I have a little bit of anecdotal information (and some research) to add to the Ozempic body of knowledge. It specifically relates to the psychological side effects of ozempic, and the emotional changes that can happen while using this medication.

A month or so ago I got ChatGPT to do a deep research dive into the possible interactions between Ozempic and amisulpride and/or mirtazapine.

Firstly, it suggested there is evidence that semaglutide has a neuro-protective effect, with currently unknown mechanisms of the drug protecting our brains from alzheimers and dementia. [1]

Secondly it found that there is no known interactions with antipsychotic or antidepressant medications.  “It is metabolized by general proteolysis (not by CYP enzymes), so it does not affect hepatic drug metabolism. Semaglutide does slow gastric emptying, but clinical studies found no significant impact on the absorption of most oral medications.” [2]

In terms of the intense effects of motivation or “the will to live” that many people who take Ozempic have reported, “GLP‑1 receptor agonists modulate reward circuits but do not block dopamine receptors as antipsychotics do. In fact, semaglutide’s effects on dopamine appear complex. Animal studies show that semaglutide increases dopamine neuron activity in the ventral tegmental area during reward consumption” [3]

One thing that I read that helped me stay the distance was the fact that over time, the side effects of semaglutide can reduce to more manageable levels. I have been on 0.5 mg for over four months now. It is not a highly effective dose for weight loss, but I wanted to know if over time, the side effects are sustainable for me, since if I do increase my dose for weight loss, I am going to need to stay on 0.5 mg of semaglutide for the forseeable future to maintain the weight loss. This is the quote from ChatGPT that gave me hope and allowed me to press on with this experiment: “In practice, if a patient at 0.5 mg experiences mental fatigue or focus problems, waiting several weeks before further dose changes or consulting a clinician can help discern whether the body will adjust or if the drug should be tapered off.” [4]

I have certainly felt less ‘at risk’ of developing a psychosis, and I have noticed some cognitive improvements from a baseline of antipsychotic and antidepressant medication use. There is no evidence to suggest that Ozempic increases the risk of psychosis. [5]

The last thing that I have noticed is that after travelling to Sydney and experiencing quite an emotionally intense period during and just after that adventure it is taking me quite a while to ‘bounce back’. One night of very minimal sleep led to a very emotionally turbulent day on the next day, and recovering from that, and the excitement from going to Sydney has been challenging to come back from. I have felt fragile, weak, teary and generally unable to work during this period. Each day I feel a little stronger, but it certainly is remarkable to me that ‘what goes up must come down’ is so true where Ozempic is concerned. I am not sure if this is more of an issue due to the other medications that I take.

I have noticed that despite the lacking motivation or ‘will to live’ especially in the mornings while taking Ozempic, the range of my emotions is much wider. I feel lower, yes, when my world comes crashing down, but I also feel higher, or happier when things are really good! I feel that this is an important bonus. Who wants to live in the bland ‘middle’ of emotional responses?

And even though it is challenging to endure these days since I have come back from Sydney with the tears, the anger and the fragile mental state, having intense feelings is pretty good too! Like life is a wonderful adventure of deep and interesting emotional states.

So, I am interested to see if there has been any impact on my macular, since I have also noticed that my vision has been impacted since being on this drug, and if not, then I might consider increasing the dose again, perhaps.

References:

  1. De Giorgi R, Koychev I, Adler AI, Cowen PJ, Harmer CJ, Harrison PJ, Taquet M. 12-month neurological and psychiatric outcomes of semaglutide use for type 2 diabetes: a propensity-score matched cohort study. EClinicalMedicine. 2024 Jul 10;74:102726. doi: 10.1016/j.eclinm.2024.102726. PMID: 39764175; PMCID: PMC11701436.

Available from: https://pubmed.ncbi.nlm.nih.gov/39764175/

    1. 2. Kommu S, Whitfield P. Semaglutide. [Updated 2024 Feb 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

Available from: https://www.ncbi.nlm.nih.gov/books/NBK603723/

3. Kooij, K. L., Koster, D. IJ., Eeltink, E., Luijendijk, M., Drost, L., Ducrocq, F., & Adan, R. A. H. (2024). GLP-1 receptor agonist semaglutide reduces appetite while increasing dopamine reward signaling. Neuroscience Applied, 3, Article 103925. https://doi.org/10.1016/j.nsa.2023.103925

4. Li JR, Cao J, Wei J, Geng W. Case Report: Semaglutide-associated depression: a report of two cases. Front Psychiatry. 2023 Aug 29;14:1238353. doi: 10.3389/fpsyt.2023.1238353. PMID: 37706035; PMCID: PMC10495976.

Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10495976/

5. Siskind D, Baker A, Russell A, Warren N, Robinson G, Parker S, Medland S, Kisely S, Hager T, Arnautovska U. Effects of semaglutide on body weight in clozapine-treated people with schizophrenia and obesity: study protocol for a placebo-controlled, randomised multicentre trial (COaST). BJPsych Open. 2023 Jul 25;9(4):e136. doi: 10.1192/bjo.2023.532. PMCID: PMC10375878.

Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10375878/