Commentary

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in his letter, or with manufacturers of competing products.

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in their response, or with manufacturers of competing products.

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in his letter, or with manufacturers of competing products.

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in their response, or with manufacturers of competing products.

The series “Neurotransmitter-based diagnosis and treatment: A hypothesis” (Part 1: Current Psychiatry, May 2022, p. 30-36, doi:10.12788/cp.0242; Part 2: Current Psychiatry, June 2022, p. 28-33, doi:10.12788/cp.0253; and Part 3: Current Psychiatry, July 2022, p. 34-40, doi:10.12788/cp.0260) translated biological psychiatry’s working causal theory into actionable clinical ideas.

The presentation of abnormal neuro­transmission may occur along a continuum. For example, extreme dopamine deficiency can present as catatonia, moderate deficiency may present with inattention, normal activity permits adaptive functioning, and excitatory delirium and sudden death may be at the extreme end of dopa­minergic excess.¹

The amplitude, rate of change, and location of neurotransmitter dysfunction may determine which specialty takes the primary treatment role. Fatigue, pain, sleep difficulty, and emotional distress require clinicians to understand the whole patient, which is why health care professionals need cross training in psychiatry, and psychiatry recognizes multisystem pathology.

The recognition and treatment of substance use disorders requires an understanding of neurotransmitter symptoms, in terms of both acute drug effects and withdrawal. Fallows² provides this information in an accessible chart. Discussions of neurotransmitters also have value in managing psychotropic medication withdrawal.³

Acetylcholine is another neuro­transmitter of importance; it is essential to normal motor, cognitive, and emotional function. Extreme cholinergic deficiency or anticholinergic crisis has symptoms of pupillary dilation, psychosis, and delirium.^4-6 The progressive decline seen in certain dementias is related in part to cholinergic deficit. Dominance of cholinergic activity is associated with depression and biomarkers such as increased rapid eye movement (REM) density, a measure of the frequency of rapid eye movements during REM sleep.⁷ Cholinergic excess or cholinergic crisis may present with symptoms of salivation, lacrimation, muscle weakness, delirium, or paralysis.⁸

The articles alluded to the interaction of neurotransmitter systems (eg, “dopamine blockade helps with endorphin suppression”). Isolating the effects of a single neurotransmitter is useful, but covariance of neurotransmitter activity also has diagnostic and treatment implications.^9-11 Abnormalities in these interactions may be part of the causal process in fundamental cognitive functions.¹² If endorphin suppression is insensitive to dopamine blockade, a relative endorphin excess may create symptoms. If acetylcholine changes are normally balanced by a relative increase in dopamine and norepinephrine, then a weak catecholamine response would fit the catecholamine-cholinergic balance hypothesis of depression. Neurotransmitter interactions are well worked out in the neurology of the basal ganglia but less clear in the frontal and limbic systems.¹³

Quantification has been applied in some areas of clinical care. Morphine equivalents are used to express opiate potency, and there are algorithms to summarize multiple medication effects on respiratory depression/overdose risk.^14,15 Chlorpromazine equivalents were used to translate a range of antipsychotic potencies in the early days of antipsychotic treatment. Adverse effects and some treatment responses partially corresponded to the level of dopamine blockade, but not without noise. There is a wide range of variance as antipsychotic potency is assessed for clinical efficacy.¹⁶ We are still working on the array of medication potency and selectivity across neurotransmitter systems.^17,18 For example, paroxetine is a potent serotonin reuptake blocker but less selective than citalopram, particularly antagonizing cholinergic muscarinic receptors.

The authors noted their hypothesis needs further elaboration and quantification as psychiatry moves from impressionistic practice to firmer science. Measurement of neuro­transmitter activity is an area of intense research. Biomeasures have yet to add much value to the clinical practice of psychiatry, but we hope for progress. Functional neuroimaging with sophisticated algorithms is beginning to detail neocortical activity.¹⁹ CSF measurement of dopamine and serotonin metabolites seem to correlate with severe depression and suicidal behavior. Noninvasive, wearable technologies to measure galvanic skin response, oxygenation, and neurotransmitter metabolic products may add to neuro-transmitter-based assessment and treatment.

Neurotransmitters are one aspect of brain function. Other processes, such as hormonal neuromodulation²⁰ and ion channels, may be over- or underactive. Channelopathies are of particular interest in cardiology and neurology but are also notable in pain and emotional disorders.^21-26 Voltage-gated sodium channels are thought to be involved in general anesthesia.²⁷ Adverse effects of some psychotropic medications are best understood as ion channel dysfunction.²⁸ Using the strategy of this hypothesis applied to activation or inactivation of sodium, potassium, and calcium channels can guide useful diagnostic and treatment ideas for further study.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in his letter, or with manufacturers of competing products.

References

1. Mash DC. Excited delirium and sudden death: a syndromal disorder at the extreme end of the neuropsychiatric continuum. Front Physiol. 2016;7:435.

2. Fallows Z. MIT MedLinks. Accessed August 8, 2022. http://web.mit.edu/zakf/www/drugchart/drugchart11.html

3. Groot PC, van Os J. How user knowledge of psychotropic drug withdrawal resulted in the development of person-specific tapering medication. Ther Adv Psychopharmacol. 2020;10:2045125320932452. doi:10.1177/2045125320932452

4. Picciotto MR, Higley MJ, Mineur YS. Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior. Neuron. 2012;76(1):116-129.

5. Nair VP, Hunter JM. Anticholinesterases and anticholinergic drugs. Continuing Education in Anaesthesia Critical Care & Pain. 2004;4(5):164-168.

6. Dawson AH, Buckley NA. Pharmacological management of anticholinergic delirium--theory, evidence and practice. Br J Clin Pharmacol. 2016;81(3):516-524.

7. Dulawa SC, Janowsky DS. Cholinergic regulation of mood: from basic and clinical studies to emerging therapeutics. Mol Psychiatry. 2019;24(5):694-709.

8. Adeyinka A, Kondamudi NP. Cholinergic Crisis. StatPearls Publishing; 2022.

9. El Mansari M, Guiard BP, Chernoloz O, et al. Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder. CNS Neurosci Ther. 2010;16(3):e1-e17.

10. Esposito E. Serotonin-dopamine interaction as a focus of novel antidepressant drugs. Curr Drug Targets. 2006;7(2):177-185.

11. Kringelbach ML, Cruzat J, Cabral J, et al. Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proc Natl Acad Sci U S A. 2020;117(17):9566-9576.

12. Thiele A, Bellgrove MA. Neuromodulation of attention. Neuron. 2018;97(4):769-785.

13. Muñoz A, Lopez-Lopez A, Labandeira CM, et al. Interactions between the serotonergic and other neurotransmitter systems in the basal ganglia: role in Parkinson’s disease and adverse effects of L-DOPA. Front Neuroanat. 2020;14:26.

