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Topics covered in this video include: monoamine hypothesis of depression, bipolar disorder, serotonin, norepinephrine, dopamine, receptors, mechanism of action of antidepressants; selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors ,tricyclic antidepressants, monoamine oxidase inhibitors, atypical antidepressants, and lithium. Antidepressants mentioned include: Citalopram, Escitalopram, Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Venlafaxine, Desvenlafaxine, Duloxetine, Levomilnacipran, Amitriptyline, Amoxapine, Clomipramine, Desipramine, Doxepin, Imipramine, Maprotiline, Nortriptyline, Protriptyline, Isocarboxazid, Phenelzine, Tranylcypromine, Selegiline, Bupropion, Mirtazapine, Trazodone, Nefazodone, Vilazodone, and Vortioxetine.
MAO actually reduce BP mildly- I think this is the same reason why this is so - this also explains the bisphasic response of adrenaline.
We have less of B2 receptors and more of Alpha 1 receptors - But the B2 receptors having a stronger affinity for Adrenaline and noradrenaline - so when there is a mild increase in adrenaline/noradrenaline the effect of B2 is dominant leading to vasodilation and reduction in BP
At higher doses(say when we take tyramine) when we have enough adrenaline/noradrenaline to bind to both Alpha1 and Beta 2 the effect of alpha1 is dominant simply because we have more of alpha1 receptors in the blood vessel.
I remember having read this on wikipedia though I cannot find it now so maybe I am extrapolating a bit.
Hope someone finds this useful, someday.
Anti depressants DON’T work. It’s merely a combination of good marketing techniques and the placebo effect. Nothing more. Furthermore, they often do MUCH more harm than good. Stay away from them at all costs.
I\'m not sure but ,if anyone else is searching for dealing with anxiety try Nadazma Destroy Depression Helper (just google it ) ? Ive heard some extraordinary things about it and my buddy got cool success with it.
man rly good tutorials. but u are making ''pharmacology'' videos-->so imo, it would be much-much better, if u would add also CI(contraindications) and DI (drug interactions), and also properly mention which drug is mostly/preferably used from such a group. simply complete pharmacology, may by time line of videos will be extended 2x, but it is definitely would by btter watch 30 mins videos than visiting boring PPT lections;)
Broken record research just diff talk do you not understand why they are little difference enough for different pattens but all basic drugs the same but lithium they are all made from same chemicals you are reading out of a book and trying to make it sound more complex like they do to sell more drugs
Each of my videos contain subtitles. Look at the bottom of the YouTube video window as the video begins playing. You need to click on a small "CC" logo that will appear in this space, beside the "Change Quality" and screen-size icons.
All these drugs r dangerous they are just as bad as Ritalin trust me do not let a doctor put you on this crap. Once you are on this drug is very difficult to get off again and the long-term side effects from taking these drugs not worth it. Pharmaceutical companies are just poison makers
MAOIs now diet-safe. No decarboxylating enzymes in foods anymore to create tyramine, meaning no tyramine to lead to high blood pressure. Food and nutrition journals have been doing these analyses for 20 years now.
It seems to me like depression, anxiety and all these disorders that are fixed by anti depressants are caused by our brains not being built for modern life. We still have the same systems that are in monkeys, pretty much.
unfortunately there is only one "antidepressant" in all of this litany of drugs that treat dopamine deficiency and that drug is really dirty. Only one antidepressant ever actually to the market, Nomifensin, treated dopamine deficiency and it was withdrawn after some rare hematologic side effect. I suspect the real reason it was withdrawn was because it actually worked.
It is a shame that selective reversible MAOIs like moclobemide (auroix) aren’t mentioned as an alternative to irreversible non selective MAOIs. Moclobemide is considered “weak”, but at the higher doses I got quite a boost from it, with very little side effects.
This video is quite excellent in summarising such a complex field of mood disorders and the different treatments.
I predict that atypical antidepressants will become the dominant “class” of medicine marketed. There are just so many different molecules that seem to have some positive effect on mood. What class people respond to is still a lottery; even if geneotyping becomes involved in predicting the probability of success to one drug over another.
Your explanations and imagery to help understand and remember the concepts is pure intelligence! These videos are simply amazing and I thank you so much for sharing your knowledge and expressing the information in terms that are understandable!!
here's a few things to try
Work out why you are shy - the first step to solving a problem is to understand why it is there.
Be comfortable about yourself - this makes it easier
Challenge youself - you will feel better by taking action - especially by doing things that push your limits.
(I discovered these and more tips on Martos magic method website )
There are some side effects to SSRI's, and they are not for everyone. SSRI's may of course help if serotonin is low. According to "WRI," about 38% of depressives have lower than normal levels of serotonin, and that is why they tend to get depressed. In this case, SSRI's may help but still have side effects. In this case, other alternatives like nutritive support for underlying imbalances causing the problem can be at least as effective. Given to the wrong people, however, SSRI's can have fatal consequences (read the PDF "A Proposal for Prevention of School Shootings" - not directly related to this article of course but...): https://www.vitacure.me/blogs/news/difference-undermethylated-vs-overmethylated-symptoms
Sorry getting confuse about SERT, SSRI's and 5-ht receptors. are you saying "hypothetically" SSRI's are slow to show a response, because even though they block SERT that they also have an effect on dysfunctional 5-ht receptors that are " in a lipid raft" and the SSRI's ( along with inhibiting serotonin reuptake) that they accumulate around these g-protein rafts, helping to separate them and in turn allowing them to function better due to an increased ability to access cAMP ?
