The sun has left us for a few rotations, only peeking out from behind the clouds in short intervals. It smiles down on us weakly, filtered through miles of gauzy cotton. How did I manage a more northern latitude? Just a day or two of relative darkness is enough to upset my balance.
Maybe I’m searching for explanations that don’t exist. To excuse my mood as simply a mirror for what’s outside. It seems impossible that such a minute change could affect me so drastically, and yet when I embark on my morning walk, the slow, chemical drip of melatonin invariably calls me back to bed. So, I hunker down, and I wait for February’s grip to loosen. Love, Your Brain
Sometimes I run because it’s when I feel strongest. I run because I love the feeling of my muscles working beneath my skin, my breath matched to my stride. Breathe in for three steps, breathe out for three steps. I love the sense of accomplishment, knowing that my body can carry me further than I think it can. Sometimes I run because it gives me joy. The simple pleasure of the wind in my hair and the sun on my face, moving with a body I’m thankful for. My body is a canvas for my mental state; when I’m well, I run for the joy of it. When I’m unwell, I run because it’s just another way to hurt myself. I run because at mile three I’m still thinking about cutting, but by mile five my brain is numb. Breathe in for three steps. Breathe out for three steps. I run because maybe if I can push my body to obey me, my brain might follow suit. I run because to be exhausted is to be empty, and where could my depression have gone except to have been left behind on the path? Expelled by my lungs, my racing heart, my wrung-out muscles. I run because it makes me feel good, and because sometimes, it makes me feel nothing at all.
Several years ago, I awoke with a slight but sharp pain in my chest. I went about my day, doing my best to ignore it. I thought it was one of those random, passing pains that bodies get sometimes. But the next day, it was much worse. Every time I inhaled, stabbing pain shot through my chest. I also was developing severe pain down my left shoulder blade and around my ribs. I debated going to the doctor for three days; meanwhile, I couldn’t sleep unless I was sitting up, and moving at a pace slightly faster than your local library’s Wi-Fi left me in breathless tears. It turned out that I had pneumonia, which was strange because I hadn’t been sick beforehand, nor was I obviously sick in any way other than having debilitating chest pain.
When I reflect on that experience, my first thought is “why did I not go to the doctor right away?” I’m certainly not a fan of going to the doctor, and I don’t like to draw attention to myself, even from concerned family and friends. But neither of those reasons fully explain why I waited.
I didn’t go right away because I didn’t know if the pain I was experiencing warranted a trip to the doctor. I distinctly remember thinking “am I imagining this?” Let’s let that sink in. I couldn’t get out of bed without first psyching myself up for several failed attempts and some tears, and I wasn’t sure if I was just~~imagining~~it.
My brain is always a little confused about the information it’s receiving because I have trouble with sensory discrimination. When someone asks me “how do you feel”, nine times out of ten I’ll go “I dunno”–because I really don’t. Especially when it’s something new, I don’t know what the heck I’m feeling from outside or inside my body. So, when I mysteriously developed pneumonia, my thought process went a little like this:
Hmm. This hurts. I think my chest definitely hurts. Should I go to the doctor? They’re gonna ask me what it feels like. Is it burning, or stabbing? What’s the difference? Maybe it’s not that bad. How bad is bad? Wait, which came first- the chest pain or the shoulder pain? Are they even the same kind of pain? Maybe I’m imagining it- if I ignore it, it might go away. Good gravy, putting on socks is really hard. I’m probably fine, though.
Because I know that sensory processing disorder (SPD) makes me sensitive to a lot of stimuli, this often leads me to understate how I feel, be it good or bad. I aim to be neutral in all aspects- I’m feeling sensations more intensely or in a mixed-up way, so it must be wrong, right? When you spend many years confused about how you feel, you get pretty good at hiding it. So, on the outside, I can appear relaxed and calm, but on the inside, I feel like that screaming bird meme. You know the one.
My nervous system 85% of the time
Anyway, do as I say, not as I do (did). The problem with approaching sensory discrimination this way is not just that you might neglect yourself when you have pneumonia, although that’s certainly not optimal. On an everyday level, taking this approach perpetuates the confusion and only makes things worse. It takes practice to start listening to your body, and it might take some serious courage to start advocating for yourself. I try to remember that the way I perceive things might be different from what other people feel, but that doesn’t mean it’s wrong.
When I was 10, I felt compelled to tell my parents “I love you” every time they left the house. Going to the grocery store? I love you. Going to work? I love you. Going to the mailbox? I love you. The fear that something catastrophic will happen to family members is a common manifestation of childhood and adolescent OCD. I thought that if I failed to carry out this ritual, my parents wouldn’t know that I loved them if or when something terrible occurred.
