Commentary

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Biologic therapies have transformed the treatment of psoriasis. Current biologics approved for psoriasis include monoclonal antibodies targeting various pathways: tumor necrosis factor α (TNF-α) inhibitors (infliximab, adalimumab, certolizumab, etanercept), the p40 subunit common to IL-12 and IL-23 (ustekinumab), the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab), IL-17A (secukinumab, ixekizumab), IL-17 receptor A (brodalumab), and dual IL-17A/IL-17F inhibition (bimekizumab). Recent research showed that risankizumab achieved the highest Psoriasis Area and Severity Index (PASI) 90 scores in short- and long-term treatment periods (4 and 16 weeks, respectively) compared to other biologics, and IL-23 inhibitors demonstrated the lowest short- and long-term adverse event rates and the most favorable long-term risk-benefit profile compared to IL-17, IL-12/23, and TNF-α inhibitors.¹

Although these monoclonal antibodies have revolutionized psoriasis treatment, they are large proteins that must be administered subcutaneously or via intravenous injection. Emerging biologics are smaller proteins administered orally via a tablet or pill. In clinical trials, oral biologics have demonstrated efficacy (eTable), suggesting that oral biologics may be the future for psoriasis treatment, as this noninvasive delivery method may help improve patient compliance with treatment.

A major inflammatory pathway in psoriasis, IL-23 has been an effective and safe drug target. The novel oral IL-23 inhibitor, JNJ-2113, was discovered in 2017 and currently is being compared to deucravacitinib in the phase III ICONIC-LEAD trial (ClinicalTrials. gov Identifier NCT06095115) in patients with moderate to severe plaque psoriasis.^2,3 In the phase IIb FRONTIER 1 trial, treatment with either 3 once-daily (25 mg, 50 mg, 100 mg) and 2 twice-daily (25 mg, 100 mg) doses of JNJ-2113 led to significant improvements in PASI 75 response at 16 weeks compared to placebo (P<.001).⁴ In the phase IIb long-term extension FRONTIER 2 trial, JNJ-2113 maintained high rates of skin clearance through 52 weeks in adults with moderate to severe plaque psoriasis, with the highest PASI 75 response observed in the 100-mg twice-daily group (32/42 [76.2%]).⁵ Responses were maintained through week 52 for all JNJ-2113 treatment groups for PASI 90 and PASI 100 endpoints. In addition to ICONIC-LEAD, JNJ-2113 is being evaluated in the phase III multicenter, randomized, double-blind, placebo-controlled trial ICONIC-TOTAL (NCT06095102) in patients with special area psoriasis and ANTHEM-UC (NCT06049017) in patients with ulcerative colitis to evaluate its efficacy and safety. The most common adverse events associated with JNJ-77242113 were mild to moderate and included COVID-19 infection and nasopharyngitis.⁶ Higher rates of COVID-19 infection likely were due to immune compromise in the setting of the recent pandemic. Similar percentages of at least 1 adverse event were found in JNJ-77242113 and placebo groups (52%-58.6% and 51%-65.7%, respectively).^4,5,7

An orally administered small-molecule inhibitor of IL-17A, LY3509754, may represent a convenient alternative to IL-17A–targeting monoclonal antibodies. In a study of 91 participants,⁸ LY3509754 showed strong target engagement indicated by elevated plasma IL-17A levels within 12 hours of dosing. Despite strong target engagement and a pharmacokinetics profile that supports once-daily administration, this study showed that oral dosing with LY3509754 was poorly tolerated, as 4.4% (4/91) of participants (3 receiving 1000 mg once daily and 1 receiving 400 mg once daily) had increased liver transaminases or acute hepatitis (onset, ≥12 days following the last dose), which was consistent with drug-induced liver injury.⁸

The small potent molecule SAR441566 inhibits TNF-α by stabilizing an asymmetrical form of the soluble TNF trimer. As the asymmetrical trimer is the biologically active form of TNF-α, stabilization of the trimer compromises downstream signaling and inhibits the functions of TNF-α in vitro and in vivo. Recently, SAR441566 was found to be safe and well tolerated in healthy participants, showing efficacy in mild to moderate psoriasis in a phase Ib trial.⁹ A phase II trial of SAR441566 (NCT06073119) is being developed to create a more convenient orally bioavailable treatment option for patients with psoriasis compared to established biologic drugs targeting TNF-α.¹⁰

