Theoretical Foundations of ACT

ACT is grounded in Relational Frame Theory (RFT), a behavioral theory of language and cognition that posits human suffering often stems from the ways in which language and thought processes contribute to experiential avoidance and cognitive fusion. Rather than attempting to eliminate distressing thoughts and emotions, ACT encourages individuals to accept them, defuse their impact, and commit to actions aligned with personal values. Psychological flexibility—the capacity to remain in contact with the present moment and act in service of chosen values despite difficult internal experiences—is the overarching aim of ACT.

This shift from symptom reduction to functional improvement is especially relevant for adolescents, whose cognitive and emotional capacities are still developing. ACT provides a developmentally appropriate framework that helps teens navigate emotional distress while fostering autonomy, identity formation, and purpose.

Core Processes in ACT and Their Application in Adolescents

ACT comprises six interrelated core processes:

1. Cognitive Defusion: Adolescents are taught to observe their thoughts without automatically accepting them as truth. Techniques like labeling thoughts (“I’m having the thought that…”) or using metaphors (e.g., leaves on a stream) help reduce the literal impact of self-critical or anxious thinking.
2. Acceptance: Rather than avoiding painful feelings—common in adolescent presentations such as self-harm or substance use—ACT promotes openness to emotion. Through mindfulness practices and experiential exercises, teens learn that distress is a normal part of human experience, not a signal to disengage.
3. Contact with the Present Moment: Adolescents are often preoccupied with past events or future worries. Grounding exercises and present-focused attention aim to build awareness and reduce rumination, improving emotional regulation.
4. Self-as-Context: Adolescents frequently struggle with self-identity and negative self-concepts. ACT fosters a perspective shift from rigid self-definitions (“I am depressed”) to a more flexible sense of self (“I notice I’m experiencing depression”), allowing for greater resilience and adaptability.
5. Values Clarification: Through guided reflection, adolescents explore what truly matters to them—relationships, creativity, justice, learning—thus anchoring their behaviors in intrinsic motivation rather than external approval or peer pressure.
6. Committed Action: ACT culminates in behavior change rooted in values. Teens are supported in setting realistic goals and taking concrete steps, even when faced with emotional discomfort.

Evidence Base for ACT in Adolescent Populations

A growing body of research supports the efficacy of ACT for adolescents across a spectrum of conditions, including anxiety disorders, depression, chronic pain, and behavioral issues. Systematic reviews and randomized controlled trials (e.g., Swain et al., 2015; Hayes et al., 2021) indicate that ACT can lead to significant improvements in psychological flexibility, mood symptoms, and overall functioning.

Notably, ACT has shown promise in school-based interventions and brief formats, making it accessible for primary care settings. Given the limited availability of specialized mental health services for youth, ACT’s adaptability enhances its utility in integrated care models.

Practical Integration into Clinical Practice

Primary care and mental health providers can incorporate ACT in both brief encounters and ongoing therapy. For example:

• During a routine visit, a provider might use a quick mindfulness exercise to help an anxious teen ground themselves.
• A pediatrician discussing adherence to medical treatment could frame the conversation around the teen’s values (e.g., staying healthy to continue playing sports).
• Mental health clinicians can use ACT metaphors and exercises to shift the focus from symptom elimination to living a meaningful life despite discomfort.

Furthermore, ACT’s emphasis on experiential learning aligns well with adolescents’ concrete thinking styles. Visual aids, metaphors, and experiential exercises (e.g., tug-of-war with a monster) make ACT both engaging and developmentally appropriate.

Challenges and Considerations

While ACT offers many benefits, providers should be aware of potential limitations. Adolescents with severe cognitive impairments or limited verbal skills may require modifications. Additionally, cultural and familial contexts should be considered when exploring values and promoting individual autonomy. Training and supervision in ACT are essential for effective delivery, especially in navigating complex cases.