I was also preoccupied with germs; my hands were cracked and bleeding from excessive washing, and I worried constantly about contamination. I always walked a specific pattern on the rug in the hallway, and I carefully watched the family dog to be sure I’d notice when he winked at me–so that I could wink back. I couldn’t tell you why I had to wink at the dog, I just had to.
I knew that these behaviors were irrational, and yet the anxiety it caused me to resist the compulsions seemed unbearable. I was afraid to go to sleep because I worried I might sleepwalk and harm my family in the middle of the night. Nearly every evening, I would tearfully confess my intrusive thoughts to my mother, convinced that she would be afraid of me for thinking such awful things. OCD commanded almost every aspect of my life.
Did I Grow Out Of It?
My parents tried to get me into therapy, but I was shy and ashamed, and simply refused to participate. So, I started taking an SSRI, slowly titrating up to the maximum dose. And incredibly, it worked. Suddenly, I was free from the torturous anxiety and embarrassing compulsions. I could be a kid again. Two years on, I slowly came off my medication. We waited, on edge, for symptoms to return, but they never did. I’ve often wondered why I never relapsed. It seemed impossible that something that had plagued me for so long had just vanished.
Thanks, PubMed
I wanted to know if other people had experiences similar to mine, so I headed over to trusty ol’ PubMed. I found several articles that explore the topic of OCD remission. Some have woefully small sample sizes and others are barely longitudinal, but there does seem to be a higher rate of OCD remission in the pediatric population than the adult population. The factors that influence this aren’t very well understood; some studies show that an earlier onset of symptoms predicts better outcomes, while others associate earlier onset with chronic, adult OCD. Don’t you just love conflicting results? I do, however, think these results can be reconciled.
Maybe It’s About Treatment, Not Age
A study published in 2014 followed up with children and adults with OCD over a three-year period. Children achieved remission more quickly than adults who had juvenile-onset of symptoms, but the age of onset did not affect the likelihood of remission. Instead, the authors show that the less time passes between the onset of symptoms and receiving treatment, the better the outcome.
This fits with the statistics on OCD treatment. In a different study by the same authors, children went an average of 1.5 years before receiving treatment, whereas adults reported a wide range of latency periods. On average, they went 14.5 years before receiving treatment, although the standard deviation was close to 12 years. Clearly, some adults suffer in silence for decades before getting treatment.
It’s plausible, then, that children who receive treatment soon after developing symptoms see remission more often, but children who endure a longer period of uninterrupted symptoms are more likely to have chronic OCD into adulthood.
The Takeaway
Multiple studies emphasized the importance of early recognition and treatment of childhood-onset OCD. Overall, I was encouraged by what I found during my deep dive into the literature. The sources I found all seemed to agree; long-term persistence of childhood-onset OCD is less common than it is for adult-onset OCD.
After all this, I’m still not sure whether I grew out of OCD. It’s difficult to determine whether anybody grows out of it without treatment because study samples come largely from inpatient and outpatient treatment centers. I will say that I occasionally get a sticky thought that reeks of OCD, but I set it aside fairly easily.
In a completely anecdotal way, this seems to me like the pathways that I was stuck in as a child had a chance to be rewired while I was on medication. Now, my brain can cope with intrusive thoughts pretty much like anybody else’s. If I had known that the chances were pretty good that I wouldn’t suffer from OCD forever, it might have been a little easier to cope as a child.
Treatment with ERP and medication offers adults and children relief from their OCD symptoms. So, if you have a kid with OCD, know that remission is possible. And for all the adults with OCD, know that there is hope, and you are not alone. Adults absolutely achieve remission as well. A 40-year follow-up study found that of 251 participants, improvement was observed in 83%. Those are pretty good odds!
Sometimes I wish someone would just roll me into the literal body shop and get me a self-care tune-up. Alas, it doesn’t work that way.
I’ve stopped using the term “self-care” to describe a lot of the things I do for myself. Hear me out, though. It’s not because there’s anything wrong with calling it self-care; it’s just that a lot of self-care tasks are not as flowery and gentle as the term implies. Sometimes you have to buckle up and make that phone call you’ve been avoiding so that your dentist doesn’t think you dropped off the face of the planet. (And so that you can get your teeth cleaned, I guess.)
I’ve found that reframing some self-care tasks as “corporeal maintenance” helps me tackle them with less procrastination. Something about approaching these tasks as simply maintenance and upkeep feels less daunting.
Here are some examples:
“Oh, my ‘check hydration tank’ light is on. Better go drink some water.”
Or “Didn’t I just go grocery shopping, like…oh, yeah, I guess it’s been a while. I should probably get some fuel for this week.”
