There has been a lot of conversation in the media recently about SSRIs and whether they might be linked to violence. While I welcome research into this area, I believe it is risky to make broad claims without careful context. We also cannot ignore that many individuals do find relief and improved functioning with this class of medications. The way we talk about them matters, both for those who are struggling and for those who are currently benefiting.
As a functional medicine provider, I always begin by addressing root causes first—nutrition, lifestyle, inflammation, gut health, toxins, infection, genetics, and more. If after thorough work, my patient and I feel an SSRI may be appropriate, we approach it thoughtfully: slowly, carefully, and with the lowest effective dose.
SSRIs are not “good” or “bad.” They can sometimes be helpful—but always as part of a comprehensive plan, not the entire plan. Unfortunately, too much of conventional psychiatry relies on a medication-first model, which ignores the broader context of mental wellness.
Depression Is Complex
Depression is never just one thing. It can be:
- psychosocial
- spiritual
- inflammatory
- toxic
- related to methylation or genetics
- driven by gut dysbiosis
- worsened by lack of sunshine
- influenced by trauma (past or present)
- triggered or sustained by infection
- associated with low thyroid function
Wellness depends on many layers: exercise, sleep, healthy relationships, meaningful connection, nutrition, and trauma work are all essential pieces of recovery. Simply prescribing medication without this context misses the mark.
Vitamins Should Be First-Line
We know deficiencies in activated B vitamins can drive mental health symptoms. Amino acids like 5-HTP and botanicals like saffron (Crocus sativus) can support serotonin synthesis and improve brain signaling.
When patients have worked through lifestyle, environmental, and nutritional foundations—and symptoms like depression, anxiety, or OCD remain—genetics often provide insight into the missing pieces. In those cases, SSRIs may have a role, but only when combined with a comprehensive, functional approach.
Genetics and Why They Matter
- MTHFR: Variants such as C677T and A1298C reduce the body’s ability to convert folate into its active form, affecting neurotransmitter methylation. Infections that increase oxidative stress can make this worse, raising homocysteine and further lowering serotonin and dopamine balance.
- MTHFD1: Mutations here impair folate cycling in the nucleus, reducing DNA repair and neurotransmitter synthesis. Chronic infections or inflammatory triggers can put added strain on this pathway, leaving patients more vulnerable to mood symptoms.
- FOLR1: Variants or autoantibodies to folate receptor alpha can limit folate transport into the brain, leading to cerebral folate deficiency. Infections and immune dysregulation are known to trigger or worsen FOLR1 autoantibodies, making folinic acid therapy especially valuable in these cases.
- HTR1A, TPH1, HTR2A: These serotonin-related genes influence production and receptor sensitivity. Infection-driven inflammation (via cytokines such as IL-6 or TNF-alpha) can downregulate tryptophan metabolism, diverting it into the kynurenine pathway. This lowers serotonin while increasing neurotoxic metabolites, which may explain why some patients experience worsening anxiety or depression after infections.
- ADRB2: Genetic variation in the beta-2 adrenergic receptor affects stress signaling, gut function, and quality of life. These pathways intersect with inflammation and neurotransmission, further shaping mental health outcomes.
We also know there are genetic differences that make SSRIs less effective, tied to low BDNF, dopamine regulation issues, or heightened stress responses. Infections can amplify these weaknesses—by lowering BDNF, increasing cortisol, and dysregulating immune-neurotransmitter signaling. Could it be that the rare but concerning reactions sometimes seen are linked to these genetic patterns, especially when infection and inflammation are not addressed before prescribing?
How I Prescribe
In my practice, SSRIs are never the first step. If prescribed, it is with the intention of supporting stability while the underlying work continues—not as a lifelong solution. Ideally, once a patient has been stable for at least a year, we can explore a careful, gradual taper.
It’s also important to emphasize: SSRIs should never be stopped abruptly. They require slow, monitored weaning, often with compounded small doses, to avoid severe withdrawal symptoms.
A Personal Note
I want to share a part of my own story. After the birth of my first child, I went through severe postpartum depression. At that time—23 years ago—the only option I was offered was Lexapro. I took it, and it helped me through one of the darkest seasons of my life.