Conclusion

ACT provides a flexible, evidence-based approach for addressing adolescent mental health concerns, emphasizing acceptance, mindfulness, and values-driven action over symptom suppression. For primary care and mental health providers, integrating ACT into practice can enhance therapeutic rapport, empower adolescents, and support long-term psychological resilience. As mental health challenges among youth continue to rise, ACT represents a timely and transformative tool in the clinician’s repertoire.

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Diagnostic Overview
SSRDs include several distinct disorders:

1. Somatic Symptom Disorder (SSD)
   Characterized by one or more distressing somatic symptoms that are accompanied by excessive thoughts, feelings, or behaviors related to those symptoms. Importantly, the symptoms may or may not be medically explained. The focus is on the psychological response to the symptoms rather than the presence or absence of a medical explanation.
2. Illness Anxiety Disorder (IAD)
   Previously known as hypochondriasis, IAD involves preoccupation with having or acquiring a serious illness despite minimal or no somatic symptoms. Patients frequently misinterpret normal bodily sensations and engage in repeated health checks or avoidant behaviors.
3. Conversion Disorder (Functional Neurological Symptom Disorder)
   This condition involves neurological symptoms (e.g., paralysis, seizures, blindness) that are inconsistent with recognized medical conditions. Symptoms often emerge in the context of psychological stress or trauma.
4. Psychological Factors Affecting Other Medical Conditions
   This diagnosis applies when psychological or behavioral factors significantly affect the course, treatment, or outcome of a medical illness.
5. Factitious Disorder
   Involves intentional falsification of physical or psychological symptoms without obvious external incentives, distinguishing it from malingering.

Epidemiology and Clinical Features
SSRDs are common across healthcare settings. SSD affects approximately 5-7% of the general population, with a higher prevalence in women. IAD affects 1.3-10% of the population, with equal gender distribution. Conversion disorder is more frequently diagnosed in females and typically presents in adolescence or early adulthood.

Patients with SSRDs often have co-occurring psychiatric disorders such as depression or anxiety. Adverse childhood experiences, trauma, and chronic stress are significant risk factors. Additionally, these patients often have complex relationships with the healthcare system—frequent visits, diagnostic procedures, and a feeling of being misunderstood or invalidated are possible.

Challenges in Diagnosis
Diagnosing SSRDs requires careful differentiation from medical conditions, malingering, and other psychiatric disorders. The DSM-5-TR emphasizes the need to avoid over pathologizing patients with medically unexplained symptoms and instead focus on the degree of psychological distress and functional impairment.

Clinicians are best served to conduct comprehensive assessments that include medical, psychiatric, and psychosocial components. Collateral information from family and medical records is often helpful. Importantly, SSRDs are not diagnoses of exclusion but require positive identification of specific clinical features.

Best Practices in Treatment

1. Psychoeducation and Therapeutic Alliance
   Establishing a strong therapeutic alliance is foundational. Patients often feel invalidated by previous medical encounters, so clinicians must acknowledge their suffering without reinforcing somatic preoccupation. Psychoeducation should reframe the illness using a biopsychosocial model, emphasizing the truly felt nature of the symptoms while introducing the role of stress and emotional factors.
2. Cognitive Behavioral Therapy (CBT)
   CBT is the most evidence-based treatment for SSRDs. It targets beliefs and thoughts about illness and health, and avoidant or excessive health behaviors. CBT helps patients develop more accurate appraisals of bodily sensations and encourages gradual re-engagement in activities.
3. Mindfulness and Acceptance-Based Therapies
   Interventions such as mindfulness-based stress reduction (MBSR) and acceptance and commitment therapy (ACT) show promise by helping patients observe their symptoms non-judgmentally and reduce experiential avoidance. These approaches may be particularly helpful in patients with chronic pain or functional neurological symptoms.
4. Pharmacotherapy
   While no medications are FDA-approved specifically for SSRDs, selective serotonin reuptake inhibitors (SSRIs) may be helpful when comorbid depression or anxiety is present. SNRIs and tricyclic antidepressants have also shown utility in somatoform pain syndromes. For example, the SNRI Duloxetine has an FDA approval for chronic pain. However, polypharmacy and iatrogenic harm should be avoided.
5. Interdisciplinary Care and Coordination
   Patients benefit from collaborative care models involving primary care providers, psychiatrists, psychologists, physical therapists, and sometimes neurologists or pain specialists. Coordinated care prevents redundant testing and provides consistent messaging. Regular case conferences and shared treatment plans are key to success.
6. Limit Medical Investigations and Set Boundaries
   While it is essential to rule out medical conditions, repeated investigations reinforce illness behavior. Providers should adopt a “diagnostic closure” strategy, providing reassurance based on appropriate evaluation, and shift focus to functional recovery. Structured visits, time-limited appointments, and continuity with a single provider help reduce fragmentation.
7. Address Trauma and Comorbidities
   Because many patients have histories of trauma, integrating trauma-informed care is essential. Screening for PTSD, dissociation, and borderline personality disorder is often appropriate. Psychotherapy targeting trauma (e.g., EMDR, trauma-focused CBT) can reduce somatic symptom intensity.

