Posted by CaptainAmerica1967 on October 20, 2011, at 17:52:15
In reply to Re: opiates and major depression, posted by sigismund on October 19, 2011, at 2:50:30
I just wanted to write this note down and wish pharmaceutical companies would take this note seriously:
By 2020, which is less than nine years away nearing eight, the second leading cause of death in the USA will be suicide and second only to heart disease and possibly the number one killer for women. This has been predicted by WHO (World Health Organization predicted this as far back as the late 1990's or early 2000's I believe).
Obviously not all suicides are caused by psychiatric diseases, but a large percent are; Others causes of suicide follow along reasons for individuals getting "reactive depression" such as death of a family member/loved one, loss of a job, divorce/breakup, longterm/lifelong chronic illness, and more which are tough enough situations but "in my opinion" don't compared to those who struggle from "daily, chronically treatment resistant depression" as I've had or have all of the above situations happen to me.
Maybe the economy is going to get really bad producing more financial hardships, divorces, loses of jobs/homes, the baby boomer ('46-'64) parents will die causing grief on their children or Social Security Disabilty will be taken away (fortunate that I saved enough money throughout my career hopefully to last a lifetime if SSD goes away or if I'm never fixed to feel confident enough to work again) by the Republicans or that's what Rick Perry wants as well as many other Republicans want to do, and this will place too much pressure or stress causing suicides to become number two or maybe it's just more genetics passed down with depression as the number of RX antidepressants have skyrocked throughout the past 10 years. I would have liked to have kids as it's only my Brother (he had a girl) and I remaining but I would never wish TRD on anyone if mine is indeed genetic (I was a 12pd baby boy and OBGYN may have damaged my temporal lobe-limbic system while trying to deliver me vaginally with too much pressure, force being placed with the foreceps on temporal lobes as I had blood on both side and still have a scar on my right temple; Neurologist gave me this hypothesis of depression as he had seen this happen quite a bit in his career prior to retiring) so I don't want children, but could always adopt.
I think the pharmaceuticals companies need to wake up and are too focused purely on the monoamine hypothesis of depression and wish they'd start focusing on other mechanisms. Prior to the first antidepressant developed in the 1950's which was discovered purely by chance when a MAOI drug used to treat tuberculosis was given to patients, the patients started feeling much better; (Other drugs are discovered this way, ie testing Viagra for heart disease, but found out Viagra worked for erectile dysfunction). Physicians used to prescribe morphine, or opiates and the opiates worked for everyone and not just a select percentage, but the fear of addiction lead to the downfall or replacement by antidepressant drugs.
Present day, upto about 45% of patients who take antidepressants don't respond or do respond but don't get completely better. Some patients may respond better to the older meds like MAOIs or tricylics as they block REM sleep better compared to the SSRI's, but probably not the SNRI but Parnate is the most potent REM blocker available (why it helps my REM sleep disorder too) and keeps the brain less active, or from being over active/hyperactive during REM sleep in which all patients with depression show this overactivity or too much glucose uptake or excessive cerebral blood flow shown on PET scans or SPECT imaging; both my pyschiatric and I believe deep brain stimulation for those with the most severe TRD will make ECT obsolete because DBS really works and hits the root cause of the depression, overactivity by stimulating the specific area every so often, it calms the brain just like DBS would for overactive brain conditions like Bipolar, ADHD, Parkinson's (DBS first used for), Anxiety, OCD, Anorexia Nervosa, Epilepsy (over and under active), hot flashes?, possibly Alheimer's whereas ECT just makes the patient have a seizure hoping that the brain corrects itself via various mechanisms. ECT didn't help me at all and probably made me feel worse as I hated the thought and feeling of being knocked out as it's a total different feeling than slowly drifting off to sleep which is a nice feeling and I felt groggy half the day from the anaesthetics and worn out.
So why do pharmaceutical companies keep coming out with tweaked or slightly changed medications like Effexor to Effexor XR to Pristiq which if the Effexor didn't work then why Effexor XR or Pristiq? Money is the reason because the company is extending the life of the medication from becoming generic and will sometimes make them into a liquid or patch therefore still extending the patent but this is not trying to necessarily really help the struggling depressed patient.
I hope to enter into a ketamine study ASAP but most likely early next year as I've been much better this past year on buprenorphine, "SUBUTEX" (not "SUBOXONE"), but still not 100% everyday and an hoping the ketamine will get me there or I'm able to start working out again, otherwise I'll try to get into a deep brain stimulation again, but was excluded twice because of one psychiatrist's mistake of giving me too much trazodone and having a medication induced seizure therefore excluding me from two DBS studies (Dallas, Emory-Mayberg at Emory) as they want patients with who've never had a seizure regardless of the reason (you can have a seizure by getting knocked over the head-knew a patient that had a seizure after a coconut fell out of a tree and hit him on the head) and I even spoke to Helen Mayberg (pioneer of DBS for TRD) regarding my situation and said I was an excellent candidate but the reviewing psychiatrist who does the inclusions/exclusions is very thorough, rigid with the rules of DBS for depression still being an investigational study.
Ketamine, from what I've read, increases brain derived neurotrophic factor (BDNF) or increases the synapses, synaptogensis. I know ketamine works as an antagonist of the glutamate NMDA receptor, a proposed mechanism for depression but have already tried meds like Namenda (Alheimer's and detxromethorphan, the newest being Nuedexta (indicated for a disease that makes individuals breakout into crying or laughing spells-pseudobulbar affect that has quinidine to elevate the detxromethorphan levels) even while on the Parnate (normally a psychiatrist or pharmacist wouldn't dare combine the two but after what TRD patient has tried everything, taking cautious risks by slowly adding a medication might be worth it but the med didn't have the desired effect either.
My goal is to conquer this as everyone's goal is an to write an autobiography in the hopes of saving individuals lives before 2020.
Best wishes to all!
poster:CaptainAmerica1967
thread:81414
URL: http://www.dr-bob.org/babble/20111016/msgs/1000333.html