But that was only the beginning of my healing. Over time, I discovered exercise for the first time, began eating well, and learned about my own genetic methylation needs. Today, instead of medication, I take a personalized compounded vitamin—something I also use with many of my patients. This targeted support has become part of my long-term stability.
When I’m not as consistent, I can feel symptoms returning. That personal experience is why I believe in a thoughtful, layered approach: Lexapro once helped me, and later functional medicine tools helped me sustain recovery. Medication can sometimes be an important bridge, but it should never be the only answer offered.
Collaboration and Consent
Medication decisions should always be a collaborative process between the patient and their provider. With informed consent, risks and benefits can be weighed openly, and close monitoring ensures safety. No one should feel pressured into medication, nor should they feel ashamed if it becomes part of their treatment plan.
My Bottom Line
The way SSRIs are often prescribed—quickly, without comprehensive evaluation—harms too many people.
The prevailing approach in allopathic psychiatry tends to rely too heavily on SSRIs, often without the thorough evaluation patients truly deserve.
At the same time, within a functional medicine approach—when used thoughtfully, alongside lifestyle, nutrition, trauma work, infection management, thyroid support, and genetic insight—SSRIs can support recovery in certain seasons of life.
Patients deserve context, collaboration, and choice—not fear, shame, or rushed prescriptions.
References
- Akbarzadeh, F., Talaei, A., Nematy, M., Ganji, D., Ebrahimi, A., & Talaei, A. (2025). Short-term effects of folate supplementation in combination with vitamin B6 for treating acute manic episodes in bipolar I disorder: A randomized controlled trial. Brain and Behavior, 15(e70432). https://doi.org/10.1002/brb3.70432
- DeVos, L., Chanson, A., Liu, Z., et al. (2008). Associations between single nucleotide polymorphisms in folate uptake and metabolizing genes with blood folate, homocysteine, and DNA uracil concentrations. American Journal of Clinical Nutrition, 88(4), 1149–1158. https://pmc.ncbi.nlm.nih.gov/articles/PMC2728423/
- Field, M. S., Kamynina, E., Watkins, D., Rosenblatt, D. S., & Stover, P. J. (2015). Human mutations in methylenetetrahydrofolate dehydrogenase 1 impair nuclear de novo thymidylate biosynthesis. Proceedings of the National Academy of Sciences, 112(13), 400–409. https://doi.org/10.1073/pnas.1414555112
- Rossignol, D. A., & Frye, R. E. (2021). Cerebral folate deficiency, folate receptor alpha autoantibodies and leucovorin (folinic acid) treatment in autism spectrum disorders: A systematic review and meta-analysis. Journal of Personalized Medicine, 11(8), 686. https://doi.org/10.3390/jpm11080686
- Vrolijk, M. F., Opperhuizen, A., Jansen, E. H., Hageman, G. J., Bast, A., & Haenen, G. R. (2017). The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function. Toxicology in Vitro, 44, 206–212. https://doi.org/10.1016/j.tiv.2017.07.004
- Molina, E., Cervilla, J., Rivera, M., Torres, F., Bellón, J. A., Moreno, B., King, M., Nazareth, I., & Gutiérrez, B. (2011). Polymorphic variation at the serotonin 1-A receptor gene is associated with comorbid depression and generalized anxiety. Psychiatric Genetics, 21(4), 195–201. https://doi.org/10.1097/YPG.0b013e3283457a48
- Wigner, P., Czarny, P., Synowiec, E., Bijak, M., Białek, K., Talarowska, M., Galecki, P., & Szemraj, J. (2018). Association between single nucleotide polymorphisms of TPH1 and TPH2 genes, and depressive disorders. Journal of Cellular and Molecular Medicine, 22(3), 1778–1791. https://doi.org/10.1111/jcmm.13459
- Kushnir, V. M., Cassell, B., Gyawali, C. P., Sayuk, G. S., Nix, B. D., Drane, W. E., & Keefer, L. (2013). Genetic variation in the beta-2 adrenergic receptor (ADRB2) predicts functional gastrointestinal diagnoses and poorer health-related quality of life. Alimentary Pharmacology & Therapeutics, 38(3), 313–323. https://doi.org/10.1111/apt.12378
