Psychosis – Vista Hill Center for Child and Youth Psychiatry

Caffeine Consumption in Individuals with Mental Health Disorders: Clinical Benefits and Risks 5/28/25

Shirley Fett — Tue, 27 May 2025 16:58:50 +0000

Caffeine, a central nervous system stimulant consumed by approximately 85% of adults in the United States daily, has complex implications for individuals with mental health disorders. Its primary mechanism involves non-selective antagonism of adenosine A1 and A2A receptors, resulting in increased dopamine and norepinephrine transmission—neurotransmitters implicated in multiple psychiatric conditions. While moderate caffeine intake may confer cognitive or mood-related benefits, the nuanced psychotropic effects of caffeine can also exacerbate psychiatric symptoms depending on the diagnosis, dose, and comorbid conditions. This review outlines the evidence-based benefits and risks of caffeine consumption across six major psychiatric conditions: ADHD, depression, anxiety, bipolar disorder, psychosis, and substance use disorders.

Attention-Deficit/Hyperactivity Disorder (ADHD)

Caffeine has stimulant-like properties that may improve attention and executive functioning in individuals with ADHD. A study in rodent models showed that caffeine improved memory and attention through enhanced dopaminergic signaling in the prefrontal cortex, paralleling the effects of prescription stimulants (Pandolfo et al., 2013). Human trials are limited, but a double-blind study in children with ADHD found that caffeine modestly improved behavior and attention, although not as effectively as methylphenidate (Lara et al., 2010). Nevertheless, caffeine may disrupt sleep—a significant concern for individuals with ADHD, as sleep impairment exacerbates core symptoms.

Depression

Caffeine’s psychostimulant properties and dopaminergic activation suggest potential antidepressant effects. A large prospective cohort study found that women who consumed ≥4 cups of caffeinated coffee daily had a 20% reduced risk of depression compared to those consuming little or none (Lucas et al., 2011). This protective effect is attributed to caffeine’s anti-inflammatory properties and its modulation of brain-derived neurotrophic factor (BDNF) (Kaster et al., 2015). However, excessive use may mask depressive symptoms or contribute to mood instability, especially when withdrawal effects are misinterpreted as depressive episodes.

Anxiety Disorders

Caffeine is a known anxiogenic agent, particularly in susceptible individuals. At high doses (e.g., >400 mg/day), caffeine can induce symptoms consistent with generalized anxiety or panic disorder, including restlessness, insomnia, palpitations, and irritability (Boulenger et al., 1984). A randomized trial demonstrated that patients with panic disorder were significantly more sensitive to caffeine’s stimulatory effects, exhibiting heightened cardiovascular and subjective anxiety responses (Charney et al., 1985). Clinical guidelines generally recommend limiting or avoiding caffeine in individuals with anxiety disorders.

Bipolar Disorder

Caffeine’s effects on mood stability in bipolar disorder are complex. While it may transiently alleviate depressive symptoms, its stimulant properties can disrupt sleep and potentially trigger manic or hypomanic episodes. Disrupted circadian rhythms are central to bipolar pathophysiology, and caffeine—especially when consumed late in the day—can exacerbate this vulnerability (Wehr et al., 1987). A study by Leibenluft and colleagues found that individuals with bipolar disorder frequently use caffeine during depressive phases but reported increased agitation during manic episodes (Leibenluft et al., 1996). Clinical prudence suggests moderating caffeine intake, especially during manic or mixed states.

Psychosis and Schizophrenia

Individuals with schizophrenia often consume caffeine at rates exceeding those of the general population. This may reflect attempts to counteract sedation from antipsychotic medications or cognitive dulling (Gurpegui et al., 2004). However, caffeine’s dopaminergic effects pose theoretical risks of exacerbating psychotic symptoms. Lucas et al. (1990) found that high caffeine intake was associated with increased positive symptoms, particularly in patients taking clozapine. Furthermore, caffeine is metabolized by cytochrome P450 1A2, the same enzyme responsible for metabolizing several antipsychotics, including olanzapine and clozapine, potentially leading to drug interactions (Carrillo et al., 2000).