14. Nielsen S, Degenhardt L, Hoban B, et al. A synthesis of oral morphine equivalents (OME) for opioid utilisation studies. Pharmacoepidemiol Drug Saf. 2016;25(6):733-737.

15. Lo-Ciganic WH, Huang JL, Zhang HH, et al. Evaluation of machine-learning algorithms for predicting opioid overdose risk among Medicare beneficiaries with opioid prescriptions. JAMA Netw Open. 2019;2(3):e190968. doi:10.1001/jamanetworkopen.2019.0968

16. Dewan MJ, Koss M. The clinical impact of reported variance in potency of antipsychotic agents. Acta Psychiatr Scand. 1995;91(4):229-232.

17. Woods SW. Chlorpromazine equivalent doses for the newer atypical antipsychotics. J Clin Psychiatry. 2003;64(6):663-667.

18. Hayasaka Y, Purgato M, Magni LR, et al. Dose equivalents of antidepressants: evidence-based recommendations from randomized controlled trials. J Affect Disord. 2015;180:179-184.

19. Hansen JY, Shafiei G, Markello RD, et al. Mapping neurotransmitter systems to the structural and functional organization of the human neocortex. bioRxiv. 2021. https://doi.org/10.1101/2021.10.28.466336

20. Hwang WJ, Lee TY, Kim NS, et al. The role of estrogen receptors and their signaling across psychiatric disorders. Int J Mol Sci. 2020;22(1):373.

21. Lawrence JH, Tomaselli GF, Marban E. Ion channels: structure and function. Heart Dis Stroke. 1993;2(1):75-80.

22. Fedele F, Severino P, Bruno N, et al. Role of ion channels in coronary microcirculation: a review of the literature. Future Cardiol. 2013;9(6):897-905.

23. Kumar P, Kumar D, Jha SK, et al. Ion channels in neurological disorders. Adv Protein Chem Struct Biol. 2016;103:97-136.

24. Quagliato LA, Nardi AE. The role of convergent ion channel pathways in microglial phenotypes: a systematic review of the implications for neurological and psychiatric disorders. Transl Psychiatry. 2018;8(1):259.

25. Bianchi MT, Botzolakis EJ. Targeting ligand-gated ion channels in neurology and psychiatry: is pharmacological promiscuity an obstacle or an opportunity? BMC Pharmacol. 2010;10:3.

26. Imbrici P, Camerino DC, Tricarico D. Major channels involved in neuropsychiatric disorders and therapeutic perspectives. Front Genet. 2013;4:76.

27. Xiao J, Chen Z, Yu B. A potential mechanism of sodium channel mediating the general anesthesia induced by propofol. Front Cell Neurosci. 2020;14:593050. doi:10.3389/fncel.2020.593050

28. Kamei S, Sato N, Harayama Y, et al. Molecular analysis of potassium ion channel genes in sudden death cases among patients administered psychotropic drug therapy: are polymorphisms in LQT genes a potential risk factor? J Hum Genet. 2014;59(2):95-99.

The authors respond

Thank you for your thoughtful commen­tary. Our conceptual article was not designed to cover enough ground to be completely thorough. Everything you wrote adds to what we wanted to bring to the reader’s attention. The mechanisms of disease in psychiatry are numerous and still elusive, and the brain’s complexity is staggering. Our main goal was to point out possible correlations between specific symptoms and specific neurotransmitter activity. We had to oversimplify to make the article concise enough for publication. Neurotransmitter effects are based on their synthesis, storage, release, reuptake, and degradation. A receptor’s quantity and quality of function, inhibitors, inducers, and many other factors are involved in neurotransmitter performance. And, of course, there are additional fundamental neurotransmitters beyond the 6 we touched on. Our ability to sort through all of this is still rudimentary. You also reflect on the emerging methods to objectively measure neuro­transmitter activity, which will eventually find their way to clinical practice and become invaluable. Still, we treat people, not tests or pictures, so diagnostic thinking based on clinical presentation will forever remain a cornerstone of dealing with individual patients.

We hope scientists and clinicians such as yourself will improve our concept and make it truly practical.

Dmitry M. Arbuck, MD
Clinical Assistant Professor of Psychiatry and Medicine
Indiana University School of Medicine
Indianapolis, Indiana
President and Medical Director
Indiana Polyclinic
Carmel, Indiana

José Miguel Salmerón, MD
Professor
Department of Psychiatry
Universidad del Valle School of Medicine/Hospital
Universitario del Valle
Cali, Colombia

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in their response, or with manufacturers of competing products.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact let[email protected].

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact let[email protected].

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact let[email protected].

Mr. F, age 42, says he has always been a very anxious person and has chronically found his worrying to negatively affect his life. He says that over the last month his anxiety has been “off the charts” and he is worrying “24/7” due to taking on new responsibilities at his job and his son being diagnosed with lupus. He says his constant worrying is significantly impairing his ability to focus at his job, and he is considering taking a mental health leave from work. His wife reports that she is extremely frustrated because Mr. F has been isolating himself from family and friends; he admits this is true and attributes it to being preoccupied by his worries.

Mr. F endorses chronic insomnia, muscle tension, and irritability associated with anxiety; these have all substantially worsened over the last month. He admits that recently he has occasionally thought it would be easier if he weren’t alive. Mr. F denies having problems with his energy or motivation levels and insists that he generally feels very anxious, but not depressed. He says he drinks 1 alcoholic drink per week and denies any other substance use. Mr. F is overweight and has slightly elevated cholesterol but denies any other health conditions. He takes melatonin to help him sleep but does not take any prescribed medications.

Although this vignette provides limited details, on the surface it appears that Mr. F is experiencing an exacerbation of chronic generalized anxiety disorder (GAD). However, in this article, I propose establishing a new diagnosis: “acute anxiety disorder,” which would encapsulate severe exacerbations of a pre-existing anxiety disorder. Among the patients I have encountered for whom this diagnosis would fit, most have pre-existing GAD or panic disorder.

A look at the differential diagnosis

It is important to determine whether Mr. F is using any substances or has a medical condition that could be contributing to his anxiety. Other psychiatric diagnoses that could be considered include:

Adjustment disorder. This diagnosis would make sense if Mr. F didn’t have an apparent chronic history of symptoms that meet criteria for GAD.

Major depressive disorder with anxious distress. Many patients experiencing a major depressive episode meet the criteria for the specifier “with anxious distress,” even those who do not have a comorbid anxiety disorder.¹ However, it is not evident from this vignette that Mr. F is experiencing a major depressive episode.

Continue to: Panic disorder and GAD...

