, and it seems 20% of my grandmother's descendants are just more fragile. It skips all around....my grandmother, dad, and I are the only direct "line." But I still think it is a susceptibility, not a given. But we definitely struggle much harder to process life than the 80%.

That must be a bit of a relief I would think, whereas I don't know of anyone in MY family.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

"There's nothing out there like Depression. Depression is absolutely crippling. Depression is incredibly pervasive.... Basically depression is like the worst disease you can get....It is devasting. It is wildly common....15% of us will get it at some point in our lifetimes. Currently, World Health Organization says that depression is the 4th leading cause of disability around the world."

 

I don't know anything at all about genetics or this professor. However, I am afraid that I could not agree that depression is like the worst disease you can get. I think that's a pretty sloppy thing to say... ALS is probably the worst disease you can get. Imagine if 15% of people lost motor neuron function?!

 

For such a wildly common problem, I'd think a simple explanation is probably the wrong explanation. That's my hunch. One thing I've learned is that reductionist explanations by experts are likely to be clever by half and incorrect or misapplied near 100% of the time. Of course, this could be an exception, but I'd look for alternative explanations.

 

Also, besides the usefulness of understanding the cause to cure the problem there seems to be a large pull to understand the answers to the 'why' questions when it comes to the neurotic and depressive maladies... As a sufferer of these diseases and their cures, I spend way more of my time doing the things that have shown a more positive risk:reward and less time wondering why they have a positive result. I hope you are able to find some relief Lilu...

 

best,

Alex

"Well my ship's been split to splinters and it's sinking fast
I'm drowning in the poison, got no future, got no past
But my heart is not weary, it's light and it's free
I've got nothing but affection for all those who sailed with me.

Everybody's moving, if they ain't already there
Everybody's got to move somewhere
Stick with me baby, stick with me anyhow
Things should start to get interesting right about now."

- Zimmerman

Link to comment
Share on other sites

  • Moderator Emeritus

There may be a gene correlated with a person's likeliness to develop depression, but that doesn't mean the gene is the cause of depression.  It's quite a leap to go from a single correlation to the idea that depression is a 'genetic disorder'.  I find it very strange that today the biological framework is treated as being synonymous with explanation.  As a psychologist, all you have to do is correlate some complex behavior with a biological event and voila!  You have yourself an explanation!  There are so many fallacies with this kind of reasoning that it'd be exhausting to try to detail them all.  Raymond Tallis is really the expert on this.  In my opinion, this is not a convincing explanation.  In fact, I don't even think it's in the realm of an explanation.  All the same, thanks for the video.

3 Years 150 mgs Effexor

2 month taper down to zero

3 terrible weeks at zero

Back up to 75 mgs

2 months at 75

6 or so months back to regular dose of 150 - was able to restabilize fine.

3 month taper back to zero

1 HORRENDOUS week at zero

2 days back up to 37.5

3 days back up to 75

One week at 150 - unable to stabilize.

Back down to 75 mgs

At 75 mgs (half original dose) and suffering withdrawal symptoms since October 2012.

 

"It is a radical cure for all pessimism to become ill, to remain ill for a good while, and then grow well for a still longer period." - Nietzsche

Link to comment
Share on other sites

There may be a gene correlated with a person's likeliness to develop depression, but that doesn't mean the gene is the cause of depression.  It's quite a leap to go from a single correlation to the idea that depression is a 'genetic disorder'.  I find it very strange that today the biological framework is treated as being synonymous with explanation.  As a psychologist, all you have to do is correlate some complex behavior with a biological event and voila!  You have yourself an explanation!  There are so many fallacies with this kind of reasoning that it'd be exhausting to try to detail them all.  Raymond Tallis is really the expert on this.  In my opinion, this is not a convincing explanation.  In fact, I don't even think it's in the realm of an explanation.  All the same, thanks for the video.