Substance Use Disorders

Caffeine interacts with reward pathways implicated in substance use. While moderate caffeine use may not pose harm, energy drink consumption (often containing high caffeine doses) has been associated with increased risk of alcohol and stimulant misuse among adolescents and young adults (Arria et al., 2011). Caffeine also carries its own dependence potential, with recognized withdrawal symptoms such as headache, fatigue, and irritability (Juliano & Griffiths, 2004). Screening for problematic use patterns is warranted, particularly in individuals with comorbid SUDs.

Conclusion

Caffeine is a psychoactive substance with condition-specific effects on mental health. While it may offer mild symptomatic relief in ADHD and depression, it can also exacerbate symptoms in anxiety, bipolar disorder, and psychosis, or complicate treatment in substance use disorders. Mental health and primary care providers should assess individual caffeine consumption patterns, explore patient motivations for use, and provide tailored guidance based on psychiatric diagnosis, comorbidities, and medication interactions.

References

Vázquez JC, et al. Effects of Caffeine Consumption on Attention Deficit Hyperactivity Disorder (ADHD) Treatment: A Systematic Review of Animal Studies. Nutrients. 2022;14(4):739. https://doi.org/10.3390/nu14040739 News-Medical
Grosso G, et al. Coffee, tea, caffeine and risk of depression: A systematic review and dose-response meta-analysis of observational studies. Mol Nutr Food Res. 2016;60(1):223-234. https://doi.org/10.1002/mnfr.201500620
Lara DR. Caffeine, mental health, and psychiatric disorders. J Alzheimers Dis. 2010;20 Suppl 1:S239-48. doi: 10.3233/JAD-2010-1378. PMID: 20164571. https://journals.sagepub.com/doi/abs/10.3233/JAD-2010-1378
Juliano LM, Griffiths RR. A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features. Psychopharmacology (Berl). 2004;176(1):1-29. https://doi.org/10.1007/s00213-004-2000-x
Charney DS, Heninger GR, Jatlow PI. Increased anxiogenic effects of caffeine in panic disorders. Arch Gen Psychiatry. 1985 Mar;42(3):233-43. doi: 10.1001/archpsyc.1985.01790260027003. PMID: 2983630. https://jamanetwork.com/journals/jamapsychiatry/article-abstract/493529
Lucas PB, Pickar D, Kelsoe J, Rapaport M, Pato C, Hommer D. Effects of the acute administration of caffeine in patients with schizophrenia. Biol Psychiatry. 1990 Jul 1;28(1):35-40. doi: 10.1016/0006-3223(90)90429-6. PMID: 2375945. https://linkinghub.elsevier.com/retrieve/pii/0006322390904296
Carrillo JA, Benitez J. Clinically significant pharmacokinetic interactions between dietary caffeine and medications. Clin Pharmacokinet. 2000 Aug;39(2):127-53. doi: 10.2165/00003088-200039020-00004. PMID: 10976659. Gurpegui M, et al. Caffeine consumption in schizophrenia: associations with clinical and sociodemographic features. Prog Neuropsychopharmacol Biol Psychiatry. 2004;28(5):945-951. https://link.springer.com/article/10.2165/00003088-200039020-00004
Meredith SE, et al. Caffeine Use Disorder: A Comprehensive Review and Research Agenda. J Caffeine Res. 2013;3(3):114-130. https://doi.org/10.1089/jcr.2013.0016
Fredholm BB, et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev. 1999;51(1):83-133. https://pubmed.ncbi.nlm.nih.gov/10049999/

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Vista Hill Native American SmartCare Program

Autism Spectrum Disorder and Psychosis 1/8/25

Shirley Fett — Fri, 03 Jan 2025 23:54:46 +0000

Patient is a 14-year-old male with history of autism spectrum disorder who presents for psychiatric evaluation. Patient was diagnosed with autism at age 3 after his pediatrician noticed concerning signs including speech delay, limited social interaction, and repetitive play. On interview, patient’s mother shares that over the past few months patient has exhibited increased aggression resulting in altercations with others and destruction of property. Furthermore, she notes that patient has started eating less and has expressed concerns about contamination of food. She has seen him talk to unseen others and laugh inappropriately. The patient endorses hearing voices but he otherwise has difficulty engaging in the interview due to internal preoccupation and thought disorganization.