Panic disorder and GAD. It is possible for a patient with GAD to develop panic disorder, which, at times, occurs after experiencing significant life stressors. Panic disorder requires the presence of recurrent panic attacks. Mr. F describes experiencing chronic, intense symptoms of anxiety rather than the discreet episodes of acute symptoms that characterize panic attacks.

Acute stress disorder. This diagnosis involves psychological symptoms that occur in response to exposure to actual or threatened death, serious injury, or sexual violation. Mr. F was not exposed to any of these stressors.

Why this new diagnosis would be helpful

A new diagnosis, acute anxiety disorder, would indicate that a patient is currently experiencing an acute exacerbation of a chronic anxiety disorder that is leading to a significant decrease in their baseline functioning. My proposed criteria for acute anxiety disorder appear in the Table. Here are some reasons this diagnosis would be helpful:

Signifier of severity. Anxiety disorders such as GAD are generally not considered severe conditions and not considered to fall under the rubric of SPMI (severe and persistent mental illness).² Posttraumatic stress disorder is the anxiety disorder–like condition most often found in the SPMI category. A diagnosis of acute anxiety disorder would indicate a patient is experiencing an episode of anxiety that is distinct from their chronic anxiety condition due to its severe impact on functional capabilities. Acute anxiety disorder would certainly not qualify as a “SPMI diagnosis” that would facilitate someone being considered eligible for supplemental security income, but it might be a legitimate justification for someone to receive short-term disability.

Treatment approach. The pharmacologic treatment of anxiety disorders usually involves a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI). However, these medications can sometimes briefly increase anxiety when they are started. Individuals with acute anxiety are the most vulnerable to the possibility of experiencing increased anxiety when starting an SSRI or SNRI and may benefit from a slower titration of these medications. In light of this and the length of time required for SSRIs or SNRIs to exert a positive effect (typically a few weeks), patients with acute anxiety are best served by treatment with a medication with an immediate onset of action, such as a benzodiazepine or a sleep medication (eg, zolpidem). Benzodiazepines and hypnotics such as zolpidem are best prescribed for as-needed use because they carry a risk of dependence. One might consider prescribing mirtazapine or pregabalin (both of which are used off-label to treat anxiety) because these medications also have a relatively rapid onset of action and can treat both anxiety and insomnia (particularly mirtazapine).

Research considerations. It would be helpful to study which treatments are most effective for the subset of patients who experience acute anxiety disorder as I define it. Perhaps psychotherapy treatment protocols could be adapted or created. Treatment with esketamine or IV ketamine might be further studied as a treatment for acute anxiety because some evidence suggests ketamine is efficacious for this indication.³

Obsessive-compulsive disorder (OCD) is typically a severe, chronic illness in which patients have recurrent, unwanted thoughts, urges, and compulsions.¹ It causes significant morbidity and lost potential over time, and is the world’s 10th-most disabling disorder in terms of lost income and decreased quality of life, and the fifth-most disabling mental health condition.² Patients with OCD (and their clinicians) are often desperate for an efficacious treatment, but we must ensure that those who are not helped by traditional psychotherapeutic and/or pharmacologic treatments are appropriate for safe neurosurgical intervention.

Pros and cons of neurosurgical therapies

Most patients with OCD are effectively treated with cognitive-behavioral therapy and pharmacotherapy in the form of selective serotonin reuptake inhibitors, clomipramine, or second-generation antipsychotics. However, up to 5% of individuals with OCD will have symptoms refractory to these traditional therapies.³ These cases require more aggressive forms of therapy, including radiofrequency ablation surgeries and deep brain stimulation (DBS). The efficacy of both therapies is similar at 40% to 60%.^4,5 While these treatments can be life-changing for patients fortunate to receive them, they are not without issue.

Only a limited number of institutions offer these neurosurgical techniques, and for many patients, those locations may be inaccessible. Patients may not experience relief simply due to where they live, difficult logistics, and the high cost requisite to receive care. If fortunate enough to live near a participating institution or have the means to travel to one, the patient and clinician must then choose the best option based on the nuances of the patient’s situation.

Ablation techniques, such as gamma knife or magnetic resonance–guided ultrasound, are simpler and more cost-effective. A drawback of this approach, however, is that it is irreversible. Lesioned structures are irreparable, as are the adverse effects of the surgery, which, while rare, may include a persistent minimally conscious state or necrotic cysts.⁴ A benefit of this approach is that there is no need for lengthy follow-up as seen with DBS.

DBS is more complicated. In addition to having to undergo an open neurosurgical procedure, these patients require long-term follow-up and monitoring. A positive aspect is the device can be turned off or removed. However, the amount of follow-up and adjustments is significant. These patients need access to clinicians skilled in DBS device management.

Finally, we must consider the chronically ill patient’s perspective after successful treatment. While the patient’s symptoms may improve, their lives and identities likely developed around their symptoms. Bosanac et al⁶ describe this reality well in a case study in which a patient with OCD was “burdened with normality” after successful DBS treatment. He was finally able to work, build meaningful relationships, and approach previously unattainable social milestones. This was an overwhelming experience for him, and he and his family needed guidance into the world in which most of us find comfort.

As ablation techniques, DBS, and other cutting-edge therapies for OCD come to the forefront of modern care, clinicians must remember to keep patient safety first. Verify follow-up care before committing patients to invasive and irreversible treatments. While general access is currently poor, participating institutions should consider advertising and communicating that there is an accessible network available for these chronically ill individuals.

Obsessive-compulsive disorder (OCD) is typically a severe, chronic illness in which patients have recurrent, unwanted thoughts, urges, and compulsions.¹ It causes significant morbidity and lost potential over time, and is the world’s 10th-most disabling disorder in terms of lost income and decreased quality of life, and the fifth-most disabling mental health condition.² Patients with OCD (and their clinicians) are often desperate for an efficacious treatment, but we must ensure that those who are not helped by traditional psychotherapeutic and/or pharmacologic treatments are appropriate for safe neurosurgical intervention.

Pros and cons of neurosurgical therapies

Most patients with OCD are effectively treated with cognitive-behavioral therapy and pharmacotherapy in the form of selective serotonin reuptake inhibitors, clomipramine, or second-generation antipsychotics. However, up to 5% of individuals with OCD will have symptoms refractory to these traditional therapies.³ These cases require more aggressive forms of therapy, including radiofrequency ablation surgeries and deep brain stimulation (DBS). The efficacy of both therapies is similar at 40% to 60%.^4,5 While these treatments can be life-changing for patients fortunate to receive them, they are not without issue.

Only a limited number of institutions offer these neurosurgical techniques, and for many patients, those locations may be inaccessible. Patients may not experience relief simply due to where they live, difficult logistics, and the high cost requisite to receive care. If fortunate enough to live near a participating institution or have the means to travel to one, the patient and clinician must then choose the best option based on the nuances of the patient’s situation.