Conclusion
Somatic Symptom and Related Disorders are complex conditions that straddle the boundary between psychiatry and medicine. When properly diagnosed and treated using evidence-based, multidisciplinary approaches, many patients experience significant improvements in functioning and quality of life. Mental health providers play a critical role in destigmatizing these conditions, guiding collaborative care, and helping patients shift from symptom preoccupation to adaptive functioning.

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Vista Hill Native American SmartCare Program

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

1. 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/nu14040739News-Medical
2. 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
3. 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
4. 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
5. 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
6. 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
7. 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
8. 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
9. 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

This medication treatment algorithm outlines evidence-based pharmacological interventions for adolescent depression, incorporating safety considerations, efficacy, and potential adverse effects. The algorithm can serve as a guide and should be individualized based on clinical judgment, patient preferences, and specific clinical circumstances. Regular monitoring and reassessment are essential throughout the treatment process.

Step 1: Initial Assessment

• Comprehensive Evaluation: Conduct a thorough assessment, including psychiatric history, symptom severity, medical history, family history, and suicidality risk. Consider differential diagnosis and co-morbidities.
• Psychotherapy: Initiate or continue evidence-based psychotherapy, such as cognitive-behavioral therapy (CBT) or interpersonal therapy (IPT). Inform psychotherapist of planned psychopharmacologic treatment and maintain ongoing collaborative dialogue as warranted
• Education and Informed Consent: Educate the patient and their family about the potential benefits, risks, and side effects of medication treatment. Obtain informed consent.

Step 2: First-Line Pharmacotherapy

• Selective Serotonin Reuptake Inhibitors (SSRIs):
  • Fluoxetine: Start with a low dose (10 mg/day) and titrate gradually to therapeutic range (20-60 mg/day).
  • Escitalopram: Initiate at 5-10 mg/day, titrate up to 10-20 mg/day.
  • Sertraline: Begin with 25-50 mg/day, titrate up to 50-200 mg/day.
• Monitoring:
  • Close monitoring for therapeutic response and adverse effects, especially during the first 4-6 weeks and following future dose increases, if instituted.
  • Assess for emergence or worsening of suicidal ideation, agitation, or behavioral activation.

Step 3: Treatment Response Assessment

• Response Evaluation: Evaluate response to SSRI treatment after 4-6 weeks.
• Adjustment: If partial response or inadequate response, consider:
  • Increasing SSRI dose, gradually at q 2-4 week intervals.
  • Switching to another SSRI.
  • Adding psychotherapy or non-pharmacological interventions.