Autism spectrum disorder (ASD) and psychosis are distinct but closely related psychiatric conditions. In the twentieth century, Swiss psychiatrist Eugen Bleuler identified autism, which he defined as withdrawal from the world, as a core, pathognomonic symptom of schizophrenia. Since the 1970s and the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), ASD and psychosis have become recognized as separate diagnoses, but they remain highly comorbid. Up to 34.8% of those with ASD exhibit psychosis and 3.6-60% of those with schizophrenia present with autistic traits. Individuals with ASD are 3.5x more likely to develop psychosis than the general population. Both conditions share risk factors including advanced paternal age, pregnancy and birth complications, migration status, specific genetic pathways, abnormalities in brain development, neuroanatomical markers, and social cognition deficits. It is thought that the impairments in information processing seen in ASD may confer a risk for later psychosis.

Identifying psychosis in individuals with ASD can be challenging. First, patients with ASD may have difficulty communicating psychotic experiences, such as delusions and hallucinations due to the social communication impairments inherent to ASD and/or insufficient cognitive ability if they have comorbid intellectual disability. Additionally, overlapping symptoms in both conditions may create complications. For example, hallucinations may be misinterpreted as the anomalous perceptual experiences reported in ASD, or negative symptoms of psychosis, such as flat affect and social withdrawal, may be confused for difficulties with socio-emotional reciprocity seen in ASD.

Considering the overall course of illness can be helpful in distinguishing psychosis from ASD. While the onset of ASD is typically in early childhood, as early as 12-24 months of age, the onset of primary psychotic disorders is typically between late adolescence and the mid-thirties (there are exceptions to this pattern; for example, childhood-onset schizophrenia can be diagnosed before 13 years old). Furthermore, negative symptoms of psychosis typically worsen over time if untreated while autistic traits remain more stable.

There are also key differences between these two disorders that can aid in diagnosis. ASD is generally associated with an impairment in understanding the rules of common social interactions, greater impairment in theory of mind (the ability to understand and predict the mental states of others) and difficulty in distinguishing between one’s subjective perceptions and reality. On the other hand, individuals with psychosis tend to have a greater tendency towards external attributions for negative events and internal attributions for positive events. They are also more likely to demonstrate hostility bias, or the tendency to interpret the ambiguous behaviors of others as hostile.

Distinguishing ASD from psychosis is important, as it can allow for early intervention and treatment. Medications for these diagnoses can overlap; for instance, the second-generation antipsychotics aripiprazole and risperidone are used for both irritability associated with ASD and for psychosis. However, higher doses of such medications may be required in primary psychotic disorders compared to ASD. Additionally, diagnostic clarification can help guide therapy. While Applied Behavior Analysis may be most appropriate for an individual with ASD, Cognitive Behavioral Therapy for Psychosis might be recommended for individuals with psychosis. Understanding the differences and shared features of ASD and psychosis is crucial for accurate diagnosis and effective intervention, ultimately leading to improved outcomes for affected individuals.

Back to the Case: Patient was diagnosed with unspecified psychosis in addition to his existing diagnosis of autism spectrum disorder. He was started on aripiprazole, which was gradually titrated to 20mg daily. He and his mother reported improvement in his aggression, hallucinations, and paranoia on this medication. He was referred to the San Diego Regional Center for interventions related to his autism spectrum disorder and to a psychosis specialty clinic for interventions related to his psychosis.