Ablation techniques, such as gamma knife or magnetic resonance–guided ultrasound, are simpler and more cost-effective. A drawback of this approach, however, is that it is irreversible. Lesioned structures are irreparable, as are the adverse effects of the surgery, which, while rare, may include a persistent minimally conscious state or necrotic cysts.⁴ A benefit of this approach is that there is no need for lengthy follow-up as seen with DBS.

DBS is more complicated. In addition to having to undergo an open neurosurgical procedure, these patients require long-term follow-up and monitoring. A positive aspect is the device can be turned off or removed. However, the amount of follow-up and adjustments is significant. These patients need access to clinicians skilled in DBS device management.

Finally, we must consider the chronically ill patient’s perspective after successful treatment. While the patient’s symptoms may improve, their lives and identities likely developed around their symptoms. Bosanac et al⁶ describe this reality well in a case study in which a patient with OCD was “burdened with normality” after successful DBS treatment. He was finally able to work, build meaningful relationships, and approach previously unattainable social milestones. This was an overwhelming experience for him, and he and his family needed guidance into the world in which most of us find comfort.

As ablation techniques, DBS, and other cutting-edge therapies for OCD come to the forefront of modern care, clinicians must remember to keep patient safety first. Verify follow-up care before committing patients to invasive and irreversible treatments. While general access is currently poor, participating institutions should consider advertising and communicating that there is an accessible network available for these chronically ill individuals.

Obsessive-compulsive disorder (OCD) is typically a severe, chronic illness in which patients have recurrent, unwanted thoughts, urges, and compulsions.¹ It causes significant morbidity and lost potential over time, and is the world’s 10th-most disabling disorder in terms of lost income and decreased quality of life, and the fifth-most disabling mental health condition.² Patients with OCD (and their clinicians) are often desperate for an efficacious treatment, but we must ensure that those who are not helped by traditional psychotherapeutic and/or pharmacologic treatments are appropriate for safe neurosurgical intervention.

Pros and cons of neurosurgical therapies

Most patients with OCD are effectively treated with cognitive-behavioral therapy and pharmacotherapy in the form of selective serotonin reuptake inhibitors, clomipramine, or second-generation antipsychotics. However, up to 5% of individuals with OCD will have symptoms refractory to these traditional therapies.³ These cases require more aggressive forms of therapy, including radiofrequency ablation surgeries and deep brain stimulation (DBS). The efficacy of both therapies is similar at 40% to 60%.^4,5 While these treatments can be life-changing for patients fortunate to receive them, they are not without issue.

Only a limited number of institutions offer these neurosurgical techniques, and for many patients, those locations may be inaccessible. Patients may not experience relief simply due to where they live, difficult logistics, and the high cost requisite to receive care. If fortunate enough to live near a participating institution or have the means to travel to one, the patient and clinician must then choose the best option based on the nuances of the patient’s situation.

Ablation techniques, such as gamma knife or magnetic resonance–guided ultrasound, are simpler and more cost-effective. A drawback of this approach, however, is that it is irreversible. Lesioned structures are irreparable, as are the adverse effects of the surgery, which, while rare, may include a persistent minimally conscious state or necrotic cysts.⁴ A benefit of this approach is that there is no need for lengthy follow-up as seen with DBS.

DBS is more complicated. In addition to having to undergo an open neurosurgical procedure, these patients require long-term follow-up and monitoring. A positive aspect is the device can be turned off or removed. However, the amount of follow-up and adjustments is significant. These patients need access to clinicians skilled in DBS device management.

Finally, we must consider the chronically ill patient’s perspective after successful treatment. While the patient’s symptoms may improve, their lives and identities likely developed around their symptoms. Bosanac et al⁶ describe this reality well in a case study in which a patient with OCD was “burdened with normality” after successful DBS treatment. He was finally able to work, build meaningful relationships, and approach previously unattainable social milestones. This was an overwhelming experience for him, and he and his family needed guidance into the world in which most of us find comfort.

As ablation techniques, DBS, and other cutting-edge therapies for OCD come to the forefront of modern care, clinicians must remember to keep patient safety first. Verify follow-up care before committing patients to invasive and irreversible treatments. While general access is currently poor, participating institutions should consider advertising and communicating that there is an accessible network available for these chronically ill individuals.

Since the first issue of GI & Hepatology News was published 15 years ago, the field of hepatology has undergone a tremendous transformation.

In the late 2000s, we witnessed revolutionary discoveries and advances in our understanding and management of chronic hepatitis C. Who knew that when IL-28B was first described in 2009, providing a genetic basis for patients’ response to interferon-based therapies, its impact would also be so swiftly supplanted by the introduction of direct acting antivirals a few years later? The pipeline for HCV treatment was feverish for several years, which resulted in a complete transformation of HCV treatment from a long, exhausting, side-effect filled course to a simple 8-to-12-week regimen. Furthermore, we now have established protocols for organ transplantation for patients without active HCV infection to receive HCV-positive organs due to the effectiveness of treatments for HCV. This kind of progress in our field demonstrates how awe-inspiring medical advances can be and how fortunate we are to have witnessed and lived this progress in such a short period of time.

Dr. Jou is associate professor of medicine, division of gastroenterology and hepatology, School of Medicine Fellowship program director, Medicine, Division of Gastroenterology and Hepatology, School of Medicine, Oregon Health and Science University, Portland. She reported no relevant financial conflicts of interest.

Since the first issue of GI & Hepatology News was published 15 years ago, the field of hepatology has undergone a tremendous transformation.

In the late 2000s, we witnessed revolutionary discoveries and advances in our understanding and management of chronic hepatitis C. Who knew that when IL-28B was first described in 2009, providing a genetic basis for patients’ response to interferon-based therapies, its impact would also be so swiftly supplanted by the introduction of direct acting antivirals a few years later? The pipeline for HCV treatment was feverish for several years, which resulted in a complete transformation of HCV treatment from a long, exhausting, side-effect filled course to a simple 8-to-12-week regimen. Furthermore, we now have established protocols for organ transplantation for patients without active HCV infection to receive HCV-positive organs due to the effectiveness of treatments for HCV. This kind of progress in our field demonstrates how awe-inspiring medical advances can be and how fortunate we are to have witnessed and lived this progress in such a short period of time.

Dr. Jou is associate professor of medicine, division of gastroenterology and hepatology, School of Medicine Fellowship program director, Medicine, Division of Gastroenterology and Hepatology, School of Medicine, Oregon Health and Science University, Portland. She reported no relevant financial conflicts of interest.

