Breaking Through Depression
theguardian.com
theguardian.com
[0] - https://www.youtube.com/watch?v=TVgQ_tgWMyU&t [1] - https://www.amazon.com/Feeling-Good-New-Mood-Therapy/dp/0380...
For example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7001356/
I wouldn't be surprised if most of the people who seek therapy don't really have any major psychological issues, but are simply in need of some advice and support - CBT would be greatly exploiting that because there isn't even a test whether or not you need CBT - it's just assumed that it's a one-size-fits-all solution.
Psychological studies are hard, and human suffering is hard to measure. CBT is abusing this fact in order to appear scientifically valid, but as the saying goes, not everything that is measurable is important, and not everything that is important is measurable.
Yes, it is important to understand the "current state of affairs" and "desired state of affairs" for goal setting (again, something common in most "talk" therapies, and definitely not a new feature of CBT). But that doesn't mean that the moment you meet a CBT therapist, they give you a pad and ask you to write down these things - good therapists actually spend the first one or two sessions talking to you to understand your issues, figure out your personality, explore your problems to diagnose you, clarify your concerns, and try and establish a rapport and boundary with you. (The whole basis of "talk" therapies is that talking and listening does qualitatively help people - and hence it is an integral part of CBT too).
> I wouldn't be surprised if most of the people who seek therapy don't really have any major psychological issues, but are simply in need of some advice and support - CBT would be greatly exploiting that because there isn't even a test whether or not you need CBT - it's just assumed that it's a one-size-fits-all solution.
Depression and anxiety are the "common cold" of mental health - everyone of us experiences it more than once in our lifetime. So yes, you would be partly right in saying people who are mildly to moderately depressed and anxious "just need some support and advise". Luckily, this is where CBT really shines - it can cure depression and anxiety without any medication (and that's been validated in many studies - in fact, it was found that not only is CBT equally as effective as anti-depressants, it is also more long-lasting than anti-depressant medication - https://pubmed.ncbi.nlm.nih.gov/15809409/ ).
> CBT would be greatly exploiting that because there isn't even a test whether or not you need CBT
While CBT has recently gained popularity as a self-help treatment mode, note that it is actually an empirically investigated systemic psychological treatment with various "schools of thoughts" including ACT (acceptance and commitment therapy), DBT (dialectic behaviour therapy), ST (schema therapy) CT (cognitive therapy). And there are CT diagnostics tests, like the Burns Depression Checklist or the Burns Anxiety Inventory test, that are used to determine depression and anxiety (respectively) to determine if someone needs CBT. On the more advanced issues, a psychiatrist has to diagnose if there are other serious issues (like personality disorders) at play before the treatment modality is decided. So yes, while you are absolutely right that CBT is not a "one-size-fits-all" solution, only an unethical therapist would try and treat you with CBT without proper diagnosis.
While the media may portray that therapists want to keep you dependent and talking with them forever (to earn money) the reality is that a good therapists will actually recommend you to someone else if they feel you aren't progressing under their care.
Placebo, maybe. Couldn’t care less. It worked, for all my purposes.
Some people take 500mg but I couldn’t find that in Canada. Also, despite selling Magnesium + Calcium supplements, apparently the Calcium competes with the Magnesium for absorption so never take those together.
I would argue with this statement. Antidepressants don’t work better than active placebos like atropine that make you feel “something is different” like dry mouth or elevated heart rate.
https://blogs.scientificamerican.com/cross-check/are-antidep...
I did however manage to recover because I got supplements (vitamins/minerals) and I think those helped me enough that I managed to stop drinking soda for a while, only tea first then water and when I lost about 20kgs, my deppression went away.
I stopped taking vitamins after I ran out for a while and I gained weight again, so I definitely think it's something I have a deficit of.
Nowadays I am diagnosed so I take concerta, but I also take additionally the supplement (vit/min) and additionally taurine (since I saw the benefits of supplements myself not gonna lie that I am biased about them, so now I saw the study that claimed that it might help prolong your life so I said why not since it's extremely cheap and just bought a 400 pills of taurine).
Is my ADD "cured"? no, but I do notice that I am somewhat more productive when I take it than not, you can't really feel the concerta, like you can a drug, it's mostly just that you without noticing lack a bit of that self restriction you have to doing mental tasks when you have ADD.
This article makes the same mistake as many other journalists: You don’t need a deficiency of a neurotransmitter for a medication to have an effect.
For an obvious example: People experiencing severe pain don’t have an “opioid deficiency”, yet opioid medications can alleviate their symptoms. Likewise, you don’t need to have a “serotonin deficiency” for drugs that interact with serotonin to have an effect on depression.
The whole “chemical imbalance” theory of depression was a reasonable guess at the time, but neuroscience largely moved past it decades ago as a singular explanation for depression. It has largely persisted among pop science, though, which creates confusion every few years when journalists get ahold of some scraps of research and try to stir up some controversy about depression medications.