AUTHOR:

Dr. Kristen Kim, MD

Child, Adolescent and Adult Psychiatrist

Vista Hill Foundation

Tapering Antipsychotic Medications in Children and Adolescents: Part 1 3/21/24

Shirley Fett — Wed, 20 Mar 2024 16:09:52 +0000

Although pediatricians do not often initiate prescriptions for antipsychotic agents, this and a subsequent e-newsletter edition discuss important issues in their use that can be of relevance to pediatric practice, both in managing acute clinical situations and in managing care for youth with longer term needs for these medicines.

About 1% of children ages 7-12 and about 1.5% of adolescents ages 13-18 are prescribed antipsychotic medications¹ some of which are FDA approved for minors with psychiatric diagnoses including schizophrenia, bipolar disorder (BD), and irritability in autism². This said, about 65% of antipsychotic medication prescribing is used off-label for issues such as severe aggression, agitation, disruptive behavior, irritability, and therapeutic augmentation when treating complex ADHD. In these cases, antipsychotic medications may be of benefit but, in general, they should not be intended for high-dose or open-ended long-term use. This said, clinicians rarely consider or discuss discontinuation of antipsychotics or any psychotropic medications with their patients⁴. In this article and a subsequent article, we will discuss guidelines on when, how and how long to use antipsychotic medications and how to reduce or discontinue them in a safe and clinically appropriate manner.

Do antipsychotics work?

The short answer is yes, which is why they are used, both for FDA approved conditions and also for non-psychotic disorders that present with very challenging behaviors and/or crisis situations. In high-risk scenarios, antipsychotics can be crucial for short-term to medium-term stabilization, such as keeping a child out of the psychiatric hospital, allowing a student to stay in a less restrictive school environment, and in reducing the risk of aggression or injury. This said, research does not clearly show that antipsychotic medication is always meaningfully helpful in some of the situations where it is commonly prescribed, such as for severe ADHD or Oppositional Defiant Disorder⁵.

How long should a patient stay on an antipsychotic medication?

Antipsychotic medication use has primarily been studied and FDA approved for short-term use (up to 6 months) in children^5or6 and, as yet, there are very few studies that assess benefits and side effects of longer-term antipsychotic use in children who are not suffering from a confirmed psychotic or bipolar disorder^6or7.

Regardless of diagnosis, common safety issues and concerns related to antipsychotic medications include: metabolic effects like weight gain, diabetes and hyperlipidemia; somnolence; prolonged QTc interval; prolactin elevation; extrapyramidal symptoms; and neuroleptic malignant syndrome. For these reasons and others, one should always have a careful conversation with patients and their families when initiating a trial of an antipsychotic medication about the planned duration of treatment of the medication, which should include factors like severity of symptoms, the natural course of the condition being treated, the age of the child, and response to other psychosocial interventions.

Particularly when used for non-psychotic illnesses, careful determination on an individual case by case basis is important, keeping in mind that the duration of treatment and dosage considerations should be carefully reviewed and reconsidered over time. Even for clinical situations when there is FDA approval, as is the case for irritability in autism, one should carefully consider if the patient truly meets criteria for prescribing (e.g., in autism, such criteria would be serious aggression, self-injury, and/or severe mood lability) and if there could be another approach such as addressing sensory or communication difficulties or using of an alternative medication with a safer side effect profile.

Need Consultation or Information about Anti-psychotic medication?

SmartCare’s On-Demand telephone consultation service is a readily accessible resource for primary care pediatricians needing support in managing patients with behavioral health challenges. Call us at (858 880-6405).

Part 2 of today’s newsletter article will discuss clinical considerations in managing patients being treated with antipsychotic medications with a focus on pragmatic strategies in tapering and discontinuing these medications when indicated.

Author:

Charmi Patel Rao, MD

Associate Medical Director, Vista Hill Foundation

Health Science Assistant Clinical Professor for UCSD Department of Psychiatry

President, San Diego Academy of Child and Adolescent Psychiatry

References:

¹Olfson M et al., JAMA Psychiatry; 2015; 72(9):867-874.