Since the first issue of GI & Hepatology News was published 15 years ago, the field of hepatology has undergone a tremendous transformation.

In the late 2000s, we witnessed revolutionary discoveries and advances in our understanding and management of chronic hepatitis C. Who knew that when IL-28B was first described in 2009, providing a genetic basis for patients’ response to interferon-based therapies, its impact would also be so swiftly supplanted by the introduction of direct acting antivirals a few years later? The pipeline for HCV treatment was feverish for several years, which resulted in a complete transformation of HCV treatment from a long, exhausting, side-effect filled course to a simple 8-to-12-week regimen. Furthermore, we now have established protocols for organ transplantation for patients without active HCV infection to receive HCV-positive organs due to the effectiveness of treatments for HCV. This kind of progress in our field demonstrates how awe-inspiring medical advances can be and how fortunate we are to have witnessed and lived this progress in such a short period of time.

Dr. Jou is associate professor of medicine, division of gastroenterology and hepatology, School of Medicine Fellowship program director, Medicine, Division of Gastroenterology and Hepatology, School of Medicine, Oregon Health and Science University, Portland. She reported no relevant financial conflicts of interest.

At the risk of losing a digit or two I am going to dip my toes into the murky waters of gender-affirming care, sometimes referred to as trans care. Recently, Moira Szilagyi, MD, PhD, president of the American Academy of Pediatrics, released two statements, one in the Aug. 22, 2022, Wall Street Journal, the other summarized in the Aug. 25, 2022, AAP Daily Briefing, in which she attempts to clarify the academy’s position on gender-affirming care. They were well-worded and heroic attempts to clear the air. I fear these explanations will do little to encourage informed and courteous discussions between those entrenched on either side of a disagreement that is unfortunately being played out on media outlets and state legislatures instead of the offices of primary care physicians and specialists where it belongs.

The current mess is an example of what can happen when there is a paucity of reliable data, a superabundance of emotion, and a system that feeds on instant news and sound bites with little understanding of how science should work.

Some of the turmoil is a response to the notion that in certain situations gender dysphoria may be a condition that can be learned or mimicked from exposure to other gender-dysphoric individuals. Two papers anchor either side of the debate. The first paper was published in 2018 by a then–Brown University health expert who hypothesized the existence of a condition which she labeled “rapid-onset gender dysphoria [ROGD]”. One can imagine that “social contagion” might be considered as one of the potential contributors to this hypothesized condition. Unfortunately, the publication of the paper ignited a firestorm of criticism from a segment of the population that advocates for the transgender community, prompting the university and the online publisher to backpedal and reevaluate the quality of the research on which the paper was based.

One of the concerns voiced at the time of publication was that the research could be used to support the transphobic agenda by some state legislatures hoping to ban gender-affirming care. How large a role the paper played in the current spate of legislation in is unclear. I suspect it has been small. But, one can’t deny the potential exists.

Leaping forward to 2022, the second paper was published in the August issue of Pediatrics, in which the authors attempted to test the ROGD hypothesis and question the inference of social contagion.

The investigators found that in 2017 and 2019 the birth ratios of transgender-diverse (TGD) individuals did not favor assigned female-sex-at-birth (AFAB) individuals. They also discovered that in their sample overall there was a decrease in the percentage of adolescents who self-identified as TGD. Not surprisingly, “bullying victimization and suicidality were higher among TGD youth when compared with their cisgender peers.” The authors concluded that their findings were “incongruent with an ROGD hypothesis that posits social contagion” nor should it be used to restrict access to gender-affirming care.

There you have it. Are we any closer to understanding gender dysphoria and its origins? I don’t think so. The media is somewhat less confused. The NBC News online presence headline on Aug. 3, 2022, reads “‘Social contagion’ isn’t causing more youths to be transgender, study finds.”

My sense is that the general population perceives an increase in the prevalence of gender dysphoria. It is very likely that this perception is primarily a reflection of a more compassionate and educated attitude in a significant portion of the population making it less challenging for gender-dysphoric youth to surface. However, it should not surprise us that some parents and observers are concerned that a percentage of this increased prevalence is the result of social contagion. Nor should it surprise us that some advocates for the trans population feel threatened by this hypothesis.

Neither of these studies really answers the question of whether some cases of gender dysphoria are the result of social contagion. Both were small samples using methodology that has been called into question. The bottom line is that we need more studies and must remain open to considering their results. That’s how science should work.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

At the risk of losing a digit or two I am going to dip my toes into the murky waters of gender-affirming care, sometimes referred to as trans care. Recently, Moira Szilagyi, MD, PhD, president of the American Academy of Pediatrics, released two statements, one in the Aug. 22, 2022, Wall Street Journal, the other summarized in the Aug. 25, 2022, AAP Daily Briefing, in which she attempts to clarify the academy’s position on gender-affirming care. They were well-worded and heroic attempts to clear the air. I fear these explanations will do little to encourage informed and courteous discussions between those entrenched on either side of a disagreement that is unfortunately being played out on media outlets and state legislatures instead of the offices of primary care physicians and specialists where it belongs.

The current mess is an example of what can happen when there is a paucity of reliable data, a superabundance of emotion, and a system that feeds on instant news and sound bites with little understanding of how science should work.

Some of the turmoil is a response to the notion that in certain situations gender dysphoria may be a condition that can be learned or mimicked from exposure to other gender-dysphoric individuals. Two papers anchor either side of the debate. The first paper was published in 2018 by a then–Brown University health expert who hypothesized the existence of a condition which she labeled “rapid-onset gender dysphoria [ROGD]”. One can imagine that “social contagion” might be considered as one of the potential contributors to this hypothesized condition. Unfortunately, the publication of the paper ignited a firestorm of criticism from a segment of the population that advocates for the transgender community, prompting the university and the online publisher to backpedal and reevaluate the quality of the research on which the paper was based.

One of the concerns voiced at the time of publication was that the research could be used to support the transphobic agenda by some state legislatures hoping to ban gender-affirming care. How large a role the paper played in the current spate of legislation in is unclear. I suspect it has been small. But, one can’t deny the potential exists.

Leaping forward to 2022, the second paper was published in the August issue of Pediatrics, in which the authors attempted to test the ROGD hypothesis and question the inference of social contagion.

The investigators found that in 2017 and 2019 the birth ratios of transgender-diverse (TGD) individuals did not favor assigned female-sex-at-birth (AFAB) individuals. They also discovered that in their sample overall there was a decrease in the percentage of adolescents who self-identified as TGD. Not surprisingly, “bullying victimization and suicidality were higher among TGD youth when compared with their cisgender peers.” The authors concluded that their findings were “incongruent with an ROGD hypothesis that posits social contagion” nor should it be used to restrict access to gender-affirming care.