 

The research shows, and as Professor Sapolsy explains, that the genetic mutation itself is NOT the cause of  Depression, nor does it predict that Depression will develop.  What it shows is that when faced with stressful situations, people with this particular mutation are 30% more likely to develop depression, than people without the mutation.  See?  And with each additional major life stress, the likelihood of a depressive episode occuring rises at twice the rate for people with this gene.  At least THAT is how I understand it.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

  • Moderator Emeritus

I see.  Sorry, I got annoyed when he used the phrase 'genetic disorder' and quit watching.  The idea that depression is really a kind of intolerance to stress is an interesting idea.  But again, simply pointing out that certain people are less tolerant to stress than others doesn't really explain anything.  The genetics are not an explanation, just a particular way of making this observation.  The question is WHY certain people are more sensitive to stress than others, and whether we can really count this sensitivity as a strict disadvantage.   

 

3 Years 150 mgs Effexor

2 month taper down to zero

3 terrible weeks at zero

Back up to 75 mgs

2 months at 75

6 or so months back to regular dose of 150 - was able to restabilize fine.

3 month taper back to zero

1 HORRENDOUS week at zero

2 days back up to 37.5

3 days back up to 75

One week at 150 - unable to stabilize.

Back down to 75 mgs

At 75 mgs (half original dose) and suffering withdrawal symptoms since October 2012.

 

"It is a radical cure for all pessimism to become ill, to remain ill for a good while, and then grow well for a still longer period." - Nietzsche

Link to comment
Share on other sites

I see.  Sorry, I got annoyed when he used the phrase 'genetic disorder' and quit watching.  The idea that depression is really a kind of intolerance to stress is an interesting idea.  But again, simply pointing out that certain people are less tolerant to stress than others doesn't really explain anything.  The genetics are not an explanation, just a particular way of making this observation.  The question is WHY certain people are more sensitive to stress than others, and whether we can really count this sensitivity as a strict disadvantage.  

 

 

I don't know if you noticed the study that I posted above the link to the study that the professor's lecture mentioned:

 

Getting the Short End of the Allele  (http://news.sciencem...3/07/18-03.html

 

Basically this is what they're saying:

 

2 short alleles (whatever those are) + 4 or more stressful experiences = 43% probability of major depression.  

2 short alleles (whatever those are) + 4 or more stressful experiences + childhood abuse = 63% probability of major depression after age 18

 

And unfortunately, they have already disproven this theory:

 

http://www.sciencemag.org/content/324/5935/1628.short

 

DEPRESSION GENE

Back to the Drawing Board for Psychiatric Genetics

In 2003, researchers landed a huge catch: a gene variant that seemed to play a major role in whether people get depressed in response to life's stresses or sail through. The find, a polymorphism related to the neurotransmitter serotonin, was heralded as a prime example of "gene-environment interaction": whereby an environmental trigger influences the activity of a gene in a way that confers susceptibility. But an exhaustive new meta-analysis published last week in The Journal of the American Medical Association suggests that the big fish may be a minnow at best. A different team reanalyzed data from 14 studies, including the original one, and found that the cumulative data fail to support a connection between the gene, life stress, and depression.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

  • Member

Looking for scientific validation for 'psychological' problems really is a snake pit, isn't it?

What happened and how I arrived here: http://survivingantidepressants.org/index.php?/topic/4243-cymbaltawithdrawal5600-introduction/#entry50878

 

July 2016 I have decided to leave my story here at SA unfinished. I have left my contact information in my profile for anyone who wishes to talk to me. I have a posting history spanning nearly 4 years and 3000+ posts all over the site.

 

Thank you to all who participated in my recovery. I'll miss talking to you but know that I'll be cheering you on from the sidelines, suffering and rejoicing with you in spirit, as you go on in your journey.

Link to comment
Share on other sites

  • Moderator Emeritus

^Indeed.Thanks for the update Lilu, I hadn't seen that.

