Creature Comforts: Pets and Mental Health


There’s nothing better than a cozy evening spent snuggled up with your dog or cat, right? Pets come with lots of responsibilities, but also with plenty of benefits for our health. I know how it weighs out for me- strongly positive. My dog has been an enormous help in my recovery from depression, and she also helps me regulate my nervous system when Sensory Processing Disorder gets in the way. But what does science say about pets and mental health?

Animal Assisted Therapy

I’m particularly interested in how pet ownership affects mental health and wellbeing, but perhaps it’s best to start with the research on therapeutic interventions. I’m guessing that it’s much easier to study the effects of human-animal interactions in the context of short visits than in the context of pet ownership for a few reasons.

  1. It’s more difficult to determine causality in cases of pet ownership. Are people with pets healthier, or are healthier people more likely to have pets?
  2. Many pet ownership studies rely on participants’ ability to report results over a long period of time, as opposed to short AAT sessions.
  3. AAT is implemented and monitored by professionals who keep detailed records.

Before I even read any articles, I was expecting to find that AAT is backed by a sizeable amount of evidence supporting the link between pets and mental health. After all, I’d seen those news stories about unconventional Emotional Support Animals, and those aren’t necessarily trained to perform a therapeutic role.

A 2017 review compiled data from 18 studies of AAT. In 15 of those studies, at least one positive effect was found, although the authors point out that most of the studies found no significant effect on treatment outcome. Overall, the review suggests that AAT, particularly dog assisted therapy, provides mild to moderate effects. Not bad, given how many variables are unavoidable when it comes to animal interactions.

Therapy dogs have been successfully used as part of treatments for elderly Alzheimer’s patients as well as in promoting social interactions in a long-stay psychiatric population.

So, if AAT is mildly or moderately effective in short “doses”, how does near-constant interaction with animals affect us? I’m wary of extrapolating too far because pet ownership is certainly not just a scaling-up of petting a therapy dog at your university’s library during finals. There’s a lot more to it; perhaps the responsibility, stress and frustration when a pet misbehaves, and of course, the emotional pain of losing a beloved companion outweigh the benefits of interacting with animals.

My Roommate is a Quadruped

Did y’all see that Reddit thread about how weird it would sound if we called our pets “roommates”?


My roommate ate every Lactaid pill out of my mother’s purse and left all the wrappers on the floor. The other day, I walked into the kitchen to find my roommate standing on the table, eating jam right out of the jar. I know someone whose roommate ate crayons and then pooped rainbows for a week.

Pet owners share their lives with their pets; not just their time and energy, but their homes, too. Many people consider their pet as part of their family, and I can see why (and not just because I’m one of those people). Anecdotally, I can understand why pets and mental health benefits are often linked in our minds.

Social Support

A qualitative study of people with mental health conditions, conducted in 2016, had participants map out their social support networks in three concentric circles, the innermost circle being the most important. 25 of the 54 participants were pet owners, and the majority of them placed their pets in the innermost circle. The researchers identified several common ways in which participants reported benefits from owning pets.

  • Establishing routines
  • Distraction from symptoms (e.g. hallucinations, suicidal ideation)
  • Sense of certainty that pets would reliably provide support
  • Caring for pets gave participants a sense of meaning
  • Reducing the stigma of mental illness through pets’ unconditional acceptance of owners
This meme will one day be horribly outdated, but that day is not today.

Another study with a similar design had me grinning from ear to ear- some of the transcripts of participants talking about their pets are delightful. Although this study focused more on chronic physical illnesses, I noticed some relevant parallels. The authors describe the apparent infantilization of pets and hypothesize that it provides a sense of reciprocity that chronic illness sufferers may not have in their human relationships. Those with chronic illness- physical or mental- often report feeling like a burden on others. Doting on a pet, it seems, alleviates some of those feelings and makes the pet owner feel needed.

Soothing or Stressful?

Everyone feels distressed from time to time. Petting an animal can help calm someone in distress by reducing blood pressure and reactions to mental stress. One study, hilariously called “Friends with Benefits: On the Positive Consequences of Pet Ownership,” experimentally found that pets were able to keep their owners from dwelling on negativity caused by social rejection.

For people with Sensory Processing Disorder, pets can provide a myriad of soothing sensory benefits. They offer tactile feedback in the form of fur, feathers, wool, etc., and the extra snuggly ones can provide deep pressure (depending on how heavy they are). Indirectly, pets provide proprioceptive and vestibular input simply by requiring interaction- walking, feeding, bathing, and training them. Pets tend to have less complex, more predictable social cues, which may make them less stressful to interact with than humans, especially for people who are easily overwhelmed.

Some of the Drawbacks

On the other hand, pets are their own entities with their own agendas. They don’t always do what we want them to. For instance, my dog barking at me while I try to drink my coffee in the morning is definitely NOT soothing. There are distinct disadvantages to owning a pet when you’re affected by SPD and/or mental illness. They can be messy and loud (unless you like those things- then add that to the advantages list), and sometimes they get in your personal space when you don’t want to be touched.

The Intersection of Pets and Mental Health for Me

Despite the frustrations and occasional discomfort, I’ve found pet ownership to be immensely helpful and rewarding. My dog reminds me to get outside and walk, to look up from my computer every once in a while (she’s being quiet…too quiet), and to enjoy all the little pleasures- long naps, eating with gusto, and rolling in smelly things.

Wait- not that last one. Don’t do that.


Can You “Grow Out Of” Childhood OCD?

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!

A black and white image of a set of human female chromosomes scattered against a black background

Understanding MTHFR and Depression

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.

By National Human Genome Research Institute – Public Domain, https://commons.wikimedia.org/w/index.php?curid=41175399

L-methylfolate: my silver bullet?

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.

By Darryl Leja, National Human Genome Research Institute – https://www.genome.gov/dmd/img.cfm?node=Photos/Graphics&id=85182, Public Domain, https://commons.wikimedia.org/w/index.php?curid=50712171

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.

Most of the studies I’ve seen, including meta-analyses, lean towards accepting a link between MTHFR and depression, especially for homozygotes, who have the least MTHFR activity. Experiments have shown evidence that active folate supplementation can be an effective adjunct therapy for treatment-resistant depression.

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.

(Featured image credited to: Abogomazova – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=25074990)