There you have it. Are we any closer to understanding gender dysphoria and its origins? I don’t think so. The media is somewhat less confused. The NBC News online presence headline on Aug. 3, 2022, reads “‘Social contagion’ isn’t causing more youths to be transgender, study finds.”

My sense is that the general population perceives an increase in the prevalence of gender dysphoria. It is very likely that this perception is primarily a reflection of a more compassionate and educated attitude in a significant portion of the population making it less challenging for gender-dysphoric youth to surface. However, it should not surprise us that some parents and observers are concerned that a percentage of this increased prevalence is the result of social contagion. Nor should it surprise us that some advocates for the trans population feel threatened by this hypothesis.

Neither of these studies really answers the question of whether some cases of gender dysphoria are the result of social contagion. Both were small samples using methodology that has been called into question. The bottom line is that we need more studies and must remain open to considering their results. That’s how science should work.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

At the risk of losing a digit or two I am going to dip my toes into the murky waters of gender-affirming care, sometimes referred to as trans care. Recently, Moira Szilagyi, MD, PhD, president of the American Academy of Pediatrics, released two statements, one in the Aug. 22, 2022, Wall Street Journal, the other summarized in the Aug. 25, 2022, AAP Daily Briefing, in which she attempts to clarify the academy’s position on gender-affirming care. They were well-worded and heroic attempts to clear the air. I fear these explanations will do little to encourage informed and courteous discussions between those entrenched on either side of a disagreement that is unfortunately being played out on media outlets and state legislatures instead of the offices of primary care physicians and specialists where it belongs.

The current mess is an example of what can happen when there is a paucity of reliable data, a superabundance of emotion, and a system that feeds on instant news and sound bites with little understanding of how science should work.

Some of the turmoil is a response to the notion that in certain situations gender dysphoria may be a condition that can be learned or mimicked from exposure to other gender-dysphoric individuals. Two papers anchor either side of the debate. The first paper was published in 2018 by a then–Brown University health expert who hypothesized the existence of a condition which she labeled “rapid-onset gender dysphoria [ROGD]”. One can imagine that “social contagion” might be considered as one of the potential contributors to this hypothesized condition. Unfortunately, the publication of the paper ignited a firestorm of criticism from a segment of the population that advocates for the transgender community, prompting the university and the online publisher to backpedal and reevaluate the quality of the research on which the paper was based.

One of the concerns voiced at the time of publication was that the research could be used to support the transphobic agenda by some state legislatures hoping to ban gender-affirming care. How large a role the paper played in the current spate of legislation in is unclear. I suspect it has been small. But, one can’t deny the potential exists.

Leaping forward to 2022, the second paper was published in the August issue of Pediatrics, in which the authors attempted to test the ROGD hypothesis and question the inference of social contagion.

The investigators found that in 2017 and 2019 the birth ratios of transgender-diverse (TGD) individuals did not favor assigned female-sex-at-birth (AFAB) individuals. They also discovered that in their sample overall there was a decrease in the percentage of adolescents who self-identified as TGD. Not surprisingly, “bullying victimization and suicidality were higher among TGD youth when compared with their cisgender peers.” The authors concluded that their findings were “incongruent with an ROGD hypothesis that posits social contagion” nor should it be used to restrict access to gender-affirming care.

There you have it. Are we any closer to understanding gender dysphoria and its origins? I don’t think so. The media is somewhat less confused. The NBC News online presence headline on Aug. 3, 2022, reads “‘Social contagion’ isn’t causing more youths to be transgender, study finds.”

My sense is that the general population perceives an increase in the prevalence of gender dysphoria. It is very likely that this perception is primarily a reflection of a more compassionate and educated attitude in a significant portion of the population making it less challenging for gender-dysphoric youth to surface. However, it should not surprise us that some parents and observers are concerned that a percentage of this increased prevalence is the result of social contagion. Nor should it surprise us that some advocates for the trans population feel threatened by this hypothesis.

Neither of these studies really answers the question of whether some cases of gender dysphoria are the result of social contagion. Both were small samples using methodology that has been called into question. The bottom line is that we need more studies and must remain open to considering their results. That’s how science should work.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

A version of this article first appeared on Medscape.com.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

A version of this article first appeared on Medscape.com.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

A version of this article first appeared on Medscape.com.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

The years start coming and they don’t stop coming.

Smash Mouth, “All Star”

Dermatologists, similar to everyone else, are subject to the inevitable: aging. More than 80% of the US population develops presbyopia, an age-related reduction in visual acuity, in their lifetime. The most common cause of refractive error in adults, presbyopia can contribute to reduced professional productivity, and individuals with uncorrected presbyopia face an estimated 8-fold increase in difficulty performing demanding near-vision tasks.¹

As specialists who rely heavily on visual assessment, dermatologists likely are aware of presbyopia, seeking care as appropriate; however, visual correction is not one size fits all, and identifying effective job-specific adjustments may require considerable trial and error. To this end, if visual correction may be needed by a large majority of dermatologists at some point, why do we not have specialized recommendations to guide the corrective process according to the individual’s defect and type of practice within the specialty? Do we need resources for dermatologists concerning ophthalmologic wellness and key warning signs of visual acuity deficits and other ocular complications?

These matters are difficult to address, made more so by the lack of data examining correctable visual impairment (CVI) in dermatology. The basis for discussion is clear; however, visual skills are highly relevant to the practice of dermatology, and age-related visual changes often are inevitable. This article will provide an overview of CVI in related disciplines and the importance of understanding CVI and corrective options in dermatology.

CVI Across Medical Disciplines

Other predominantly visual medical specialties such as pathology, radiology, and surgery have initiated research evaluating the impact of CVI on their respective practices, although consistent data still are limited. Much of the work surrounding CVI in medicine can be identified in surgery and its subspecialties. A 2020 study by Tuna et al² found that uncorrected myopia with greater than 1.75 diopter, hyperopia regardless of grade, and presbyopia with greater than 1.25 diopter correlated with reduced surgical performance when using the Da Vinci robotic system. A 2002 report by Wanzel et al³ was among the first of many studies to demonstrate the importance of visuospatial ability in surgical success. In radiology, Krupinski et al⁴ demonstrated reduced accuracy in detecting pulmonary nodules that correlated with increased myopia and decreased accommodation secondary to visual strain.

Most reports examining CVI across medical disciplines are primarily conversational or observational, with some utilizing surveys to assess the prevalence of CVI and the opinions of physicians in the field. For example, in a survey of 93 pathologists in Turkey, 93.5% (87/93) reported at least 1 type of refractive error. Eyeglasses were the most common form of correction (64.5% [60/93]); of those, 33.3% (31/93) reported using eyeglasses during microscopy.⁵

The importance of visual ability in other highly visual specialties suggests that parallels can be drawn to similar practices in dermatology. Detection of cutaneous lesions might be affected by changes in vision, similar to detection of pulmonary lesions in radiology. Likewise, dermatologic surgeons might experience a similar reduction in surgical performance due to impaired visual acuity or visuospatial ability.

