There is no drug without side effects or complications. The same drug that is a lifesaver for one may land another person in the hospital. Everything is a balance of risks and rewards. Tradeoffs are a given in this life.
An incredible piece of teaching. So consistent and clear. And it is also reassuring to see the coherency of the research that is being carried out. The mystery of depression - what it is and how the medication treats it - is receding nicely.
I have tried 3 of the most terrifying drugs ever, finasteride destruction of hormones, then effexor destruction of my dopamine serotonin and norepinephrine receptors, then valium destruction of my gaba system.I am 3 years clean of all this,the withdrawal was hell. what it help me was cbd zinc vitamin c whatever reduce inflammation, i am not what used to be, but i can function, also my sexual life is back, not more errection problems from effexor usage and finasteride
Excellent information. Thank you for publishing! (The binding profile in patients in remission provides a salutatory warning for medication compliance!)
Hello from England UK I'm disabled and in chronic pain I also have suffered for over 25 years with chronic anxiety and reasurance seeking OCD about contamination which involves nearly touching everything without washing my hands , I'm obsessed with my clothes being contaminated with dirty toilet water backsplash on my butt getting on my trousers and bottom rear end of my jumper , and on and on . I'm taking 150mg sertraline and 100mg amitriptyline.
Great info! I learned a lot and I read a lot about depression. I had several ketamine infusions and they were wonderful and very helpful. The infusions are extremely expensive, tho. I am going to try the nasal spray but I have heard things that it’s not as effective. Thanks for your research and please update us if you can!
Great talk, thank you very much. Was amazed to see the proliferation of serotonin autoreceptor 5-HT1A on one of the slides. Big question for me is - is that proliferation caused by stress, or was it pre-existing?
I have few questions: I) How does an SNRI differ from a SSRI? II) Could Gluten we eat be a problem on any of those arguments? III) If SSRI help reducing serotonin receptors, what would be the effect in the long-term, usage?
I) Noradrenalin vs Serotonin For a chart and explaination on difference, watch this video: ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-u_7LwL5EmAs.html
*"I have few questions:* *I) How does an SNRI differ from a SSRI?* II) Could Gluten we eat be a problem on any of those arguments? *III) If SSRI help reducing serotonin receptors, what would be the effect in the long-term, usage?"* Serotonin deficit theory was proved wrong many decades ago. Long term effect of supposed antidepressants is getting persistent non reversible neurological damage and worse depression. Hope this helps you get the answers, sources: ISSM Webinar on Post SSRI Sexual Dysfunction ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-yFxMeoaIc3c.html PETER GØTZSCHE about many his studies on SSRIs/psychiatric drugs English Español ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-Vw6v9a-rylg.html David Healy, MD: Sex, SSRI's & Medical Groupthink ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE--iY30swDoyw.html The multiple damage these drugs cause is not reversible. So called antidepressants / SSRIs / SNRIs are very damaging, should be a very last resort on people with very acute problems (probably 0,01% of the people that get them now).
This is a masterpiece. I recently read something similar, and it was a masterpiece in its own right. "Unlocking the Brain's Full Potential" by Alexander Sterling
I took 2 pills and ended up having serotonin syndrome. Stuff is nasty in the end no pills few years later anxiety is minimal as normal background from work deadlines and court
Focusing on the downstream effect of ssri (neuroplasticity) I believe they can find new ways to specifically target receptors (such as BDNF receptors) without causing too many side effects.
@ Brain & Behavior Research Foundation My question is that, if amount of 5-HT1a receptors are proportional to gray matter in various brain areas and it provides neurogenesis and synapsogenesis, does not taking SSRI's leads to reducing in gray matter and ability of synapsogenesis? Because doctor said that, SSRI reduces the 5-HT1a receptors. Does this means, SSRI antidepressants cause decrease in neuroplasticity and gray matter and even decline in intelligence? (since we are correlating intelligence with gray matter)
SSRI’s work because they downregulate the receptors. HT2a receptors are are implicated in plasticity and creativity. Unless you take a HT2a antagonist with the SSRI then other receptors can be affected by the increase in serotonin. Haha that’s all I know. Good question
@@zaheerahman7266 Actually, the 5HT1a receptor that provides therapeutic benefits when downregulated is the pre-synaptic one (the autoreceptor one), not the post synaptic). Subtype and location in the synapse will make it have different functions. Even though, not only the pre synaptic one is down regulated. The post synaptic one is too, alongside with the other 5HT receptors. The down regulation of the 5HT3 receptor, the only ionotropic sertoninergic receptor, also provides clinical benefits because it stops the dopaminergic signaling, and this receptor is a very unique one because it actually interfere with the signaling even when not bound to serotonin, therefore, the downregulation of this subtype will actually lead to substantial decrease on it's activity (thus, an increase in dopaminergic signaling).
They actually lead to a downstream effect that increases BDNF, reduces cortisol effect, has anti inflammatory activity, removes cytokines from the membranes and some other features that will result in neuroprotection and actually increase synaptogenesis. Even with the post synaptic receptors being downregulated, the SSRIs won't cause a reduced serotoninergic activity. The receptor is downregulated as a response to the increased serotoninergic signaling.
@@user-yy8dh7bd4k In short, "[SSRIs] result in neuroprotection and actually increase synaptogenesis." So NO the opposite (positive) affect on gray-matter & neuroplasticity. Correct?
