Hormone Augmentation of Anti-Depressants

So, those who have been following my blog for a bit know that I’ve been having health and mood issues for the past year or so. Well, I’ve entered yet another chapter of this epic saga, and thought I would give you an update.

Art thou ready, Harold?

So the last time I posted on this, the endocrinology appointment I had been waiting for THREE MONTHS had been postponed by a week, and I was feeling rather upset about it. Well, the appointment came at last. However, it didn’t get off to the best start. I told her I had lyme, I told her I had endometriosis (both of which could cause fatigue, my main complaint), and I told her about starting the hypothyroid meds and them getting rid of my depression.

And she goes, “Well, I don’t think you have hypothyroidism. I think that was the placebo effect.”

I felt like she had slapped me. I just blinked at her.

Like, I have no problem with the idea of something being the placebo effect. The placebo effect is very real–and growing!–and can work even when you know it’s the placebo effect that’s doing the work. Some researchers have also suggested that a lot of anti-depressants are actually just super-charged placebos. But it was just the sudden and total dismissal of my interpretation of my experience that was so stunning. She said this before she had done any blood tests or asked about my symptoms or my family history. And in fact, after I had told her about my symptoms and my family history, she agreed that after all, it MIGHT be hypothyroidism, and said she would do blood tests. Fine.

So she listens to my symptoms. I impress upon her that fatigue is my main symptom, but she seems to latch on to some of my other symptoms more, especially the fact that sometimes my hands shake. Now, they were shaking THEN because I was nervous, but they do shake sometimes. So do my brother’s–he thinks we both have benign essential tremor, which does run in siblings, and it basically means “sometimes you shake a little and we don’t know what’s causing it but meh, it’s fine. *handwaves*” Anyway, she started suggesting things I might have, like excess testosterone, Cushing’s disease (excess cortisol from your adrenal glands) and freaking acromegaly (WTF?).

You know, like Abraham Lincoln.

Interestingly, I have found in my research since then that most of these, though they CAN cause fatigue, cause it by hyping you up too much rather than by slowing you down. So, like, it’s not like she DIDN’T listen, but at the same time… I kinda felt like she didn’t listen.

Anyway, at least she ordered tons of tests (TONS. Like, twelve. The phlebotomist I saw said she’d never seen this doc order so many), so she must have taken me seriously. She also listened when I said I had crappy insurance, and she suggested a cheaper lab to go to, which was nice. I had to spit in test tubes at 11 PM for three nights running and essentially pee in a jar for 24 hours. It was delightful. [/sarcasm]

I’m just gonna leave this here.

Meanwhile, of course, I was researching, because that’s what I do. While it didn’t sound to ME like I had excess testosterone or excess cortisol, it DID sound like I had deficiencies in one of those, likely testosterone. So I fully expected that when all my tests came back, they would find something.

Finally I got the call. And the receptionist was like, “All your tests are normal! 😀 😀 ” like this is a GOOD thing.

Someone needs to be tested for inappropriate smiling disorder.

They just never seem to get that a negative test isn’t necessarily a good thing: now, not only do I still have the symptoms, but we STILL don’t know what’s causing them, so we can’t treat them. DOES THAT SOUND TO YOU LIKE A REASON TO SMILE??

I was pretty upset.

So I do what I always do when I’m upset about my health:

(I’m sure you can hear this coming)

I started Googling again.

I looked up Chronic Fatigue Syndrome, because I was afraid that was what I might actually have, and there are no effective treatments for CFS. Turns out that, in order to be diagnosed with CFS, you have to have unexplained, persistent fatigue for six months or more, along with at least four out of a list of eight symptoms. I had three.

Never been so relieved to get a failing grade!

But that still didn’t tell me what I had.  So, back to Google again: disorders and illnesses that may be mistaken for CFS. Well, it turned out there were a lot of them–including lyme and endometriosis! But one caught my eye: hormone imbalances.