In short: SSRI inhibit SERT & re-establish 5-HT functionality ( g-proteins in a lipid raft ) which takes a few weeks before effects are noticeable. ?
Recent evidence revealed that antidepressant pills increase suicide risks by 2-5 times. [a][b][c][d][e][h]
Cognitive behavioural therapy halves the risk of repeated suicide attempts. [k]
Furthermore, antidepressants increased all cause mortality by 33%! [i][j]
Another meta-analysis published in the British Journal of Psychiatry has found that even patients with the most severe depression can expect to get as much benefit from cognitive behavioural therapy (CBT) as those with less severe symptoms. [f]
Even Behavioural Activation effectively decreases depressive symptoms. [g]
Trained grandmothers are better than psychiatrists.
Anti depression pills should be used to make a balance to ur mind . U also have to make positive life changes ,change diet , exercise , positive thinking , and so on. If depression last more then a month it probably is a chemical imbalance.
Thank you very much your videos are really helpful and the presentation is great!!! Could you please make videos about antipsychotics, anti mania, sedative hypnotics, antiepilectics and anti-parkinson drugs?
12:50 -- FALSE. If you had only read even ONE journal article on MAOIs and food interactions in THE LAST 30 YEARS, you would know that there is hardly any risk of MAOI - food interactions anymore. Interestingly, MAOIs increase serotonin levels several times more than do (S)SRI anti-depressants. This ought to be of great import to those pitiable chronic depressives whom the new-age (SSRI) anti-depressants don't serve.
Peter Hell Hello Peter: 30 mg of Parnate is unlikely to constitute a therapeutic dose in most people, the end result of which is that the imbecilic doctors (and NHS) will say, well, Parnate doesn't work for you. To test for the minimum dose that will have a therapeutic effect on a patient, blood pressure should be taken, then after you stand, take it again. A blood pressure drop of 15 points systolic on standing indicates that initially sufficient MAO is being inhibited. Doctor and patient can then track depression symptoms and increase if necessary, up to 90 - 120mg per day. I say 120mg as some psychiatrists have found that even after all MAO has been inhibited by Parnate, that there is additional benefit up to 120mg - this is anectdotal but a possibility.
Peter Hell I would second what D Snyder said. The literature and expert opinion supports that doses over 60mg can give increasing therapeutic benefits. A systolic BP drop of 15+ points standing (orthostatic) indicates that a therapeutic dose has been reached, but doesn't indicate a max.
DISCLAIMER: your treatment is up to your psychiatrist and I am not diagnosing you or giving medical advice as I am not familiar with your case or treatment history. Anything I write is informational only and not meant to be taken as medical advice. The American Psychiatric Association 2010 guidelines endorse going up to 60 mg/day in divided doses if needed (other tertiary sources back this up as well). If your psychiatrist goes by the British Association of Psychopharmacology then there is no dosing statement in those guidelines. Using a 60mg dose comes with the risk of increased side effects (activation, insomnia) but it is a well-studied dose.
I am a psychopharmacologist and I want to thank you for pointing this out. The fears of prescribing MAOIs (dietary concerns and pharmacodynamic interactions) are vastly overblown and limit exposure for many people who could benefit from this class. I've even recommended starting low-dose nortriptyline and phenelzine at the same time (TCA + phenelzine combo has been studied for decades; https://www.ncbi.nlm.nih.gov/pubmed/6376486 ) in a patient with ECT non-responsiveness and had a good result with no safety concerns.
thank you so much for posting! My teacher keeps saying i don't have to know how these medicines work but i do need to know the side effects. Because of this video i can finally relate the drug to the side effects.
i was prescribed effexor for minor anxiety by my doctor i looked this drug up and people saw it has withdrawl symptoms worse than heroin some people say withdrawl will cause horrible migrains brain zaps feelings of no emotions at all (zombie like) and many more terrifying symptoms. I think something as serious as this shouldnt be prescribed for minor anxiety what the hell these are dangerous drugs why are they prescribed for any social or mental problems however minor??
Antidepressants are medications that can help relieve symptoms of depression, social anxiety disorder, anxiety disorders, seasonal affective disorder, and dysthymia, or mild chronic depression, as well as other conditions.
They aim to correct chemical imbalances of neurotransmitters in the brain that are believed to be responsible for changes in mood and behavior.
Depression Medications (Antidepressants)
These are the most commonly prescribed type of antidepressant.
Serotonin and noradrenaline reuptake inhibitors (SNRIs) are used to treat major depression, mood disorders, and possibly but less commonly attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), anxiety disorders, menopausal symptoms, fibromyalgia, and chronic neuropathic pain.
SNRIs raise levels of serotonin and norepinephrine, two neurotransmitters in the brain that play a key role in stabilizing mood.
Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. They are effective in treating depression, and they have fewer side effects than the other antidepressants.
SSRIs block the reuptake, or absorption, of serotonin in the brain. This makes it easier for the brain cells to receive and send messages, resulting in better and more stable moods.
They are called "selective" because they mainly seem to affect serotonin, and not the other neurotransmitters.