3 Years 150 mgs Effexor

2 month taper down to zero

3 terrible weeks at zero

Back up to 75 mgs

2 months at 75

6 or so months back to regular dose of 150 - was able to restabilize fine.

3 month taper back to zero

1 HORRENDOUS week at zero

2 days back up to 37.5

3 days back up to 75

One week at 150 - unable to stabilize.

Back down to 75 mgs

At 75 mgs (half original dose) and suffering withdrawal symptoms since October 2012.

 

"It is a radical cure for all pessimism to become ill, to remain ill for a good while, and then grow well for a still longer period." - Nietzsche

Link to comment
Share on other sites

  • Administrator

They cannot separate nature from nurture in these things. People who come from stressed families often display stress.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

Link to comment
Share on other sites

To paraphrase an old line, "Fools and psychiatrists are both blind men in an unlit cellar at midnight, looking for a black cat that isn't there. The difference is, the psychiatrist finds it".

Ed

Link to comment
Share on other sites

To paraphrase an old line, "Fools and psychiatrists are both blind men in an unlit cellar at midnight, looking for a black cat that isn't there. The difference is, the psychiatrist finds it".Ed

LOL I've never heard that one!

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

They cannot separate nature from nurture in these things. People who come from stressed families often display stress.

 

What do you mean by that?  I guess I cannot relate it to my family. My parents are both quite hyper and often agitated. Whereas I'm always calm. Doesn't mean that I'm not stressed, but it doesn't get exhibited outwardly.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

  • Moderator Emeritus

To paraphrase an old line, "Fools and psychiatrists are both blind men in an unlit cellar at midnight, looking for a black cat that isn't there. The difference is, the psychiatrist finds it".Ed

 

Love it!  Thank you, Edted.

Psychotropic drug history: Pristiq 50 mg. (mid-September 2010 through February 2011), Remeron (mid-September 2010 through January 2011), Lexapro 10 mg. (mid-February 2011 through mid-December 2011), Lorazepam (Ativan) 1 mg. as needed mid-September 2010 through early March 2012

"Never attribute to malice that which is adequately explained by stupidity." -Hanlon's Razor


Introduction: http://survivingantidepressants.org/index.php?/topic/1588-introducing-jemima/

 

Success Story: http://survivingantidepressants.org/index.php?/topic/6263-success-jemima-survives-lexapro-and-dr-dickhead-too/

Please note that I am not a medical professional and my advice is based on personal experience, reading, and anecdotal information posted by other sufferers.

 

Link to comment
Share on other sites

  • 3 months later...

Very Interesting.

 

Both my parents are clinically depressed and are on anti depressants. So I do believe that you can have the right genetic traits to be biologically determined to get depressed.

 

But I do agree on Jemma's point also. After all we are nothing but a product of our environment and the behavioural  programing of our parents.

 

All good stuff!

2013-July 1st Citalopram 20mg ()

2013-August 19th ended Citalopram cold turkey

med free.  (Took them for 7 weeks)

 

When I was a child, I spoke as a child,

I understood as a child, I thought as a child;

But when I became a man,

I put my childish things away.

 

- 1 Corinthians 13:11

 

Link to comment
Share on other sites

  • 1 year later...

I have been looking into this because of an article Sapolsky wrote about the German pilot which I think was full of holes. He said depression is 100% biological. I searched the literature for proof, and this was the study I found--the one in the first post.

 

Then I read it. Want to see what they actually concluded? The following os excerpted from a letter I wrote to Mad in America yesterday:

 

In 2011, a meta-analysis revealed that “...there probably is a real, if small, effect...” How small was this “probable” “real” effect? This small: “We agree with Lewis et al that testing for 5-HTTLPR genotype on its own is not likely to be clinically useful.”

 

And how can something be real while also being merely probable?

2009: Cancer hospital said I had adjustment disorder because I thought they were doing it wrong. Their headshrinker prescribed Effexor, and my life set on a new course. I didn't know what was ahead, like a passenger on Disneyland's Matterhorn, smiling and waving as it climbs...clink, clink, clink.