Step 4: Second-Line Pharmacotherapy

• Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs):
  • Venlafaxine: Initiate at 37.5 mg/day, titrate up to 75-225 mg/day.
  • Duloxetine: Start with 30 mg/day, titrate up to 60-120 mg/day.
  • Bupropion: Consider in cases with atypical depression symptoms or when SSRIs or SNRIs are ineffective or not tolerated. Begin with 75 mg/day, titrate up to 150-300 mg/day.
• Monitoring:
  • Continuously monitor for therapeutic response and adverse effects.
  • Assess for potential drug interactions, especially with other psychotropic medications.

Step 5: Consultation and Collaboration

• Collaboration: Maintain open communication with the patient, their family, and involved healthcare professionals throughout treatment.
• Consultation: Consider consultation with a child and adolescent psychiatrist for complex cases, treatment-resistant depression, or significant comorbidities.

Step 6: Continuation and Maintenance

• Continuation Phase: Once remission is achieved, continue the effective medication at the same dose for at least 6-12 months to prevent relapse.
• Maintenance Phase: For recurrent depression or chronic conditions, consider long-term maintenance treatment with medication and/or psychotherapy.

Safety Considerations:

• Suicidality Risk: Monitor closely for emergence or worsening of suicidal ideation, especially during the initial weeks of treatment.
• Serotonin Syndrome: Educate about symptoms and signs, especially if combining SSRIs or SNRIs with other serotonergic medications.
• Drug Interactions: Be cautious with concomitant use of other medications metabolized by cytochrome P450 enzymes. Avoid monoamine oxidase inhibitors (MAOIs).
• Monitoring Parameters: Regularly assess for efficacy, adverse effects, vital signs, and growth parameters in adolescents.

Author:

Shawn Singh Sidhu, M.D., DFAPA, DFAACAP

​Medical Co-Director, Vista Hill Foundation

References:

• American Academy of Child and Adolescent Psychiatry (AACAP). (2019). Practice parameter for the assessment and treatment of children and adolescents with depressive disorders.
• Cheung, A. H., & Emslie, G. J. (2015). Treatment-resistant depression in adolescents. Pediatric Drugs, 17(6), 383-392.
• National Institute for Health and Care Excellence (NICE). (2019). Depression in children and young people: identification and management (Clinical guideline [CG) 28).
• Zhou, X., Hetrick, S. E., Cuijpers, P., Qin, B., Barth, J., Whittington, C. J., … & Xie, P. (2015). Comparative efficacy and acceptability of psychotherapies for depression in children and adolescents: A systematic review and network meta-analysis. World Psychiatry, 14(2), 207-222.
• Baldwin, D. S., & Montgomery, S. A. (2005). Serotonin selective reuptake inhibitors. Journal of Psychopharmacology, 19(2_suppl), 4-6.
• Rush, A. J., Trivedi, M. H., Wisniewski, S. R., Nierenberg, A. A., Stewart, J. W., Warden, D., … & Fava, M. (2006). Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. The American Journal of Psychiatry, 163(11), 1905-1917.
• Cipriani, A., Furukawa, T. A., Salanti, G., Chaimani, A., Atkinson, L. Z., Ogawa, Y., … & Geddes, J. R. (2018). Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. The Lancet, 391(10128), 1357-1366.
• Taylor, D., Paton, C., & Kapur, S. (2019). The Maudsley prescribing guidelines in psychiatry. John Wiley & Sons.
• Nutt, D. J. (2008). Relationship of neurotransmitters to the symptoms of major depressive disorder. The Journal of Clinical Psychiatry, 69, 4-7.

The symptoms of depression can be the same for older patients as younger adults. However, older patients with depression can often deny feeling sad or depressed. Here are some clues to indicate that an older patient might have depression.

• unexplained or aggravated aches and pains
• feelings of hopelessness or helplessness
• anxiety and worries
• concentration problems
• lack of motivation and energy
• slowed movement and speech
• irritability
• loss of interest in socializing and hobbies
• neglecting personal care

It can be easy to think of a patient’s presenting symptoms as a normal part of aging, for example it is common for people to experience trouble with concentration and difficulty maintaining sleep as they get older. Even feelings of guilt and worthlessness can appear to be a reaction to losing a loved one or retiring, respectively. One important factor is looking at the level of impairment to help determine if a more serious process is occurring.