Few trials have focused on investigating the antipsoriatic effects of orally administered small molecules. Some of these small molecules can enter cells and inhibit the activation of T lymphocytes, leukocyte trafficking, leukotriene activity/production and angiogenesis, and promote apoptosis. Oral administration of small molecules is the future of effective and affordable psoriasis treatment, but safety and efficacy must first be assessed in clinical trials. JNJ-77242113 has shown a more promising safety profile, has recently undergone phase III trials, and may represent the newest wave for psoriasis treatment. While LY3509754 had a strong pharmacokinetics profile, it was poorly tolerated, and study participants' laboratory results suggested the drug to be hepatotoxic.⁸ SAR441566 has been shown to be safe and well tolerated in treating psoriasis, and phase II readouts are expected later in 2025. We can expect a new wave of psoriasis treatments with emerging oral therapies.

Psoriasis treatments have come a long way in the past 20 years. We now have more than a dozen systemic targeted treatments for psoriatic disease, with more on the way; however, with each successive class of medications introduced, the gap has narrowed in terms of increasing efficacy. In an era of medications reporting complete clearance rates in the 70% range, the average improvement in Psoriasis Area and Severity Index (PASI) for most biologics has remained at 90% to 95% in the past half-decade. While this is a far cry from the mean PASI improvements of 70% seen with the first biologics,¹ it is becoming more challenging to base our treatment decisions solely on PASI outcome measures.

How, then, do we approach rational selection of a systemic psoriasis treatment? We could try to delineate based on mechanism of action, but it may be disingenuous to dissect minor differences in pathways (eg, IL-17 vs IL-23) that are fundamentally related and on the same continuum in psoriasis pathophysiology. Therefore, the most meaningful way to select an appropriate therapeutic may be to adopt a patient-centered approach that accounts for both individual preferences and specific medical needs by evaluating for other comorbidities² to exclude or select certain medicines or types of treatments. We have long known to avoid tumor necrosis factor (TNF) α inhibitors in patients with congestive heart failure or a history of demyelinating disorders while regularly considering the presence of psoriatic arthritis and family planning when making treatment decisions. Now, we can be more nuanced in our approaches to psoriasis biologics. Specifically, the most important comorbidities to consider broadly encompass cardiometabolic disorders, gastrointestinal conditions, and psychiatric conditions.

Cardiometabolic Disorders

Possibly the hottest topic in psoriasis for some years now, the relationship between cardiometabolic disorders and psoriasis is of great interest to clinicians, scientists, and patients alike. There is a clear link between development of atherosclerosis and Th17-related immune mechanisms that also are implicated in the pathogenesis of psoriasis.³ Furthermore, the incidence of cardiovascular disease is markedly increased in patients with psoriasis, which is an independent risk factor for myocardial infarction, particularly among younger patients.^4,5 Although several retrospective studies^6-8 have shown that TNF-α inhibitors are associated with a reduction in cardiovascular outcomes, it is yet to be seen whether biologic treatment actually has a direct impact on cardiovascular outcomes, multiple studies investigating the effect of biologics on arterial inflammation markers notwithstanding.⁹

There are some direct factors to keep in mind when considering cardiometabolic comorbidities in patients with psoriasis. Obesity is common in the psoriasis population and can have a direct negative effect on cardiovascular health.¹⁰ However, the data on obesity and psoriasis are somewhat mixed with regard to treatment outcomes. In general, with increased volumes of distribution for biologics in patients with obesity, it has been shown that treatment success is more difficult to achieve in those with a body mass index greater than 30.¹¹ Rather surprisingly, a separate nationwide study in South Korea found that patients on biologics for psoriasis were more likely to experience weight gain, even after controlling for factors such as exercise, smoking, and drinking,¹² but it is unclear whether this is driven mostly by a known connection between weight gain and TNF-α inhibitors.¹³ These contrasting results point to the need for further studies in this area, as our intuitive approach would involve promoting weight loss while starting on a systemic treatment for psoriasis—but perhaps it is important not to assume that one will come with the other in tow, reinforcing the need to discuss a healthy diet with our patients with psoriasis regardless of treatment decisions.