2010: Post surgical accidental Effexor discontinuation by nurses, masked by intravenous Dilaudid. (The car is balanced at the top of the track.) I get home, pop a Vicodin, and ...

Whooosh...down, down, down, down, down...goes the trajectory of my life, up goes my mood and tendency to think everything is a good idea.
2012: After the bipolar jig was up, now a walking bag of unrelated symptoms, I went crazy on Daytrana (the Ritalin skin patch by Noven), because ADHD was a perfect fit for a bag of unrelated symptoms. I was prescribed Effexor for the nervousness of it, and things got neurological. An EEG showed enough activity to warrant an epilepsy diagnosis rather than non-epileptic ("psychogenic") seizures.

:o 2013-2014: Quit everything and got worse. I probably went through DAWS: dopamine agonist withdrawal syndrome. I drank to not feel, but I felt a lot: dread, fear, regret, grief: an utter sense of total loss of everything worth breathing about, for almost two years.

I was not suicidal but I wanted to be dead, at least dead to the experience of my own brain and body.

2015: I  began to recover after adding virgin coconut oil and organic grass-fed fed butter to a cup of instant coffee in the morning.

I did it hoping for mental acuity and better memory. After ten days of that, I was much better, mood-wise. Approximately neutral.

And, I experienced drowsiness. I could sleep. Not exactly happy, I did 30 days on Wellbutrin, because it had done me no harm in the past. 

I don't have the DAWS mood or state of mind. It never feel like doing anything if it means standing up.

In fact, I don't especially like moving. I'm a brain with a beanbag body.   :unsure:

Link to comment
Share on other sites

since this thread is still going, ill mention something from previous study: there is no genetic causes for diseases, most especially 'brain diseases' like psych diagnoses. there are genetic enablers that can help set the scene for illness, but even hard physical diseases that are genetic and degenerative rely on more than just DNA---environmental factors and bodily stressors play a requisite role in the development of illness. even fetal formation in the womb that is already running the course of some of these inherited diseases requires an active cycle to continue along its path. thats sort of the entire point of/impetus behind medical science (and also a big focus of more modern fields like gene therapy).

 

in terms of mental health, there are a variety of partially identified genes that are related (neither solely nor exclusively) to things like disposition and coping method preferentiality, and measuring these constellations can give you a slight edge on predicting the potential for mental health experiences, but we are fundamentally far more complex than we are capable of understanding or scrutinizing. we dont even understand DNA or the implications of gene sequences---we are largely just shooting off conjectures; theres real-world application, but something doesnt have to be correct to have successful application. the interaction of different elements within genomes is NOT understood by science, and our experimentation has also led to a lot of dangerous application, like GMO foods that lose quality or become toxins within the human body because you cant play pick-and-choose with gene sequences and expect everything else to operate as usual.

 

its also important to note how easily we can change our genes, both activating and inactivating particulars, and most especially damaging, mutating, and altering our own DNA---even the DNA we pass on to children. a lot of processes of illness or fatal physical collapse reflect a breakdown of genetic functioning due to internal and external factors. even aside from the question of human mortality or morbidity, its staggering how easily we can alter our own 'predispositions' to diseases or non-disease traits simply through lifestyle and exposure to environmental factors. people tend to think of genetic lineage as a rather linear thing, but we are more...fuzzy. so tackling a problem as complex as depression, which lacks unifying diagnostic criteria and expression, it seems quite unfeasible to reduce incidence to clean-cut gene sequences and heredity.