²Harrison J et al., Journal of Pediatric Health Care; 2012; 26(2): 139-145

³Sohn M et al., Medicine 2016; 95(23): e3784

⁴Dinnessen M et al., European Child and Adolescent Psychiatry; 2020; 29 (12): 1717-1727

⁵ Lentini G et al., Biomedicines 2022;10(11): 2818

⁶Aman M et al., Journal of Child and Adolescent Psychopharmacology; 2015; 25(6):482-493

⁷Singappuli P et al., CNS Spectrums 2022; 27(5):570-587

Managing Mood Disorders for Pregnant Patients and Their Progeny 6/11/2020

Shirley Fett — Thu, 11 Jun 2020 15:48:51 +0000

Optimizing treatment intervention for individuals with clinically significant mood disorders during pregnancy can be fraught with conflicting influences and requires careful consideration and sensitivity, as whatever actions you take (or don’t take) for the mother, will also affect the fetus. Following are a number of clinical considerations identified in a recent article published in Psychiatric Times.

Pregnancies happen– and dialogue with all female patients of child bearing ages about the potential impacts of their becoming pregnant should be a routine part of their care and should be documented. In this context, it is far better to explore the individual issues for each patient prior to a pregnancy occurring than to have to respond after the fact.
While there is a very natural impulse to want all pregnancies to be “natural”, a reflex response of stopping all medications is not appropriate, nor is a rigid stance against any changes in treatment —the risks and benefits of continuing meds or stopping meds should be considered carefully and be individualized to each patient. Relapse rates in the face of medication discontinuation can be as high as 70% for women with depression and as high as 85% for those with bipolar depression. This is contrast to reported relapse rates of only 30% when a pregnant patient continues her medication.
A depressed mom means a distressed fetus and it is important to consider the potential impacts of a mother’s recurring or worsening mood disorder on the child. Research shows a clear association between maternal depression and negative consequence such as preterm delivery, low birth weight, poor reflexes in the baby, and both increased risk of preeclampsia and gestational diabetes for the mother.
For a patient whose illness history indicates that discontinuation of medication is likely to be associated with a relapse or significant worsening of symptomatology, the impulse to reduce medication dosage should be carefully reconsidered as fetal exposure to the drug will occur in this scenario and a compromise in the mother’s mood state, with impacts on the fetus, would be anticipated.
With an unanticipated pregnancy it would be highly appropriate to consider switching from an agent such as paroxetine with known fetal risk to another agent if this has not been considered prior to the onset of the pregnancy.
Regardless of the prescription choices made with regard to psychiatric medications, counseling and attention to an expecting mother’s potential use of substances such as tobacco, alcohol, marijuana, opiates and other drugs is always warranted given the documented risks to both mom and child.
Continuing with an antidepressant following pregnancy during the breastfeeding period is another consideration to address with the pregnant mom-to-be and the family in recognition of the very substantial health and emotional benefits of breastfeeding and the limited risks of medication exposure for the infant.
For mood disordered patients with more complicated treatment regimens that have included the use of benzodiazepines prior to the start of a pregnancy, gradual tapering off the benzodiazepine is ideal and a scheduled taper over the course of several weeks is recommended to avoid withdrawal symptoms such as increased blood pressure and pulse, seizures, and heightened anxiety.
For patients with complex co-occurring disorders and symptoms with psychotic symptoms or manic tendencies, careful management of antipsychotic and/or mood stabilizing medications is required in association with enhanced psychosocial and psychotherapeutic supports. Coordinated interventions by a multidisciplinary team for these high risk situations is ideal and the active evaluation and subsequent ongoing management of the potential risks and benefits of psychopharmacologic interventions is necessary. Patients who have required use of mood stabilizer medications such as lithium, valproic acid and carbamazepine will require particular attention as each of these agents have significant potential fetal toxicities.

Reference: Psychiatric Times, March 2020 (p16-17) Common Errors Psychiatrists Make When Managing Mood Disorders In Pregnant Patients