If I call it “self-care,” I’m likely to not do it – either because I don’t care, or because I don’t feel worthy of being cared for. But, if you want to keep driving to the things you do care about, you have to get the oil changed every once in a while.
There’s a lot of talk about self-care these days; some criticize it and some embrace it whole-heartedly. There tends to be an atmosphere of self-indulgence when we discuss it; as if every act of caring for ourselves is rooted in all-encompassing positivity. And yes, self-care can be self-indulgent and rooted in self-love. Those things are necessary. But self-care is also doing the things that aren’t very fun but are kind of non-negotiable when it comes to being healthy.
It may very well be the case that you do complete these tasks out of self-love, and I think that’s great. In fact, that seems like a wonderful goal to work towards. But if you’re not there yet, and calling those unpleasant/boring tasks “self-care” feels insincere, go ahead and call them something else. Whatever floats your goat.
“I need a new bathing suit”, I told my mother before heading out the door. A list of criteria floated through my mind. It needed to have shorts, or maybe a skirt, which had to go down to my mid-thigh. Of course, it should be cute so as not to arouse suspicion or too many questions.
Buying a bathing suit with a skirt was just one of many ways I hid my self-harm from those around me. In my third year of college I became depressed, and the following summer I started self-harming. I did it in secret and hid the evidence. I knew that altering my clothing choices would spark concern, so I continued to wear shorts that barely covered the still-healing wounds. Looking at photos from this time is painful. I remember desperately trying to appear well; smiling while anxiously pulling my shorts down to cover my secret. It consumed me entirely until cutting was all I thought about. Fighting the urge to do it was like trying not to sneeze. I would think about it constantly for days or weeks until I could take no more, and give in just to make the thoughts stop.
At age 4, I was diagnosed with Sensory Processing Disorder, a neurological condition that affects the brain’s ability to make sense of a world filled with sensory stimuli. I screamed getting my hair washed, I refused to go outside until my mittens were tucked into my sleeves, and anytime I fell down, I held my breath until I passed out. As a child, the world was a scary place, and although I learned to cope with my differences, the pressure of college and my looming adult life plunged me into numbness and depression. I began to feel outside of myself when in busy areas, and when I closed my eyes, I felt a gentle rocking as if I were on a boat. Cutting was a way for me to ground myself when things felt out of control.
All of this has taken me months to discover, though, and it was terrifying to not understand my own actions. Reaching out to my loved ones helped immensely. After months of hiding my self-harm from my mother, I told her about it the night before I moved back to school. When I showed her, she looked at the rows of raised, red scars and softly said: “that’s what I thought was happening.” All of the effort I had put into protecting her from the truth, for nothing. She had known for weeks, and I probably caused her more worry by staying silent. The next day, I left to begin my final year of college, four states away. I began seeing a therapist who encouraged me to create art that expressed my emotions, and when I found myself in a hazy stupor, I would open my sketchbook instead of turning to self-harm. But removing self-harm from my list of coping mechanisms made me feel wildly out of control, and I spiraled into a state of suicidal ideation. By the time I reached one month without engaging in self-harm, my therapist was gently suggesting hospitalization. Thankfully, I switched medications, and although it wasn’t the right one for me, it helped enough to keep me safe.
What I’ve learned about self-harm and other damaging coping behaviors is that they give you the illusion of control. Over time, however, it grows into a slippery beast of its own. You may eventually wonder how this action that you perceived as giving you control has come to hold you so tightly, until it doesn’t feel like a choice at all. Months of therapy, various medications, and the unwavering support of my friends and family have slowly allowed me to come out of the darkness. Today, I have gone over 10 months without self-harm, and I’ve come to understand that saying “no” to that self-harm voice gives me true control that is much more effective than self-harm ever was.
A couple of years ago, my psych nurse suggested we send some of my cheek cells to a lab for genetic testing. I was severely depressed and hadn’t had much success with the antidepressants I’d tried. With a significant family history of depression and other mental health issues, it seemed likely that there was a genetic component for me.
My psych nurse told me that for some people, a genetic abnormality affects the activity of a particular enzyme that’s implicated in psychiatric conditions (and many other illnesses). People with this mutation can be helped by taking what’s essentially a supplement (I believe she even said it was “like a vitamin”), l-methylfolate. By taking the product of this hindered metabolic process in pill form, it fills in the gaps that your faulty enzymes have left behind. Because it was a rather serious situation, we decided that we may as well add this supplement to see if it helped. I told her I’d think about the genetic testing.
A couple of weeks later, we revisited the idea. The l-methylfolate seemed to be helping a little, but not dramatically. I had figured that the testing would be unnecessary; if the l-methylfolate helped, we’d know I was a mutant. If it didn’t, we’d move on to something else. It wasn’t that cut and dry.
Why the reluctance, you ask?