 

im sorely missing sleep, i hope this is at least half-way legible.

from 2005-2012, i spent 7 years taking 17 different psychotropic medications covering several classes.  i would be taking 3-7 medications at a time, and 6 out of the 17 medications listed below were maxed or overmaxed in clinical dosage before i moved on to trying the next unhelpful cocktail.
 
antidepressants (SSRIs, SNRIs, NDRIs, tetracyclics): zoloft, wellbutrin, effexor, lexapro, prozac, cymbalta, remeron
antipsychotics (atypical): abilify, zyprexa, risperdal, geodon
sleep aids (benzos, off-label antidepressants & antipsychotics, hypnotics): seroquel, temazepam, trazodone, ambien
anxiolytics: buspar
anticonvulsants: topamax
 
i tapered off all psychotropics from late 2011 through early 2013, one by one.  since quitting, ive been cycling through severe, disabling withdrawal symptoms spanning the gamut of the serious, less serious, and rather worrisome side effects of these assorted medications.  previous cross-tapering and medication or dosage changes had also caused undiagnosed withdrawal symptoms.
 
brainpan addlepation

Link to comment
Share on other sites

I have been looking into this because of an article Sapolsky wrote about the German pilot which I think was full of holes. He said depression is 100% biological. I searched the literature for proof, and this was the study I found--the one in the first post.

 

Then I read it. Want to see what they actually concluded? The following os excerpted from a letter I wrote to Mad in America yesterday:

 

In 2011, a meta-analysis revealed that “...there probably is a real, if small, effect...” How small was this “probable” “real” effect? This small: “We agree with Lewis et al that testing for 5-HTTLPR genotype on its own is not likely to be clinically useful.”

 

And how can something be real while also being merely probable?

The same way being shy is a disease and ssris are like insulin.... 

is there money behind it... 

take a jump in the dark and grab some cash... 

put the marketing machine to work 

walla patent money in the bank... 

 

makes me want to gag I see if from a mile away.

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

Link to comment
Share on other sites

  • 2 weeks later...

New study:

http://www.alphagalileo.org/ViewITem.aspx?Itemid=151616&CultureCode=en

 

Suffering from abuse during childhood increases the chances of depression, above all in those adults who are genetically predisposed
13 April 2015 11:07 University of Granada

 

An international research project led by scientists from the U. of Granada has demonstrated that the risk of suffering from depression due to abuse during childhood is significantly higher in those patients who are genetically predisposed.

This research has been published in the prestigious Journal of Psychiatry and Neuroscience, and it has been coordinated by Prof.Blanca Gutiérrez, from the Psychiatry Department at the U. of Granada. Participants include researchers from the CIBERSAM group (UGR Centre for Biomedical Research), the Biostatistics Department at the U. of Granada, King’s College in London, Loyola University in Andalusia, the University of Seville, the University of Zaragoza, the Health Service of La Rioja, the Health Service of the Canary Islands, and the San Cecilio Clinical University Hospital in Granada.

Scientists analysed a sample which consisted of 2.679 primary health care patients from 41 different health clinics in seven different Spanish provinces, between the ages of 18 and 75. They were all followed during a period of three years, and the survey included genetic tests.

The results demonstrated that those individuals who have scarcely functional genes implied in neurotrophism (BDNF) and in serotonin transmission are particularly vulnerable to the noxious effects that childhood abuse (either psychological, physical or sexual) has upon general mood and as a risk factor in clinical depression.

According to prof. Gutiérrez “it is an important result, which proves a triple genetic-environmental sort of interaction whose relevance is even more important if we take into consideration that the response to antidepressants appears to be fundamentally mediated through proteins codified by the two genes we have studied.”

“Our results present a fundamental genetic-environmental model to explain this sort of therapeutic response”, concludes this researcher from the U. of Granada.