The data that we have do not directly answer the big questions about biologic treatment and cardiovascular health, but we are starting to see interesting signals. For example, in a report of tildrakizumab treatment in patients with and without metabolic syndrome, the rates of major adverse cardiovascular events as well as cardiac disorders were essentially the same in both groups after receiving treatment for up to 244 weeks.¹⁴ This is interesting, more because of the lack of an increase in cardiovascular adverse events in the metabolic syndrome group, who entered the trial on average 25 kg to 30 kg heavier than those without metabolic syndrome. There is an increased risk for adverse cardiovascular events among patients with metabolic syndrome, a roughly 2-fold relative risk in as few as 5 to 6 years of follow-up.¹⁵ While the cohorts in the tildrakizumab study¹⁴ were too small to draw firm conclusions, the data are interesting and a step in the right direction; we need much larger data sets for analysis. Among other agents, similar efficacy and safety have been reported for guselkumab in a long-term psoriasis study; as a class, IL-23 inhibitors also tend to perform well from an efficacy standpoint in patients with obesity.¹⁶

Overall, when assessing the evidence for cardiometabolic disorders, it is reasonable to consider starting a biologic from the IL-17 or IL-23 inhibitor classes— thus avoiding both the potential downside of weight gain and contraindication in patients with congestive heart failure associated with TNF-α inhibitors. It is important to counsel patients about weight loss in conjunction with these treatments, both to improve efficacy and reduce cardiovascular risk factors. There may be a preference for IL-23 inhibitors in patients with obesity, as this class of medications maintains efficacy particularly well in these patients. Patients with psoriasis should be counseled to follow up with a primary care physician given their higher risk for metabolic syndrome and adverse cardiovascular outcomes.

Gastrointestinal Conditions

Psoriasis and inflammatory bowel disease (IBD) have a bidirectional association, and patients with psoriasis are about 1.7 times more likely to have either Crohn disease or ulcerative colitis.^17,18 This association may be related to a shared pathogenesis with regard to immune dysregulation and overactivated inflammatory pathways, but there are some important differences to consider from a therapeutic standpoint. Given the increased expression of IL-17 in patients with IBD,¹⁹ a phase II trial of secukinumab yielded surprising results—not only was secukinumab ineffective in treating Crohn disease, but there also were higher rates of adverse events²⁰ (as noted on the product label for all IL-17 inhibitors). We have come to understand that there are regulatory subsets of IL-17 cells that are important in mucosal homeostasis and also regulate IL-10, which generally is considered an anti-inflammatory cytokine.²¹ Thus, while IL-17 inhibition can reduce some component of inflammatory signaling, it also can increase inflammatory signaling through indirect pathways while increasing intestinal permeability to microbes. Importantly, this process seems to occur via IL-23–independent pathways; as such, while direct inhibition of IL-17 can be deleterious, IL-23 inhibitors have become important therapeutics for IBD.²²

IL-17 family, IL-17A clearly is the culprit for worsening colitis as evidenced by both human and animal models. On the contrary, IL-17F blockade has been shown to ameliorate colitis in a murine model, whereas IL-17A inhibition worsens it.²³ Furthermore, dual blockade of IL-17A and IL-17F has a protective effect against colitis, suggesting that the IL-17F inhibition is dominant. This interesting finding has some mechanistic backing, since blockade of IL-17F induces Treg cells that serve to maintain gut epithelium homeostasis and integrity.²⁴

Overall, IL-17A inhibitors should be avoided in patients with a history of IBD—namely, secukinumab and ixekizumab. While there may be theoretical reasons that brodalumab or bimekizumab may confer a somewhat different risk for IBD exacerbation, there may be better choices that would be expected to effectively treat both the psoriasis and IBD manifestations. Given the US Food and Drug Administration approval of IL-23 inhibitors for IBD and their high levels of efficacy in treating psoriasis, these likely will be the best choice for most patients. Another mainstay of IBD treatment is TNF-α inhibitors, but they come with other risks such as increased immunosuppression and increased risk for nonmelanoma skin cancer.