Depression can occur co-morbidly with dementia and the two disorders each increase the risk of the other, but the cognitive concerns that occur with each are different. Persons with depression commonly report trouble concentrating and being motivated. Persons with dementia present with short-term memory loss and word finding difficulties, and may not be aware of the cognitive challenges. The cognitive decline seen in dementia is mostly a slow process whereas the cognitive decline seen in depression is more rapid. Here is a helpful chart to distinguish between depression and dementia.

One very important thing to be aware of is that the suicide risk is high among older patients with depression, particularly in Caucasian males. Research shows that 75% of people who commit suicide have visited their PCPs in the previous month but their symptoms of depression were either not disclosed or not assessed for. This is a serious and potentially preventable problem, and starts with improving psycho-education and awareness of depression in older patients.

It is also important to be aware that medical problems and medications can cause depressive symptoms in older adults. Medical problems that can cause depressive symptoms, either directly or as a psychological reaction to the illness, include Parkinson’s disease, stroke, heart disease, cancer, diabetes, thyroid disorders, vitamin B12 deficiency, dementia, lupus and multiple sclerosis. Medications that can cause of worsen depression include: beta-blockers, sleeping medications, benzodiazepines, calcium-channel blockers, ulcer medications, steroids, cholesterol medications, and pain medications. While the mood-related side effects of prescription medication can affect anyone, older adults are more sensitive because of less efficient metabolism of medication.

Treatment for depression should include treating underlying medical factors, increasing social engagement and therapy. Medication (primarily the SSRIs) can be an important part of the treatment as well, but it is important to utilize the lowest effective dose and monitor closely for side effects, which can include bone loss and increased risk for falls and fractures in elderly patients. Measures to reduce the risk of bone loss, like exercise and calcium and vitamin D supplementation, are important to consider adjunctively.

As mentioned previously, it is important to improve awareness of and assessment for depression in older patients, It not only can be a debilitating condition on its own, but it can also complicate the presentation of other medical problems and limit effectiveness of treatment for those other medical problems.

Females in their 40s and 50s often present to their primary care providers with new-onset depressive symptoms. In developing a treatment plan, it is important to assess if the symptoms are part of menopause or perimenopause or if they represent a new-onset depressive disorder. A complicating factor is that menopause can independently increase the risk of a depressive episode even in a woman without a history of depression.

During the assessment, it is important to obtain a thorough menstrual history as well as ask if the patient is experiencing other physical symptoms of menopause. The menstrual history should include if her cycle is regular or irregular, the heaviness of the flow, and when she had her last menses. Perimenopause begins when the cycle begins to vary and ends 12 months after the last menses. If it is clinically unclear if a patient is in perimenopause, one can measure FSH and estrogen levels during the early follicular phase. During perimenopause, vasomotor symptoms (VMS) and mood lability may worsen. Vasomotor symptoms include hot flashes and night sweats. Other physical symptoms of menopause include: forgetfulness, insomnia, sexual changes (decreased desire, vaginal atrophy), vaginal dryness, joint pains, bladder discomfort, breast pain, and headaches.

Menopausal patients with vasomotor symptoms are more likely to have mood symptoms as well, which can include: irritability, insomnia, mood lability, and anxiety. Both the mood changes associated with menopause as well as the vasomotor symptoms are linked to dysregulation of monoaminergic neurotransmitter systems caused by fluctuating estrogen levels.

Treatment is based on where the patient is in the course of perimenopause/ menopause and on the severity of the mood symptoms. The other factor is the appropriateness of hormone replacement therapy (HRT). While there has been much controversy about HRT since the Women’s Health Initiative study in 2002 showed concerns about possible increased risk of breast cancer and limited cardiac protection of HRT, more recent evaluation of the study results has reduced many of these concerns. As a result estrogen is the only FDA approved treatment for VMS, and since mood symptoms of menopause are so intimately linked to VMS, theoretically estrogen would be a good treatment for depression linked to menopause as well.