2005-2008: Effexor; 1/2008 Tapered 3 months, then quit. 7/2008-2009 Reinstated Effexor (crying spells at start of new job.)
2009-3/2013: Switched to Pristiq 50 mg then 100 mg
3/2013: Switched to Lexapro 10mg. Cut down to 5 mg. CT for 2 weeks then reinstated for 6 weeks
8/2013-8/2014: Tapering Lexapro (Lots of withdrawal symptoms)
11/2014 -8/2015: Developed severe insomnia and uncontrollable daily crying spells
12/2014-6/2015: Tried Ambien, Klonopin,Ativan, Lunesta, Sonata, Trazadone, Seroquel, Rameron, Gabapentin - Developed Anxiety disorder, PTSD, and Psychogenic Myoclonus
7/2015-1/2016: Reinstated Lexapro 2 mg (mild improvement, but crying spells still present)

1/2016-5/2017: Lexapro 5 mg ( helped a lot, but poor stress tolerance & depressive episodes)

5/20/2017 - Raised dose to Lexapro 10 mg due to lingering depression(Total of 2 failed tapers & severe PAWS)

9/11/2018 - Present: Still on 10 mg Lexapro and mostly recovered.(Extremely sensitive to stress which triggers Myoclonus.)

10/7/2022 - 20 mg Lexapro (brand only) Plus occasional Klonopin for anxiety and Ambien for insomnia.

Link to comment
Share on other sites

New study:

http://www.alphagalileo.org/ViewITem.aspx?Itemid=151616&CultureCode=en

 

Suffering from abuse during childhood increases the chances of depression, above all in those adults who are genetically predisposed

13 April 2015 11:07 University of Granada

 

An international research project led by scientists from the U. of Granada has demonstrated that the risk of suffering from depression due to abuse during childhood is significantly higher in those patients who are genetically predisposed.

This research has been published in the prestigious Journal of Psychiatry and Neuroscience, and it has been coordinated by Prof.Blanca Gutiérrez, from the Psychiatry Department at the U. of Granada. Participants include researchers from the CIBERSAM group (UGR Centre for Biomedical Research), the Biostatistics Department at the U. of Granada, King’s College in London, Loyola University in Andalusia, the University of Seville, the University of Zaragoza, the Health Service of La Rioja, the Health Service of the Canary Islands, and the San Cecilio Clinical University Hospital in Granada.

Scientists analysed a sample which consisted of 2.679 primary health care patients from 41 different health clinics in seven different Spanish provinces, between the ages of 18 and 75. They were all followed during a period of three years, and the survey included genetic tests.

The results demonstrated that those individuals who have scarcely functional genes implied in neurotrophism (BDNF) and in serotonin transmission are particularly vulnerable to the noxious effects that childhood abuse (either psychological, physical or sexual) has upon general mood and as a risk factor in clinical depression.

According to prof. Gutiérrez “it is an important result, which proves a triple genetic-environmental sort of interaction whose relevance is even more important if we take into consideration that the response to antidepressants appears to be fundamentally mediated through proteins codified by the two genes we have studied.”

“Our results present a fundamental genetic-environmental model to explain this sort of therapeutic response”, concludes this researcher from the U. of Granada.

" antidepressants appears to be fundamentally mediated through proteins codified by the two genes we have studied.”"

 

see that word "appears"  that is like we are guessing... it is the like the word "thought" they use to say serotonin is "thought" to be involved with depression... another bit of double talk from those who are best at it. 

 

Scientists analysed a sample which consisted of 2.679 primary health care patients from 41 different health clinics in seven different Spanish provinces, between the ages of 18 and 75. "

 

How did they pick these people... the worst of the worst?  What is the criteria?  We all know that participants and how the study is designed can be how trials can predict the outcome... if you want all the people to be better on a drug pick the best to start with ect we have seen all sorts of ticks and slight of hand in studies to get the results the study designers wanted to get.  

 

"The same way being shy is a disease and ssris are like insulin.... 

is there money behind it... 

take a jump in the dark and grab some cash... 

put the marketing machine to work 

walla patent money in the bank... 

 

makes me want to gag I see if from a mile away."

 

JADED not buying but then again I am done shopping

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

Link to comment
Share on other sites

Please sign in to comment

You will be able to leave a comment after signing in



Sign In Now
 Share

×
×
  • Create New...

Important Information

Terms of Use Privacy Policy