@@agceh Antidepressants are not prescribred only for depression but for other 100 problems and off label. Antidepressants induced anhedonia is more devastating than depression! I have it, it's terrible!
The biggest joke of all is if the suicides were known to be depressed were they taking the depression medication? Because if they were then that leads to increase serotonin and receptors that's the whole point of what they are supposed to do. Also these drugs actually cause increased number of relapses. Quite frankly anyone who can hold a mouse by the tail and when it stops struggling shows its depression really needs some urgent psychiatric help himself. Does it not occur to him maybe the mouse is simply tired?? Also it is shown that these drugs increase suicidality, cause agitation etc. Such a dangerous talk, plus the withdrawal problems are horrendous, but also what is happening in someone's life in the first place, ie not what's wrong with you but what's happened to you? But oh yes that won't need drugs but you will need to talk to them, maybe un dealt with trauma? Oh but then big pharma? Yes of course, money the root of all evil
Wow, an intelligent comment! This guy is basically getting paid to characterize depression as a disease, and to then describe any brain difference he can find as a defect. In reality, there is no disease and there is no medical treatment, only synthetic drug consumption with increased dysfunction and disability. The drugs don't work anyway, whether or not you think it's a disease.
Quetiapine make me overdose on 80 paracetamols . I'm still on it with conjuction of venlafaxine. I'm addicted to these medicines and struggling to reduce .
Research for clinical trials. They are the best tests / use specialized scans that show abnormalities that regular scans don't. I've been researching low dose naltrexone. So many studies are linking depression partly to neuroinflammation.
Should You Take Antidepressants? I think you can put it this way: Depression itself damages the body. It is now known that depression leads to a higher risk of cardiovascular diseases and diabetes. Depression significantly shortens life expectancy. Depression also damages the brain. The brain volume decreases, the risk of dementia increases. Antidepressants can partially reduce the harmful effects of depression. On the other hand, they themselves increase the risk of dying earlier and can have many bad side effects. Some antidepressants lead to obesity, others increase the risk of bleeding etc. etc. In the end, one can say: With depression you will die earlier. In addition, the risk of numerous illnesses increases. With and through antidepressants you will also die earlier and risk numerous illnesses. So what's left for you? I think you should see if taking antidepressants improves quality of life. If antidepressants make you feel better, happier, and work better, then you should take them. You should also have a look at possible side effects and have yourself examined regularly. But always remember: Depression also has side effects. In addition, you should - generally - eat as healthy as possible and do a lot of sport. This also reduces the risk of gaining weight through antidepressants. All the best!
@@johanngotlub7662 But those drugs don't allow you to deal with the underlying trauma. They almost debilitate you. Agreed, if someone has to choose between life-threatening depression, then those medications might be a great idea. But if you don't cope with the underlying trauma, then how is it probable to really move forward?
Tried it. Doesn't work save your money. Even the clinical trials done for TMS & RTMS show it to be effective at about the same rate as placebo... So, don't make the same mistake I did save your money.,
A systematic review of the available literature was published in arguably the most prestigious medical journal (the Lancet) just last month (October 2019). The authors concluded that there is a lack of quality evidence (especially clinical evidence) to support the efficacy of CBD as an antidepressant. So there's not really much to discuss. There are anecdotes abound, but that doesn't mean anything... CBD is being aggressively marketed as a magical panacea, but in many cases this is unwarranted. Here's a link to the Lancet review (sadly it's behind a paywall but you can find it for free elsewhere): www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(19)30401-8/fulltext
I see that there has been a great following, well 5 comments uahooo !!! I wonder if it is because of the great trust that people have towards psychotherapy or because they have broken their balls to get themselves fucked. Then I'd like to know if with all this funding they have taken into consideration, even minimally, the natural active ingredients, those not monopolized, because they seem to work quite well, aside from LSD, but which is already your patent. Then I'd like to know why the ketamine molecules, which are of two different types, have been chosen the most harmful one. Thanks.....
Thank you, Angie and Dr. Kirsch! After watching this fascinating interview, I’m wondering about a few things. If SSRI’s are basically placebos... 1. How do you explain the positive neuroplastic changes in folks with MDD who’ve been on SSRIs vs. those with MDD who have not taken SSRIs? PET scans prove that positive structural changes occur with SSRIs vs no SSRIs. Granted, they don’t have PET scans of people who were given a placebo, so maybe they’d have neuroplastic changes, too. 2. How do you explain the positive neuroplastic (and behavioral) changes in mice that are given an SSRI? 3. Would SSRIs show a more significant effect (vs. placebo) the longer folks take them? It seems that most studies aren’t long enough. Here’s an example of the neuroplasticity I mentioned: ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-k2AdebIbx5Y.html
It basically explained how untreated depression can lead to neuronal death in some critical brain circuits resulting in treatment resistant depression and how such treatment resistant depression may amendable to treatment with ketamine which works by a different physiological mechanism. This knowledge is potentially very helpful to those reluctant to take antidepressants and those who have developed treatment resistant depression over the years.
13:21 but was suicider depressed? maybe not at all or wrongfully ruled suicide.. just devils advocate because exponential variables in every study make me have these intrusive room for error thoughts