An important question remains: What about patients who do not have known IBD? Do we proactively change our treatment choice due to fear of IBD development given the higher incidence of both Crohn disease and ulcerative colitis in patients with psoriasis? What about patients with a family history of IBD? First-degree relatives of patients with Crohn disease and ulcerative colitis have an 8- and 4-fold higher risk for those same conditions, respectively.²⁵ Postmarketing surveillance and database findings of low rates of IBD development with IL-17 inhibitors gives only modest reassurance, as dermatologists generally know to avoid these medications for patients with even questionable IBD symptoms. It is important to emphasize to our patients that in no case do we believe that a psoriasis medication actually will cause IBD—rather, someone with subclinical IBD could experience a flare and a first manifestation of colitis. The drug is not the culprit in inducing IBD but rather may serve to unmask existing disease.

One study suggested that for patients who move on to the IL-17 inhibitor secukinumab after being treated with TNF-α inhibitors for psoriasis, the rates of IBD development are higher (4.8%) than in those who start IL-17A inhibition without prior treatment (1%)(OR, 8.38; P=.018).²⁶ This begs the question of whether subclinical IBD in many patients with psoriasis who are treated with TNF-α inhibitors can be unmasked later when they are transitioned to a treatment that either does not treat the IBD or could worsen it. There may be a mechanistic drive behind this sequencing of treatments that predisposes patients to colitis, which would suggest selecting an IL-23 inhibitor after failing/trying a TNF-α inhibitor. However, the data are very preliminary, and in real practice, other concerns such as severe psoriatic arthritis may outweigh these considerations, as the IL-17 inhibitor class still is considered to be more effective than IL-23 inhibition at treating psoriatic arthritis overall. For most patients with no personal history of IBD and no strong family history of IBD (ie, first-degree relatives), the choice of biologic should not be affected by concern over gastrointestinal issues.

Psychiatric Conditions

It has been well established that psoriasis is linked to higher rates of depression, anxiety, and suicidality.²⁷ How do we take this into account when treating patients with psoriasis, especially when we have biologics with a warning label for suicidality and a Risk Evaluation and Mitigation Strategies program (brodalumab) and language around suicidal ideation in the label (bimekizumab)? While it is challenging to discuss mental health, it is not a conversation that we as dermatologists should shy away from. Appropriate treatment of psoriasis is an important tool to get our patients on the path to better mental health. A recent database study of more than 4000 patients showed that patients with psoriasis treated with biologics had a 17% lower risk for depression than those treated with conventional disease-modifying drugs such as methotrexate.²⁸ The comparator of the conventional disease-modifying drug class is important as it serves as a control for disease severity. Too often, a higher rate of depression, anxiety, or suicidality can be attributed to a medication when we in fact may just be capturing the background of higher incidence of all 3 in patients with severe psoriasis.

Indeed, even with the medication that many worry about on this front (brodalumab), multiple studies have confirmed that the effect on mental health generally is a positive one, with decreases in depressive symptoms.²⁹ In a cohort switched from TNF-α inhibitors to brodalumab, symptoms of depression actually improved,³⁰ so attributing a direct treatment effect to negative mental health outcomes does not seem to be justified, especially in light of the low number of suicide events in global postmarketing surveillance for brodalumab, comparable to or lower than other biologics for psoriasis.³¹ Similarly, bimekizumab has language in the label about discussing suicidality with patients, although the rates of suicidal ideation and behavior are no different from other biologics and rates of depression improved with its use.³²

Heightened awareness of our patients’ mental health is something that we as providers should embrace, even when it seems that we do not have much time to see each patient. The priority when a patient comes in with mental health symptoms should be to treat what is within our scope (ie, psoriasis) as quickly and effectively as possible— with a newer-generation biologic such as an IL-17 or IL-23 inhibitor—while encouraging the patient to seek care from a mental health professional. In these cases, one might even argue that the rapidity of action of IL-17 inhibitors may be of additional benefit.

Final Thoughts

We as dermatologists generally are tasked with seeing high volumes of patients, and an initial psoriasis consultation can be a lengthy visit; however, it is rewarding to establish this relationship with patients and a reminder of why we practice medicine to begin with. Psoriasis can be satisfying to treat, and we have so many highly effective medicines that can completely transform our patients’ lives. Applying an understanding of the interplay between psoriasis, its related comorbidities, and treatment choices can be a fulfilling exercise that captures the essence of shared decision-making, which can lead to better outcomes and satisfaction for both providers and patients.