The Importance of Visual Performancein Dermatology

With presbyopia often becoming clinically apparent at approximately 40 years of age,^1,6 CVI has the potential to be present for much of a dermatologist’s career. Responsibility falls on the individual practitioner to recognize their visual deficit and seek appropriate optometric or ophthalmologic care. It should be emphasized that there are many effective avenues to correct refractive error, most of which can functionally restore an individual’s vision; however, each option prioritizes different visual attributes (eg, contrast, depth perception, clarity) that have varying degrees of importance in particular areas of dermatologic practice. For example, in addition to visual acuity, dermatologic surgeons might require optimized depth perception, whereas dermatologists performing detailed visual inspection or dermoscopy might instead require optimized contrast sensitivity and acuity. At present, the literature is silent on guiding dermatologists in selecting corrective approaches that enhance the visual characteristics most important for their practice. Lack of research and direction surrounding which visual correction techniques are best suited for individual tasks risks inaccurate and nonspecific conversations with our eye care providers. Focused educated dialogues about visual needs would streamline the process of finding appropriate correction, thereby reducing unnecessary trial and error. As each dermatologic subspecialty might require a unique subset of visual skills, the conceivable benefit of dermatology-specific visual correction resources is evident.

Additionally (although beyond the scope of this commentary), guidance on how a dermatologist should increase their awareness and approach to more serious ophthalmologic conditions—including retinal tear or detachment, age-related macular degeneration, and glaucoma—also would serve as a valuable resource. Overall, prompt identification of visual changes and educated discussions surrounding their correction would allow for optimization based on the required skill set and would improve overall outcomes.

Final Thoughts

Age-related visual changes are a highly prevalent and normal process that carry the potential to impact clinical practice. Fortunately, there are multiple corrective mechanisms that can functionally restore an individual’s eyesight. However, there are no resources to guide dermatologists in seeking specialty-specific correction centered on their daily tasks, which places the responsibility for such correction on the individual. This is a circumstance in which the task at hand is clear, yet we continue to individually reinvent the wheel. We should consider this an opportunity to work together with our optometry and ophthalmology colleagues to create centralized resources that assist dermatologists in navigating age-related visual changes.

Acknowledgments—The authors thank Delaney Stratton, DNP, FNP-BC (Tucson, Arizona); J. Daniel Twelker, OD, PhD (Tucson, Arizona); and Julia Freeman, MD (Pittsburgh, Pennsylvania), for their contributions to the manuscript, as well as Susan M. Swetter, MD (Palo Alto, California) for reviewing and providing feedback.

The years start coming and they don’t stop coming.

Smash Mouth, “All Star”

Dermatologists, similar to everyone else, are subject to the inevitable: aging. More than 80% of the US population develops presbyopia, an age-related reduction in visual acuity, in their lifetime. The most common cause of refractive error in adults, presbyopia can contribute to reduced professional productivity, and individuals with uncorrected presbyopia face an estimated 8-fold increase in difficulty performing demanding near-vision tasks.¹

As specialists who rely heavily on visual assessment, dermatologists likely are aware of presbyopia, seeking care as appropriate; however, visual correction is not one size fits all, and identifying effective job-specific adjustments may require considerable trial and error. To this end, if visual correction may be needed by a large majority of dermatologists at some point, why do we not have specialized recommendations to guide the corrective process according to the individual’s defect and type of practice within the specialty? Do we need resources for dermatologists concerning ophthalmologic wellness and key warning signs of visual acuity deficits and other ocular complications?

These matters are difficult to address, made more so by the lack of data examining correctable visual impairment (CVI) in dermatology. The basis for discussion is clear; however, visual skills are highly relevant to the practice of dermatology, and age-related visual changes often are inevitable. This article will provide an overview of CVI in related disciplines and the importance of understanding CVI and corrective options in dermatology.

CVI Across Medical Disciplines

Other predominantly visual medical specialties such as pathology, radiology, and surgery have initiated research evaluating the impact of CVI on their respective practices, although consistent data still are limited. Much of the work surrounding CVI in medicine can be identified in surgery and its subspecialties. A 2020 study by Tuna et al² found that uncorrected myopia with greater than 1.75 diopter, hyperopia regardless of grade, and presbyopia with greater than 1.25 diopter correlated with reduced surgical performance when using the Da Vinci robotic system. A 2002 report by Wanzel et al³ was among the first of many studies to demonstrate the importance of visuospatial ability in surgical success. In radiology, Krupinski et al⁴ demonstrated reduced accuracy in detecting pulmonary nodules that correlated with increased myopia and decreased accommodation secondary to visual strain.

Most reports examining CVI across medical disciplines are primarily conversational or observational, with some utilizing surveys to assess the prevalence of CVI and the opinions of physicians in the field. For example, in a survey of 93 pathologists in Turkey, 93.5% (87/93) reported at least 1 type of refractive error. Eyeglasses were the most common form of correction (64.5% [60/93]); of those, 33.3% (31/93) reported using eyeglasses during microscopy.⁵

The importance of visual ability in other highly visual specialties suggests that parallels can be drawn to similar practices in dermatology. Detection of cutaneous lesions might be affected by changes in vision, similar to detection of pulmonary lesions in radiology. Likewise, dermatologic surgeons might experience a similar reduction in surgical performance due to impaired visual acuity or visuospatial ability.

The Importance of Visual Performancein Dermatology

With presbyopia often becoming clinically apparent at approximately 40 years of age,^1,6 CVI has the potential to be present for much of a dermatologist’s career. Responsibility falls on the individual practitioner to recognize their visual deficit and seek appropriate optometric or ophthalmologic care. It should be emphasized that there are many effective avenues to correct refractive error, most of which can functionally restore an individual’s vision; however, each option prioritizes different visual attributes (eg, contrast, depth perception, clarity) that have varying degrees of importance in particular areas of dermatologic practice. For example, in addition to visual acuity, dermatologic surgeons might require optimized depth perception, whereas dermatologists performing detailed visual inspection or dermoscopy might instead require optimized contrast sensitivity and acuity. At present, the literature is silent on guiding dermatologists in selecting corrective approaches that enhance the visual characteristics most important for their practice. Lack of research and direction surrounding which visual correction techniques are best suited for individual tasks risks inaccurate and nonspecific conversations with our eye care providers. Focused educated dialogues about visual needs would streamline the process of finding appropriate correction, thereby reducing unnecessary trial and error. As each dermatologic subspecialty might require a unique subset of visual skills, the conceivable benefit of dermatology-specific visual correction resources is evident.