If the patient is in perimenopause and HRT is an option, studies have shown that HRT can be helpful for both the mood symptoms of perimenopause as well as VMS, so it can be an appropriate treatment for women presenting with mild-moderate mood symptoms related to perimenopause. If HRT is not an option or if the mood symptoms are more severe, treatment with an antidepressant is an option. Studies have shown that the selective norepinephrine reuptake inhibitors (venlafaxine, duloxetine) are more helpful for VMS than the selective serotonin reuptake inhibitors (SSRIs), so if HRT is not an option, one might consider starting with an SNRI to treat both the mood symptoms as well as the VMS. If HRT is an option, one might consider a combination of HRT and an SSRI as an alternative

Adequate Trial Length: These medications can take 4-6 weeks to see the full positive effect once reaching a therapeutic dose. It is important to discuss this with patients prior to starting the medication so they have a realistic expectation about how long it may take to feel relief from their symptoms. And it is important for the prescriber to wait the full 4 weeks at a therapeutic dose prior to changing the medication. Of course the dose can be optimized based on the patients’ response in the meantime.

“Starting Low and Going Slow”: Particularly when treating anxiety disorders and drug naïve patients, it is important to “start low and go slow” to avoid problematic side effects. This is particularly true when prescribing these medications to children and adolescents as well as older patients. Slow titration has been shown to decrease the risks for increased anxiety, increased agitation and akathisia (internal restlessness) in patients being treated with SSRIs. For example when using fluoxetine in these situations, the prescriber might consider starting at 10 mg per day for one week prior to increasing to 20 mg per day, and then waiting at 20 mg for one month to assess response.

Higher Therapeutic Dose for Anxiety Disorders: While it is important to “start low and go slow” when treating anxiety disorders, many anxious patients require a higher dose for full efficacy. Using the same example of fluoxetine, while a dose range of 20-40 mg per day is adequate for treating depression, doses in the 40-80 mg range are often needed to treat anxiety disorders effectively, particularly obsessive-compulsive disorder. In these cases, it can take 3-4 months to get to a full therapeutic dose and to see full relief from symptoms.

Discontinuation Syndrome: The SSRIs, particularly the ones with shorter half-lives like paroxetine, fluvoxamine, and sertraline, can have a discontinuation syndrome if they are stopped abruptly. While the discontinuation syndrome is not dangerous or life threatening, it can be very uncomfortable for patients. Symptoms include: gastrointestinal upset, sleep disturbance, flu-like symptoms and an electrical shock sensation. The best way to avoid it is to taper SSRIs that have a shorter half-life. Fluoxetine on the other hand does not necessarily require a taper because it has a very long half-life.

Serotonin Syndrome: Serotonin syndrome is a potentially life threatening drug reaction that occurs when the body is exposed to too much serotonin. It most commonly occurs when two medications that increase serotonin in the central nervous system are taken together. Aside from the SSRIs, other medications that can increase serotonin in the brain include the triptans (used for migraines), certain pain medications (including Tramadol and Demerol), the MAOIs, and dextromethorphan (cough medication). Drugs of abuse like LSD and ecstasy have also been associated with serotonin syndrome. The symptoms of serotonin syndrome include: agitation, restlessness, diarrhea, nausea, vomiting, increased heart rate, increased blood pressure, increased body temperature, hallucinations, loss of coordination, overactive reflexes, myoclonus, and tremor. It is important to discuss this risk with patients, especially if they are taking more than one medication that can increase serotonin levels, so that they can seek immediate medical attention if they exhibit these symptoms.