Psoriasis treatments have come a long way in the past 20 years. We now have more than a dozen systemic targeted treatments for psoriatic disease, with more on the way; however, with each successive class of medications introduced, the gap has narrowed in terms of increasing efficacy. In an era of medications reporting complete clearance rates in the 70% range, the average improvement in Psoriasis Area and Severity Index (PASI) for most biologics has remained at 90% to 95% in the past half-decade. While this is a far cry from the mean PASI improvements of 70% seen with the first biologics,¹ it is becoming more challenging to base our treatment decisions solely on PASI outcome measures.

How, then, do we approach rational selection of a systemic psoriasis treatment? We could try to delineate based on mechanism of action, but it may be disingenuous to dissect minor differences in pathways (eg, IL-17 vs IL-23) that are fundamentally related and on the same continuum in psoriasis pathophysiology. Therefore, the most meaningful way to select an appropriate therapeutic may be to adopt a patient-centered approach that accounts for both individual preferences and specific medical needs by evaluating for other comorbidities² to exclude or select certain medicines or types of treatments. We have long known to avoid tumor necrosis factor (TNF) α inhibitors in patients with congestive heart failure or a history of demyelinating disorders while regularly considering the presence of psoriatic arthritis and family planning when making treatment decisions. Now, we can be more nuanced in our approaches to psoriasis biologics. Specifically, the most important comorbidities to consider broadly encompass cardiometabolic disorders, gastrointestinal conditions, and psychiatric conditions.

Cardiometabolic Disorders

Possibly the hottest topic in psoriasis for some years now, the relationship between cardiometabolic disorders and psoriasis is of great interest to clinicians, scientists, and patients alike. There is a clear link between development of atherosclerosis and Th17-related immune mechanisms that also are implicated in the pathogenesis of psoriasis.³ Furthermore, the incidence of cardiovascular disease is markedly increased in patients with psoriasis, which is an independent risk factor for myocardial infarction, particularly among younger patients.^4,5 Although several retrospective studies^6-8 have shown that TNF-α inhibitors are associated with a reduction in cardiovascular outcomes, it is yet to be seen whether biologic treatment actually has a direct impact on cardiovascular outcomes, multiple studies investigating the effect of biologics on arterial inflammation markers notwithstanding.⁹

There are some direct factors to keep in mind when considering cardiometabolic comorbidities in patients with psoriasis. Obesity is common in the psoriasis population and can have a direct negative effect on cardiovascular health.¹⁰ However, the data on obesity and psoriasis are somewhat mixed with regard to treatment outcomes. In general, with increased volumes of distribution for biologics in patients with obesity, it has been shown that treatment success is more difficult to achieve in those with a body mass index greater than 30.¹¹ Rather surprisingly, a separate nationwide study in South Korea found that patients on biologics for psoriasis were more likely to experience weight gain, even after controlling for factors such as exercise, smoking, and drinking,¹² but it is unclear whether this is driven mostly by a known connection between weight gain and TNF-α inhibitors.¹³ These contrasting results point to the need for further studies in this area, as our intuitive approach would involve promoting weight loss while starting on a systemic treatment for psoriasis—but perhaps it is important not to assume that one will come with the other in tow, reinforcing the need to discuss a healthy diet with our patients with psoriasis regardless of treatment decisions.

The data that we have do not directly answer the big questions about biologic treatment and cardiovascular health, but we are starting to see interesting signals. For example, in a report of tildrakizumab treatment in patients with and without metabolic syndrome, the rates of major adverse cardiovascular events as well as cardiac disorders were essentially the same in both groups after receiving treatment for up to 244 weeks.¹⁴ This is interesting, more because of the lack of an increase in cardiovascular adverse events in the metabolic syndrome group, who entered the trial on average 25 kg to 30 kg heavier than those without metabolic syndrome. There is an increased risk for adverse cardiovascular events among patients with metabolic syndrome, a roughly 2-fold relative risk in as few as 5 to 6 years of follow-up.¹⁵ While the cohorts in the tildrakizumab study¹⁴ were too small to draw firm conclusions, the data are interesting and a step in the right direction; we need much larger data sets for analysis. Among other agents, similar efficacy and safety have been reported for guselkumab in a long-term psoriasis study; as a class, IL-23 inhibitors also tend to perform well from an efficacy standpoint in patients with obesity.¹⁶