Additionally (although beyond the scope of this commentary), guidance on how a dermatologist should increase their awareness and approach to more serious ophthalmologic conditions—including retinal tear or detachment, age-related macular degeneration, and glaucoma—also would serve as a valuable resource. Overall, prompt identification of visual changes and educated discussions surrounding their correction would allow for optimization based on the required skill set and would improve overall outcomes.

Final Thoughts

Age-related visual changes are a highly prevalent and normal process that carry the potential to impact clinical practice. Fortunately, there are multiple corrective mechanisms that can functionally restore an individual’s eyesight. However, there are no resources to guide dermatologists in seeking specialty-specific correction centered on their daily tasks, which places the responsibility for such correction on the individual. This is a circumstance in which the task at hand is clear, yet we continue to individually reinvent the wheel. We should consider this an opportunity to work together with our optometry and ophthalmology colleagues to create centralized resources that assist dermatologists in navigating age-related visual changes.

Acknowledgments—The authors thank Delaney Stratton, DNP, FNP-BC (Tucson, Arizona); J. Daniel Twelker, OD, PhD (Tucson, Arizona); and Julia Freeman, MD (Pittsburgh, Pennsylvania), for their contributions to the manuscript, as well as Susan M. Swetter, MD (Palo Alto, California) for reviewing and providing feedback.

The years start coming and they don’t stop coming.

Smash Mouth, “All Star”

Dermatologists, similar to everyone else, are subject to the inevitable: aging. More than 80% of the US population develops presbyopia, an age-related reduction in visual acuity, in their lifetime. The most common cause of refractive error in adults, presbyopia can contribute to reduced professional productivity, and individuals with uncorrected presbyopia face an estimated 8-fold increase in difficulty performing demanding near-vision tasks.¹

As specialists who rely heavily on visual assessment, dermatologists likely are aware of presbyopia, seeking care as appropriate; however, visual correction is not one size fits all, and identifying effective job-specific adjustments may require considerable trial and error. To this end, if visual correction may be needed by a large majority of dermatologists at some point, why do we not have specialized recommendations to guide the corrective process according to the individual’s defect and type of practice within the specialty? Do we need resources for dermatologists concerning ophthalmologic wellness and key warning signs of visual acuity deficits and other ocular complications?

These matters are difficult to address, made more so by the lack of data examining correctable visual impairment (CVI) in dermatology. The basis for discussion is clear; however, visual skills are highly relevant to the practice of dermatology, and age-related visual changes often are inevitable. This article will provide an overview of CVI in related disciplines and the importance of understanding CVI and corrective options in dermatology.

CVI Across Medical Disciplines

Other predominantly visual medical specialties such as pathology, radiology, and surgery have initiated research evaluating the impact of CVI on their respective practices, although consistent data still are limited. Much of the work surrounding CVI in medicine can be identified in surgery and its subspecialties. A 2020 study by Tuna et al² found that uncorrected myopia with greater than 1.75 diopter, hyperopia regardless of grade, and presbyopia with greater than 1.25 diopter correlated with reduced surgical performance when using the Da Vinci robotic system. A 2002 report by Wanzel et al³ was among the first of many studies to demonstrate the importance of visuospatial ability in surgical success. In radiology, Krupinski et al⁴ demonstrated reduced accuracy in detecting pulmonary nodules that correlated with increased myopia and decreased accommodation secondary to visual strain.

Most reports examining CVI across medical disciplines are primarily conversational or observational, with some utilizing surveys to assess the prevalence of CVI and the opinions of physicians in the field. For example, in a survey of 93 pathologists in Turkey, 93.5% (87/93) reported at least 1 type of refractive error. Eyeglasses were the most common form of correction (64.5% [60/93]); of those, 33.3% (31/93) reported using eyeglasses during microscopy.⁵

The importance of visual ability in other highly visual specialties suggests that parallels can be drawn to similar practices in dermatology. Detection of cutaneous lesions might be affected by changes in vision, similar to detection of pulmonary lesions in radiology. Likewise, dermatologic surgeons might experience a similar reduction in surgical performance due to impaired visual acuity or visuospatial ability.

The Importance of Visual Performancein Dermatology

With presbyopia often becoming clinically apparent at approximately 40 years of age,^1,6 CVI has the potential to be present for much of a dermatologist’s career. Responsibility falls on the individual practitioner to recognize their visual deficit and seek appropriate optometric or ophthalmologic care. It should be emphasized that there are many effective avenues to correct refractive error, most of which can functionally restore an individual’s vision; however, each option prioritizes different visual attributes (eg, contrast, depth perception, clarity) that have varying degrees of importance in particular areas of dermatologic practice. For example, in addition to visual acuity, dermatologic surgeons might require optimized depth perception, whereas dermatologists performing detailed visual inspection or dermoscopy might instead require optimized contrast sensitivity and acuity. At present, the literature is silent on guiding dermatologists in selecting corrective approaches that enhance the visual characteristics most important for their practice. Lack of research and direction surrounding which visual correction techniques are best suited for individual tasks risks inaccurate and nonspecific conversations with our eye care providers. Focused educated dialogues about visual needs would streamline the process of finding appropriate correction, thereby reducing unnecessary trial and error. As each dermatologic subspecialty might require a unique subset of visual skills, the conceivable benefit of dermatology-specific visual correction resources is evident.

Additionally (although beyond the scope of this commentary), guidance on how a dermatologist should increase their awareness and approach to more serious ophthalmologic conditions—including retinal tear or detachment, age-related macular degeneration, and glaucoma—also would serve as a valuable resource. Overall, prompt identification of visual changes and educated discussions surrounding their correction would allow for optimization based on the required skill set and would improve overall outcomes.

Final Thoughts

Age-related visual changes are a highly prevalent and normal process that carry the potential to impact clinical practice. Fortunately, there are multiple corrective mechanisms that can functionally restore an individual’s eyesight. However, there are no resources to guide dermatologists in seeking specialty-specific correction centered on their daily tasks, which places the responsibility for such correction on the individual. This is a circumstance in which the task at hand is clear, yet we continue to individually reinvent the wheel. We should consider this an opportunity to work together with our optometry and ophthalmology colleagues to create centralized resources that assist dermatologists in navigating age-related visual changes.

Acknowledgments—The authors thank Delaney Stratton, DNP, FNP-BC (Tucson, Arizona); J. Daniel Twelker, OD, PhD (Tucson, Arizona); and Julia Freeman, MD (Pittsburgh, Pennsylvania), for their contributions to the manuscript, as well as Susan M. Swetter, MD (Palo Alto, California) for reviewing and providing feedback.

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].