FDA Black Box Warning: In 2004, the FDA issued a black box warning for all antidepressants and mood stabilizer medications based on research that showed an increased rate of spontaneous reporting of suicidal thoughts in adolescents and young adults treated with SSRIs. The FDA is currently re-evaluating the black box warning but for now it is important to discuss it with young patients who are being treated with these medications. It is important to keep in mind that the rate of the side effect did not increase by much, from 2/1000 patients to 4/1000 patients. In addition while there was in increase in the rate of reporting suicidal thoughts there was not an increase in actual suicidal gestures, suicide attempts or completed suicides. Some hypotheses about why the increase in reporting is seen includes: patients who are being treated with medications have more contact with mental health and medical providers and therefore may be more comfortable disclosing their suicidal thoughts; patients may experience improvements in their energy levels prior to improvements in their mood; the suicidal thoughts might be related to the increase in activation seen in young patients with SSRI treatment; and that spontaneous reporting of already present suicidal thoughts is a sign that the patient’s depression is improving. It is also important to remind patients and their families that these medications overall decrease the rate of suicide. Therefore they are an important part of treatment, with close monitoring, which includes phone or in person contact within 1-2 weeks after starting medication or increasing the dose.

It is our hope that this discussion about the nuances of using the SSRIs and other antidepressant medications helps for more effective usage of these important medication treatments in the primary care setting. Please feel free to call PC2 for specific questions related to specific patients.

Guidelines exist to urge primary care providers and cardiologists who see patients with coronary artery disease to screen for depression and refer for treatment as appropriate. It is therefore worthwhile to review appropriate treatment recommendations, both pharmacological and non-pharmacological, for these cases.

For mild-moderate cases and/or based on patient preference, a referral for psychotherapy can be appropriate as a first line intervention. This removes the concern about problematic side effects that might occur from a medication intervention. Of course, close follow-up is necessary, typically within 2-3 months, to make sure there is improvement in depression symptoms with therapy or if there is a need to consider a medication intervention.

Multiple well-designed studies have shown the effectiveness of selective serotonin reuptake inhibitors (SSRIs) for treating depression in patients with coronary artery disease. The SSRIs sertraline (Zoloft), citalopram (Celexa), escitalopram (Lexapro) and fluoxetine (Prozac) have been studied in short-term trials and found to be effective. Many of these studies have assessed for cardiovascular safety measures related to the prescribed medication, and most show no difference between the medication arm and placebo arm. The caveat is that most of these studies have looked at safety of short-term use of SSRIs but not long-term use in patients with coronary artery disease. This still needs to be studied.

Other antidepressant classes have either not been studied in patients with coronary artery disease or the use is not recommended. The tricyclic antidepressants are not commonly used in patients with coronary artery disease because of possible side effects, including orthostatic hypotension, effects on cardiac conduction, and anticholinergic effects.

When considering an SSRI, it is important to pay attention to possible drug interactions. Strong 2D6 inhibitors like fluoxetine and paroxetine can increase blood levels of beta-blockers, which are commonly used in patients with coronary artery disease. Increased blood levels of beta-blockers can lead to bradycardia. SSRIs may also interact with antiplatelet agents and anticoagulants to raise the risk of bleeding but this needs to be studied more to determine the exact risk and resulting clinical implications. There have been concerns raised with respect to citalopram about QT interval prolongation at higher doses, but upon further investigation, the concern may be overstated.

The bottom line is that for patients with coronary artery disease who are assessed to also have depression, the first-line recommendation, especially for mild-moderate cases, should be psychotherapy, with consideration of an SSRI for moderate-severe cases or if psychotherapy is not effective on its own. If considering an SSRI, sertraline and escitalopram have been found to be effective with minimal concerns about problematic side effects. As always, primary care providers are welcome to consult with SmartCare PC2 to help determine a best treatment course of action.