Overall, when assessing the evidence for cardiometabolic disorders, it is reasonable to consider starting a biologic from the IL-17 or IL-23 inhibitor classes— thus avoiding both the potential downside of weight gain and contraindication in patients with congestive heart failure associated with TNF-α inhibitors. It is important to counsel patients about weight loss in conjunction with these treatments, both to improve efficacy and reduce cardiovascular risk factors. There may be a preference for IL-23 inhibitors in patients with obesity, as this class of medications maintains efficacy particularly well in these patients. Patients with psoriasis should be counseled to follow up with a primary care physician given their higher risk for metabolic syndrome and adverse cardiovascular outcomes.

Gastrointestinal Conditions

Psoriasis and inflammatory bowel disease (IBD) have a bidirectional association, and patients with psoriasis are about 1.7 times more likely to have either Crohn disease or ulcerative colitis.^17,18 This association may be related to a shared pathogenesis with regard to immune dysregulation and overactivated inflammatory pathways, but there are some important differences to consider from a therapeutic standpoint. Given the increased expression of IL-17 in patients with IBD,¹⁹ a phase II trial of secukinumab yielded surprising results—not only was secukinumab ineffective in treating Crohn disease, but there also were higher rates of adverse events²⁰ (as noted on the product label for all IL-17 inhibitors). We have come to understand that there are regulatory subsets of IL-17 cells that are important in mucosal homeostasis and also regulate IL-10, which generally is considered an anti-inflammatory cytokine.²¹ Thus, while IL-17 inhibition can reduce some component of inflammatory signaling, it also can increase inflammatory signaling through indirect pathways while increasing intestinal permeability to microbes. Importantly, this process seems to occur via IL-23–independent pathways; as such, while direct inhibition of IL-17 can be deleterious, IL-23 inhibitors have become important therapeutics for IBD.²²

IL-17 family, IL-17A clearly is the culprit for worsening colitis as evidenced by both human and animal models. On the contrary, IL-17F blockade has been shown to ameliorate colitis in a murine model, whereas IL-17A inhibition worsens it.²³ Furthermore, dual blockade of IL-17A and IL-17F has a protective effect against colitis, suggesting that the IL-17F inhibition is dominant. This interesting finding has some mechanistic backing, since blockade of IL-17F induces Treg cells that serve to maintain gut epithelium homeostasis and integrity.²⁴

Overall, IL-17A inhibitors should be avoided in patients with a history of IBD—namely, secukinumab and ixekizumab. While there may be theoretical reasons that brodalumab or bimekizumab may confer a somewhat different risk for IBD exacerbation, there may be better choices that would be expected to effectively treat both the psoriasis and IBD manifestations. Given the US Food and Drug Administration approval of IL-23 inhibitors for IBD and their high levels of efficacy in treating psoriasis, these likely will be the best choice for most patients. Another mainstay of IBD treatment is TNF-α inhibitors, but they come with other risks such as increased immunosuppression and increased risk for nonmelanoma skin cancer.

An important question remains: What about patients who do not have known IBD? Do we proactively change our treatment choice due to fear of IBD development given the higher incidence of both Crohn disease and ulcerative colitis in patients with psoriasis? What about patients with a family history of IBD? First-degree relatives of patients with Crohn disease and ulcerative colitis have an 8- and 4-fold higher risk for those same conditions, respectively.²⁵ Postmarketing surveillance and database findings of low rates of IBD development with IL-17 inhibitors gives only modest reassurance, as dermatologists generally know to avoid these medications for patients with even questionable IBD symptoms. It is important to emphasize to our patients that in no case do we believe that a psoriasis medication actually will cause IBD—rather, someone with subclinical IBD could experience a flare and a first manifestation of colitis. The drug is not the culprit in inducing IBD but rather may serve to unmask existing disease.