Perhaps there was a little anxiety about what I might find out about myself, but I suppose that’s a topic for my therapist. Mostly, I was skeptical. Genetic research has advanced tremendously, but the mechanistic aspects of mental illnesses are still rather poorly understood. Could a DNA profile really tell me why I was depressed?
Well, I’ll spoil the ending for you and say “Yes. Kind of.” Curiosity won out, and I agreed to part with some of my genetic material in the name of science and not wanting to be depressed forever. The results, pared down to what’s important for clinicians and patients to understand, were interesting- and rather ambiguous.
The science behind MTHFR mutations
The gene in question is called methylenetetrahydrofolate reductase (MTHFR). Our genes code for proteins, and enzymes like MTHFR are one type of protein. MTHFR is involved in something called one-carbon metabolism, which has effects on the production of neurotransmitters.
First, some genetics background
Harken back to your high school or college biology class; remember alleles? A gene and an allele are not exactly the same thing. A gene is essentially a small segment of a chromosome. The DNA sequence of a gene codes for a specific sequence of amino acids, which comprise proteins. An allele, however, is a variation of a gene. For each gene, you got one allele from your mom and one from your dad. I received a combination of normal and mutated MTHFR genes. Mutation is how variation occurs, and the process itself is neither good nor bad; it just is. Some mutations are adaptive, some are neutral, and some are deleterious.
Two MTHFR mutations
There are two main mutations on the same allele that seem to affect this enzyme’s activity. As usual, the names are cryptic; they’re called C677T and A1298C. The numbers and letters refer to where in the allele one nucleotide (or one “digit” in the DNA code) has been changed to another, and the substitution that’s taken place. In general genetics contexts, heterozygotes have different alleles from mom and dad, while homozygotes have identical alleles.
In the context of mutation research, there is typically one genotype that is referred to as “wild type,” meaning it contains no mutations and has full function. In this case, imagine the big “B” homozygous chromosome in the image above as the “wild type” and the little “b” as the mutation in question. The letters in examples like this are simply ways to represent alleles in a theoretical framework. The order of the letters is written out because, without further research, it’s difficult to tell which parent the mutation came from.
To bring it around to MTHFR, I’m a heterozygote for both of the main mutations (this is called “compound heterozygosity”). My genotype for C677T is C/T. The C (cytosine) is the nucleotide in the normal allele and the T (thymine) is the substituted nucleotide in my mutated version. I got the C from one parent and the T from the other. I’m also a heterozygote when it comes to the A1298C mutation. My genotype is A/C, where the A (adenosine) is the normal one and the C is the mutant.
The problem lies in the metabolism of a key metabolic precursor: a biologically-active form of folate. The product of this reaction is 5-tetrahydrofolate, which provides a methyl group for epigenetic regulation. In other words, when MTHFR is mutated, the system that controls gene expression and, ultimately, neurotransmitter production, is affected by a lack of this enzyme’s product because the enzyme’s function is reduced. This is the gap that the supplement I take fills in.
Enzyme activity
Meta-analyses suggest that C677T homozygous mutants (they have two mutated copies) have a 75% reduction in MTHFR activity, and A1298C homozygous mutants have a 39% reduction in enzyme activity. Heterozygotes for each mutation have less severe reductions in activity, but if you’re a compound heterozygote (like me), that results in a 52% reduction. So, I have slightly less than half the enzymatic activity for MTHFR than a normal, non-mutant.
MTHFR and depression
That all seems pretty straightforward, but take a look at the plethora of studies that exist on the internet, and you’ll see why I was cautious. Some have found significant relationships between MTHFR polymorphisms and psychiatric conditions, and yet others haven’t. There are some studies that say that there is no difference between mutant and control subjects when it comes to depression. Others suggest that carrying a mutated MTHFR allele predicts depression when the person is exposed to childhood trauma.
The consensus seems to be that more research is needed, although increasingly, there does seem to be a relationship between MTHFR and depression.
For me, I’m content to believe that at least some of my struggles can be traced back to MTHFR. The supplement does seem to make my antidepressants more effective. Plus, that’s not all that my genetic report showed. I also have a weird serotonin transporter that makes SSRIs less effective and increases my cortisol release in response to stress. I’m glad I did the test, at the very least because it helped me to accept my disorder as valid and offered insights into my mental health..
The future of mental health treatment
Is this a sure-fire way to treat mental illness? I’d say not yet, but it’s certainly valuable. Personalized medicine seems to be a buzzword floating around these days, and the implications of genetic research for how we approach mental illness are fascinating. Maybe when the relationships between genes and mental illness are elucidated a little more clearly, we can finally kick the stigma and misconceptions out the door. One can hope, at least.
Love, Your Brain 