•  Fatigue/low energy
•  Trouble initiating or maintaining sleep
•  Hypersomnia
•  Significant change in appetite, leading to change to weight
• Poor concentration
• Depressed mood

When someone presents with new onset depressive symptoms, it is important to obtain a thorough history, conduct a review of systems to determine if there are abnormal findings in other body systems, obtain a family history, and perform a physical exam. These can point the provider in the right direction in terms of a differential diagnosis. Medical conditions that can mimic symptoms of depression include:

• Hypothyroidism
• B12 deficiency
• Iron deficiency anemia
• Autoimmune disorders – fibromyalgia, lupus
• Sleep apnea
• Seasonal allergies
• Medication side effect – ex: pain medication, beta blockers, Accutane, Chantix

If there is a concern for a medical condition leading to depressive symptoms, consider appropriate lab tests and imaging studies to confirm or rule out the diagnosis. To be clear, not everyone who presents with depressive symptoms needs to have other medical conditions ruled out, just in situations when it makes sense clinically.

Case Study:
9 year old female who presents with fatigue and low energy and trouble with concentration x 2 months. She reports she does not understand why she feels so tired because she sleeps 7-8 hours per night. The daytime fatigue is causing her to feel sad some days because it is affecting her energy level with her 1 year old and at work. She does not have a history of depression. Medically she is healthy except she experienced significant blood loss during her delivery.

Next Steps?
Given that she does not have a history of depression, it is important to rule out other medical causes for her symptoms. Basic labs are ordered and show low Hb/Hct. Additional studies ordered to assess for iron-deficiency anemia and confirm the diagnosis. She is started on iron supplementation and encouraged to eat more iron- rich foods in her diet and sees improvement in her symptoms over the next 3 months.
It is hopeful that this discussion and case example give clearer guidelines on when to consider a medical workup for a patient presenting with classically depressive symptoms. One take home point is that it is important to conduct a brief review of systems even in a patient presenting with depressive symptoms as her chief complaint.

Call: Provider Consultations 858-880-6405 Email: BHCS.provider@vistahill.org Webpage: www.pc2education.org

A recent consult received on our provider triage line [(858) 880-6405] involved a single, middle aged gentleman who had presented on his own steam to a clinic with a mix of mental health, substance use and medical problems— each presenting the provider with risk concerns of various dimensions.  Sorting through these issues with appropriate deference to confidentiality concerns was the focus of the consultation process.

The patient appeared marginally competent with prior behavioral health problems including a history of episodic substance abuse binges.  He also had underlying medical problems that had potential to spin out of control if his medication compliance and self-care were to falter, as seemed likely were he on his own.   He was depressed and angry, not well organized in his thinking, and made several veiled passing references to both potential self-harm and/or harm to others.   There was no clear indication of intoxication, but his past history of substance abuse was well documented. Though he might likely benefit from psychotropic medication intervention, he showed little insight or motivation to request or obtain care.

While not deemed to be acutely or intensively at-risk, the PCP called SmartCare wondering how to respond.  Would it be appropriate to contact law enforcement?  And if so, could he be safely maintained at the clinic until they responded?  If contacted, would the officers come in a timely manner and then be willing to bring him to the “not so” nearest psychiatric facility?   And, finally, if transferred would he ultimately be admitted for treatment or, as seemed more likely, would he simply be released angrier, more frustrated and perhaps a greater risk?

On the other hand, it was felt that the patient could not be released to his own recognizance given his clear deficits in judgement, insight and impulse control.  The patient’s visit to the clinic had been occasioned by a relatively minor medical concern.  He was clearly not seeking a behavioral health intervention, yet the clinic provider felt on the horns of a dilemma given the potential for harm.

After review of the presenting problems and past history, it was decided to ask the patient for his permission to contact his relatives, so that the safety concerns and a management plan could be discussed with them.   He agreed and details of monitoring, oversight, follow up care, and a safety plan were put into place with the family.

Bottom line:  Family, neighbors, friends and others in the community can be an important resource for patients and providers when additional information or community support is required as part of addressing a perceived safety concern—psychiatric or medical.  With patient consent, confidentiality requirements can be waived and provider confidence restored.