One study suggested that for patients who move on to the IL-17 inhibitor secukinumab after being treated with TNF-α inhibitors for psoriasis, the rates of IBD development are higher (4.8%) than in those who start IL-17A inhibition without prior treatment (1%)(OR, 8.38; P=.018).²⁶ This begs the question of whether subclinical IBD in many patients with psoriasis who are treated with TNF-α inhibitors can be unmasked later when they are transitioned to a treatment that either does not treat the IBD or could worsen it. There may be a mechanistic drive behind this sequencing of treatments that predisposes patients to colitis, which would suggest selecting an IL-23 inhibitor after failing/trying a TNF-α inhibitor. However, the data are very preliminary, and in real practice, other concerns such as severe psoriatic arthritis may outweigh these considerations, as the IL-17 inhibitor class still is considered to be more effective than IL-23 inhibition at treating psoriatic arthritis overall. For most patients with no personal history of IBD and no strong family history of IBD (ie, first-degree relatives), the choice of biologic should not be affected by concern over gastrointestinal issues.

Psychiatric Conditions

It has been well established that psoriasis is linked to higher rates of depression, anxiety, and suicidality.²⁷ How do we take this into account when treating patients with psoriasis, especially when we have biologics with a warning label for suicidality and a Risk Evaluation and Mitigation Strategies program (brodalumab) and language around suicidal ideation in the label (bimekizumab)? While it is challenging to discuss mental health, it is not a conversation that we as dermatologists should shy away from. Appropriate treatment of psoriasis is an important tool to get our patients on the path to better mental health. A recent database study of more than 4000 patients showed that patients with psoriasis treated with biologics had a 17% lower risk for depression than those treated with conventional disease-modifying drugs such as methotrexate.²⁸ The comparator of the conventional disease-modifying drug class is important as it serves as a control for disease severity. Too often, a higher rate of depression, anxiety, or suicidality can be attributed to a medication when we in fact may just be capturing the background of higher incidence of all 3 in patients with severe psoriasis.

Indeed, even with the medication that many worry about on this front (brodalumab), multiple studies have confirmed that the effect on mental health generally is a positive one, with decreases in depressive symptoms.²⁹ In a cohort switched from TNF-α inhibitors to brodalumab, symptoms of depression actually improved,³⁰ so attributing a direct treatment effect to negative mental health outcomes does not seem to be justified, especially in light of the low number of suicide events in global postmarketing surveillance for brodalumab, comparable to or lower than other biologics for psoriasis.³¹ Similarly, bimekizumab has language in the label about discussing suicidality with patients, although the rates of suicidal ideation and behavior are no different from other biologics and rates of depression improved with its use.³²

Heightened awareness of our patients’ mental health is something that we as providers should embrace, even when it seems that we do not have much time to see each patient. The priority when a patient comes in with mental health symptoms should be to treat what is within our scope (ie, psoriasis) as quickly and effectively as possible— with a newer-generation biologic such as an IL-17 or IL-23 inhibitor—while encouraging the patient to seek care from a mental health professional. In these cases, one might even argue that the rapidity of action of IL-17 inhibitors may be of additional benefit.

Final Thoughts

We as dermatologists generally are tasked with seeing high volumes of patients, and an initial psoriasis consultation can be a lengthy visit; however, it is rewarding to establish this relationship with patients and a reminder of why we practice medicine to begin with. Psoriasis can be satisfying to treat, and we have so many highly effective medicines that can completely transform our patients’ lives. Applying an understanding of the interplay between psoriasis, its related comorbidities, and treatment choices can be a fulfilling exercise that captures the essence of shared decision-making, which can lead to better outcomes and satisfaction for both providers and patients.

Psoriasis treatments have come a long way in the past 20 years. We now have more than a dozen systemic targeted treatments for psoriatic disease, with more on the way; however, with each successive class of medications introduced, the gap has narrowed in terms of increasing efficacy. In an era of medications reporting complete clearance rates in the 70% range, the average improvement in Psoriasis Area and Severity Index (PASI) for most biologics has remained at 90% to 95% in the past half-decade. While this is a far cry from the mean PASI improvements of 70% seen with the first biologics,¹ it is becoming more challenging to base our treatment decisions solely on PASI outcome measures.