Now, that makes sense, because testosterone and cortisol are both hormones. Plus, I had long felt that I had symptoms of inadequate progesterone, and one of those was fatigue.

And then I thought about it: I have a Mirena IUD, which works by releasing progesterone. I was also taking a progestin-only birth control pill, trying to flood my system with a lot of progesterone in order to stop my endometriosis from spreading/shut down my insane period. It hasn’t worked. But I got the Mirena in October of 2015 and got depression in December of that year, developing fatigue by June. The timeline made sense: I might have excess progesterone.

Sure enough, the symptoms of excess progesterone sounded pretty familiar, and included fatigue–as well as SEDATION! So I quit taking my birth control pill (I still have the Mirena).

I’ve started to feel a little more energetic–although part of that may be that it’s spring (I also have seasonal affective disorder) and I’ve started my new hobby of painting, which has helped my mood and given me something to look forward to. But I do think that stopping the birth control pill helped.

So here’s the question: why did an endocrinologist, who is supposed to be an expert on hormones, not look at my medications and figure this out long before I did?

Anybody?

But that’s not the end of it. Because I did… (drumroll…) some more Googling! And guess what? The National Institute of Health says that hypothyroid meds can help relieve symptoms in people who haven’t responded to traditional antidepressants like SSRIs.

T3 has most commonly been used to augment response to antidepressants in those who failed to respond to an antidepressant trial. These studies are reviewed in Table III These studies, whether open-label or controlled, generally show that up to half of patients who do not respond to an antidepressant trial will respond within 2 to 3 weeks after the addition of 25 to 50 g of T3. The notable exception is the study by Gitlin et al34 who failed to find a significant difference between T3 and placebo in the potentiation of imipramine in 16 patients with major depression. This study, however, involved a 2- week, double-blind, crossover design, which can be problematic in evaluating antidepressant treatment response. Another study compared T3 augmentation to lithium augmentation in tricyclic antidepressant nonresponders.37 Both augmentation strategies were found to be comparable in a 2-week placebo-controlled trial. This was the first study to directly compare lithium and T3 in tricyclic augmentation, but later studies did examine T3 versus lithium with SSRI nonresponders41,42 (see Table III). In view of the limitations of the individual studies involving tricyclics, a meta-analysis of these studies concluded that T3 may increase response rates and decrease severity of depression scores in patients refractory to tricyclic antidepressant treatment.43 Patients with T3 augmentation were approximately twice as likely to respond as were controls. Recently, there has been emerging data on the use of T3 to augment SSRIs,3942 the most commonly used antidepressants. The findings with the SSRIs are generally consistent with those for the tricyclics. Both open and controlled studies are generally positive, and indicate that T3 may be an effective augmentation agent for SSRI nonresponders. Recent data from the STAR*D trial42 showed that T3 augmentation had comparable response and remission rates to other augmentation options such as lithium, and a more favorable adverse event dropout rate, despite the fact that response and particularly remission rates were low in all treatment groups. (Source)

So it wasn’t placebo after all. Which makes a lot of sense, as my mom pointed out, because there were a number of things I tried before desiccated thyroid meds that I thought were going to help my depression–lyme treatment, getting back on Effexor, basically any SSRI I ever tried–and they never did. So if it had been placebo effect, wouldn’t it have worked a lot earlier? It seems most likely it was the augmentation effect of the T3.

TL;DR: I AM NOT GOING OFF MY DESICCATED THYROID MEDS, EVEN IF THE ENDOCRINOLOGIST TELLS ME TO. THEY CAN PRY THEM OUT OF MY COLD, DEAD HANDS.

So, being the irritating little know-it-all I am, I sent the link and quote above to my endocrinologist.

Because that’s how I roll.

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5 thoughts on “Hormone Augmentation of Anti-Depressants

  1. Pingback: My Miracle | A Little Gentian

  2. Pingback: The Thyroid Saga Continues! | A Little Gentian

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