Basically, ignore this section of the article. Serotonin deficiency was never necessary for SSRIs to work and we’ve known that for decades. The authors of these books throw out some vague explanations for why they think they work, but the reality is that it’s all very complex and our understandings are still evolving. Engineers tend to hate medicine because they want to think of the brain as a well-understood computer program that can be debugged and treated with the right inputs (medications) but ultimately a lot of what we know is from empirical testing. We can throw theories out all day long, but at the end of the day the only thing that matters is what shows results in studies.
Why this unnecessary dig in an otherwise good comment? As an engineer, I don't even think of most programs as being "well-understood".
https://www.nccih.nih.gov/research/research-results/painindu...
A nail gun shoots a nail through your foot. You go to the hospital and the nail is removed, but the pain remains.
There's nothing wrong with your opioid receptors: the pain you feel doesn't result from some kind of imbalance in them. It's 'valid' pain - no malfunction there - telling you that your foot is in a bad way.
When they give you opioids for this, it's not treating the core problem, at all (no problem w/the receptors). Yet it's still helpful, and does good, because it's dulling the overwhelming and excessive amount of pain you would otherwise be feeling.
Getting a nail stuck through your foot is more like a close friend or relative dying. Having chronic pain is more like having depression (well, that and chronic pain very often leads to depression, and the reduction in opioid receptor availability may be somehow related, but that's a whole other thing).
The parent comment's point about opioid receptors becoming less available in chronic pain (and the linked article pointing out that opioids are generally terrible for dealing with chronic pain) is quite relevant here. Opioids kind of work at first for chronic pain, but they progressively work less and less and have increasingly negative side effects over time. There are certainly some parallels with many people's experience with some neurotransmitter targeting meds.
None of this means that GP is necessarily wrong about their assertions regarding SSRI and similar medications, but it is worth stopping to consider the possibility at least.
Me most of all. I haven’t had intense thoughts for years, whereas they were a daily occurrence before.
I started in 2016, and can safely say I’d be a worse person without it. I only wish I’d started when I was 17, but unfortunately my mom had the brilliant idea of slipping me antidepressants while saying they were something else, which made it rather hard to trust anything to do with antidepressants. I imagine people here have different horror stories that make it hard to just try them for a few months.
There may be no clear evidence that they work, but they do something for me. What do they do, if not work? It produced a positive outcome which wasn’t placebo.
Post SSRI sexual dysfunction. SSRIs cause decrease in sexual function for most people who take them while they're on them, but for some, it's permanent. There is no effective treatment, you are stuck sexually dysfunctional for the rest of your life.
Doctors do not warn you this is a possibility. Just bam, no warning, life ruined forever.
Since we’re being honest, the only effects I’ve noticed are going soft after 20 minutes or so, and more difficulty finishing. Sidenafil helps with the former. As for the latter, it isn’t every time, and I don’t mind it much, but everyone’s different.
I think it’s important to address this issue head on though. The horror stories of sexual dysfunction were one reason I put off trying antidepressants. But (a) you’ll see the effects coming on gradually, (b) it’s not permanent, and (c) for me it wasn’t nearly as intense as people made it seem.
If yours goes away when you stop taking SSRIs, then you aren't suffering PSSD (post SSRI sexual dysfunction) in the first place.
From https://annals-general-psychiatry.biomedcentral.com/articles...
> A 19-year retrospective cohort analysis was conducted using a computerized database of the largest HMO in Israel. ED was defined by phosphodiesterase-5 inhibitors prescriptions. 12,302 males aged 21–49 met the following criteria: non-smokers, no medical or psychiatric comorbidities or medications associated with ED, no alcohol or substance use.
> SAs were associated with an increased risk for ED (cOR = 3.6, p < 0.000001, 95% CI 2.8–4.8), which remained significant after adjusting for age, SES, BMI, depression and anxiety (aOR = 3.2, p < 0.000001, 95% CI 2.3–4.4). The risk for PSSD was 1 in 216 patients (0.46%) treated with SAs. The prevalence of PSSD was 4.3 per 100,000.
4.3 per 100k is lower than the US murder rate (6.8 per 100k). You’re right that it’s a consideration, but it seems pretty rare.
> Out of the 866 subjects of the study group, four subjects (0.46%) met full case criteria for PSSD (see Fig. 1B). These subjects were 32, 34, 37, and 42 years-old. They used antidepressants with at least a partial serotonergic mechanism (escitalopram, paroxetine, imipramine, or nortriptyline) for 4–8 months before initiating treatment for erectile dysfunction with PDE-5 inhibitors (all used tadalafil and vardenafil, but not sildenafil). They continued to have erectile dysfunction after drug discontinuation as evidenced by 3.6–14.8 months of PDE-5 inhibitor treatment at the end of the study period. The prevalence of PSSD in males of ages 21–49 years of the population of the CHS Tel-Aviv district is 4.3 per 100,000 (4 in 92,476).
4 in 866 is pretty good odds, but everyone has different risk profiles. I’ll be sure to mention it next time Prozac comes up.
I got to watch in real time as my libido evaporated, immediately desisted the pills and yet...
