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I have been known to lament that there’s nothing new under the sun when it comes to depression treatment, and thus, there is little hope for people with true treatment-resistant depression. (And by treatment-resistant depression I mean people who really have tried everything, and there are few in this category.)
But I forget how far we’ve come and how fast. It isn’t fair to say there aren’t new approaches to treatment-resistant depression because there are new approaches being researched and approved every year. Here are a few noted by Current Psychiatry article Innovative approaches to treatment-resistant depression:
We did think that we would be able to find a “bipolar or depression gene,” just as we’ve found a Huntington’s gene, that would allow for genetic testing of bipolar disorder and depression. Now we know, though, that hundreds of genes make up the cause of bipolar disorder and depression and the environment plays a key role in whether bipolar or depression manifest.
We once called depression a “chemical imbalance” and even though professionals have known this wasn’t the case for decades we haven’t really had any model that stood in for the chemical imbalance one. Now we’re considering that depression is related to an inflammatory process (yes, anti-inflammatories are being tested) and “studies show levels of inflammatory cytokines and interleukins rise during a depressive episode and decline when the depression remits.”
We once thought that depression was all wrapped up in neurotransmitters like serotonin, but we’re now realizing this is only part of the picture. One of the things we have now realized is that depressed brains shrink and this is likely due to a decrease in brain derived neurotropic factor (BDNF) and other factors involved in neuroplasticity and neurogenesis (the brain being healthy and able to properly create new cells).
As I mentioned, we used to think that serotonin was where it was at in terms of the causes of depression. We then widened our net to include the neurotransmitters norepinephrine and dopamine and while all three of these have a role to play in depression, we now realize that glutamate does too. I’ve been saying for a while that I think glutamate is the next big thing in antidepressant medication. We can see an example of that in n-acetlycysteine treatment.
5. From Pills to InfusionsPersonally, I’m not sure this is super-good news because it’s an expensive form of treatment, but we are now looking at intravenous (IV) infusions of medications as well as pills for the treatment of depression. The key example of this is ketamine. A ketamine infusion (NOT the street drug) produces an acute antidepressant response in people within 1-2 hours of taking it, and this includes people with treatment-resistant depression. The antidepressant effect may be due to a surge in BDNF and neuroplasticity changes probably due to the direct concentrations of the drug that are possible through an IV infusion. However, this happens after the acute effects and the mechanism of action for those is not yet known.
Well, this isn’t new if you ask me but we are getting more intelligent about it. We now are using more evidence-based research in deciding what drug to add to another in cases of treatment-resistant depression. Additions to antidepressants for depression may be:
This isn’t overly new either, but the idea is because medication affects all parts of the body, neuromodulation – which affects only the brain – is superior in terms of side effects. Neuromodulation includes:
The theory is that one day deep brain stimulation – where electrodes are implanted directly into your brain – will be as commonly used for treatment-resistant depression as it is in Parkinson’s disease. (DBS, by the way, is very promising for long-term, highly effective treatment of treatment-resistant depression but the test population sizes have been small for obvious reasons.)
So we are making headway. It’s important to understand that and not give up hope. We learn more about depression every year and new treatments become viable every year so look for one of the above treatments to be available near you sometime soon.
Natasha Tracy is an award-winning writer, speaker, advocate, and consultant from the Pacific Northwest. She has been living with bipolar disorder for 26 years and has written more than 2000 articles on the subject.
Find more of Natasha’s work in her acclaimed book: "Lost Marbles: Insights into My Life with Depression & Bipolar" on Amazon.
Connect with Natasha at the social media links below.
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I Got a Nclex question that read like this, Which approach by an UAP indicates the most effective approach to a depressed patient. and the answers choices were: A) Cheerful B) Empathetic C) Serious D) Humorous
So can anyone tell me what research shows to be the correct answer? Getting Depressed here
Natasha Tracy; I just wanted to say what great articles you have written, as well as being interesting and fact-filled they give me some degree of hope. BPII, still having meds adjusted…. anyhow
Thank you very much.
Do you have more information on ALKS 5461? Supposedly this looks promising.
Always worthwhile.
Natasha–this is such an excellent piece: cutting edge, wide-ranging, well-researched, hopeful, that I’m so pleased to have come across it. Am busy forwarding it to all the social media sites, since I don’t think it can get too much play. I don’t know how you consistently churn out one relevant, well-done post after another–but I’m glad you do! (Must sign off to I can take care of reddit, google+, digg. . . .). Best wishes, Candida
Hi Candida,
Thanks so much for all the sharing. I believe that it _should_ be widely shared as it’s important information for many people to have but, in truth, it can be hard to get people interested in “research” posts because they’re dryer than other types. I understand this but I will continue to write them as I consider them important.
Again, that’s for your support.
– Natasha Tracy
hello, i reckon that “compassionate use” can be given by governing bodies as a designation to a compound that shows great promise for a disorder that is difficult to treat. this precludes the need for the compound to undergo extensive multi-year even multi-decade clinical trials. it also permits government health programs to pay for it, either in part or fully. it seems reasonable to apply this to ketamine hcl treatment for bi-polar and uni-polar depression, and perhaps ptsd. these disorders notorious for their resistance to treatment. in lieu of a compassionate use designation, those who can afford to pay will get the treatment that can help them immediately, and those who don’t, will not. kind regards, g saint
Hi G Saint,
That sounds reasonable to me, but I’m not the one who makes the law on that sort of thing. I’m not sure how common that sort of action is by the government but I would think, not very.
– Natasha Tracy
dear ms.natash tracy, thanks, ever so for your kind words. studies look quite promising for ketamine. it appears 70% of seriously ill people are helped significantly. there are no long term studies, however. anecdotaly, one woman of 41 years w/ trd who had also tried ect w/ no positive result, was reported by her doctors to be doing well after 15 months of ketamine treatments. might you know how all of us might influence medicare and medicaid to approve payment of ketamine hcl treatment by having them designate this medication for “compassionate use”? some doctors in private practice and hospitals are currently utilising this protocol on an out-patient basis, however, i reckon yearly costs would be in the five-figure area, an out-of-pocket expense impossible for most patients. hoping all’s well w/natasha tracy. kind regards, g saint
Hi G Saint,
I’m sorry, I don’t know how to influence your healthcare system in that way. I’m sure you’re right that it would be very expensive but I suspect that you would have to wait for more research before it’s approved for that kind of coverage.
– Natasha Tracy
the anti-depressant effects of ketamine hcl 0.5 mg. per kg. i.v. are reported to occur shortly after administration of a forty minute drip. the increase of bdnf followed by the emergence of neurogenisis occur later, therefore the acute and immediate anti-depressant effects of ketamine hcl appear due to a mechanism of action other than bdnf induced neurogenisis. hopefully current and future studies will provide greater insights and could lead to a new class of medications.
Hi G Saint,
Thanks for the clarification. Honestly, that makes more sense. I’m going to update the article to reflect this. Thank-you.
– Natasha
Amazing ! I like the way you are writing more and more !
Thanks for a great article, it gives a lot of hope for folks ;)
One love.
Hi Ernest,
Thanks. I like to think it gives hope to people; I feel like it gives hope to me.
– Natasha Tracy