I say this as someone who kept his SSRI induced asexuality to himself for 20 years; I was ashamed and humiliated.
Zyban though, somehow that made girls pretty again.
And mushrooms dragged me back from a long bout of suicidality with a single dose.
I just want to point out for understanding, that placebo effects are real effects; and even more surprisingly, they can work even if you know you are taking a placebo. It's completely legitimate to consider placebo effects part of the efficacy of a medication.
> For some commentators, the recent downfall of the chemical imbalance theory has cast doubt on the use of existing antidepressant drugs, which were meant to restore the lost serotonin. Yet the data certainly suggests that they work better than placebos – and the authors of these two new books can explain why. For Nord, it is because antidepressant drugs help to correct the fundamental biases in someone’s perceptions of the world. This change occurs incredibly quickly. People with depression are more likely to see anger, and less likely to see happiness, in neutral facial expressions – but in many patients, this tendency begins to disappear after they have taken just one antidepressant pill. Gold, meanwhile, points to studies showing that our current antidepressant pills encourage the birth of new brain cells and neural connections, which would help people to break free of the hyperactive stress response.
Over the course of 25 years I tried 42 different anti-depressants (practically all of them across all classes), atypicals, mood stabilizers, off-label Parkinson’s drugs, off-label anti-seizure drugs, benzodiazepines, you name it. Often multiple times (because time, age, etc) in incredible varieties of combinations, dosages, etc, etc.
The 43rd changed my life.
It’s rough, frustrating, and long but you need to keep trying keys until one (or more) fits the lock. Whether that’s these kinds of medications, ketamine, mushrooms, therapy, selling your worldly possessions and becoming a monk, whatever.
It doesn’t really matter how you do it - it’s life or death.
Yeah, off-label is something I hear a lot... and indeed it's super super frustrating
and thanks.. :)
Easily available online (at the moment) through telemedicine from places like this one https://www.joyous.team/ (no affiliation) that charges $129/mo.
It does sound interesting though.. maybe I should poke him a bit more about it.. thanks :)
It’s worth keeping in mind that long ago I was prescribed Prozac but didn’t take it consistently, so I didn’t notice any effect. It wasn’t until I did it every day for 60 days that I noticed changes. It’s like https://youtu.be/D8BZPAeCGEc?si=xjYSD9t5DprFfMRm but easier, since you just need to take a pill every day.
So keep consistent, and keep your head up. I believe in you.
some days are better than others I guess... lot of not so fun ones. that particular day was just a minefield I guess
I have something new to try though. So I guess it's something.
Intense in both directions or only intensely negative?
But again, everyone is different, and you should monitor your own condition along with your doctor and adjust dosage accordingly.
The article does disambiguate between (what they call) "true sadness" and depression:
> Gold dismisses the common idea that depression is medicalised sadness, noting that “true sadness is often associated with cherished, loving memories of, for instance, a lost loved one, combined with grief over their loss, and, at times, a bittersweet feeling encompassing both the bounties of life and the harsh reality that all relationships must come to an end”. Such feelings, he says, are typically unavailable to seriously depressed individuals, whose emotional repertoire is constricted to “a deadening litany of self-excoriation and hopelessness”.
And I think it is an important distinction. "Depression" has been treated as a catch-all term for what turns out to be a myriad of different causes that happen to look the same to an outside observer.
I personally experience chronic inflammation due to Crohn's disease and it does cause depressive symptoms even though there isn't any major external reason that I should feel that way.
And it makes no sense that the same treatment should be used in both of our cases.
-- Carol Hanisch, 1970
> If you get exposed to a lot of glucocorticoids, you're more at risk now for depression. You can see this epidemiologically: you get people, and statistically, before their first major depressive episode something awful stressful occurs. Have one of those first depressive episodes, due to some stressful event, you come out the other side eventually. You are no more at risk for depression than anybody else. Along comes a second major stressor, and you fall into depression, come out the other end, no more at risk than anyone else for depression. Somewhere around the fourth or fifth stress-induced depression, something happens and things start cycling on their own there and you no longer need a major stressor to cause you to get depressed like that. That's when the clocks are off and running. That's the transition.[0]
Will your life ever have meaning again? Probably not, no. Not the meaning it had before those three very important people were taken from you. Probably nothing of value makes sense, anymore, not in light of their absence. What's the point of watching TV you can't talk about with them? What's the point of going on trips you can't share photos of with them? At least, that's how I've been thinking about my losses.
I'm just a stranger on the internet, but if you told me life had lost its meaning I would believe you, and you would be right.
...but there is also a neurological component.
0. Dr. Robert Sapolsky, PhD, 2009 - https://youtu.be/NOAgplgTxfc?t=2165&si=P0pg-W5lOe3n0LWb
Time theoretically will help heal your wounds but for many it's not that simple (as the article points out, we're still trying to figure it out).
An incredibly bitter irony is that one can take steps to ameliorate the condition but when in the throes of it, finding the strength and ability to do so is incredibly challenging.
If you want someone to talk to, you can email me or DM via Twitter. Happy to just listen.