How, then, do we approach rational selection of a systemic psoriasis treatment? We could try to delineate based on mechanism of action, but it may be disingenuous to dissect minor differences in pathways (eg, IL-17 vs IL-23) that are fundamentally related and on the same continuum in psoriasis pathophysiology. Therefore, the most meaningful way to select an appropriate therapeutic may be to adopt a patient-centered approach that accounts for both individual preferences and specific medical needs by evaluating for other comorbidities² to exclude or select certain medicines or types of treatments. We have long known to avoid tumor necrosis factor (TNF) α inhibitors in patients with congestive heart failure or a history of demyelinating disorders while regularly considering the presence of psoriatic arthritis and family planning when making treatment decisions. Now, we can be more nuanced in our approaches to psoriasis biologics. Specifically, the most important comorbidities to consider broadly encompass cardiometabolic disorders, gastrointestinal conditions, and psychiatric conditions.

Cardiometabolic Disorders

Possibly the hottest topic in psoriasis for some years now, the relationship between cardiometabolic disorders and psoriasis is of great interest to clinicians, scientists, and patients alike. There is a clear link between development of atherosclerosis and Th17-related immune mechanisms that also are implicated in the pathogenesis of psoriasis.³ Furthermore, the incidence of cardiovascular disease is markedly increased in patients with psoriasis, which is an independent risk factor for myocardial infarction, particularly among younger patients.^4,5 Although several retrospective studies^6-8 have shown that TNF-α inhibitors are associated with a reduction in cardiovascular outcomes, it is yet to be seen whether biologic treatment actually has a direct impact on cardiovascular outcomes, multiple studies investigating the effect of biologics on arterial inflammation markers notwithstanding.⁹

There are some direct factors to keep in mind when considering cardiometabolic comorbidities in patients with psoriasis. Obesity is common in the psoriasis population and can have a direct negative effect on cardiovascular health.¹⁰ However, the data on obesity and psoriasis are somewhat mixed with regard to treatment outcomes. In general, with increased volumes of distribution for biologics in patients with obesity, it has been shown that treatment success is more difficult to achieve in those with a body mass index greater than 30.¹¹ Rather surprisingly, a separate nationwide study in South Korea found that patients on biologics for psoriasis were more likely to experience weight gain, even after controlling for factors such as exercise, smoking, and drinking,¹² but it is unclear whether this is driven mostly by a known connection between weight gain and TNF-α inhibitors.¹³ These contrasting results point to the need for further studies in this area, as our intuitive approach would involve promoting weight loss while starting on a systemic treatment for psoriasis—but perhaps it is important not to assume that one will come with the other in tow, reinforcing the need to discuss a healthy diet with our patients with psoriasis regardless of treatment decisions.

The data that we have do not directly answer the big questions about biologic treatment and cardiovascular health, but we are starting to see interesting signals. For example, in a report of tildrakizumab treatment in patients with and without metabolic syndrome, the rates of major adverse cardiovascular events as well as cardiac disorders were essentially the same in both groups after receiving treatment for up to 244 weeks.¹⁴ This is interesting, more because of the lack of an increase in cardiovascular adverse events in the metabolic syndrome group, who entered the trial on average 25 kg to 30 kg heavier than those without metabolic syndrome. There is an increased risk for adverse cardiovascular events among patients with metabolic syndrome, a roughly 2-fold relative risk in as few as 5 to 6 years of follow-up.¹⁵ While the cohorts in the tildrakizumab study¹⁴ were too small to draw firm conclusions, the data are interesting and a step in the right direction; we need much larger data sets for analysis. Among other agents, similar efficacy and safety have been reported for guselkumab in a long-term psoriasis study; as a class, IL-23 inhibitors also tend to perform well from an efficacy standpoint in patients with obesity.¹⁶

Overall, when assessing the evidence for cardiometabolic disorders, it is reasonable to consider starting a biologic from the IL-17 or IL-23 inhibitor classes— thus avoiding both the potential downside of weight gain and contraindication in patients with congestive heart failure associated with TNF-α inhibitors. It is important to counsel patients about weight loss in conjunction with these treatments, both to improve efficacy and reduce cardiovascular risk factors. There may be a preference for IL-23 inhibitors in patients with obesity, as this class of medications maintains efficacy particularly well in these patients. Patients with psoriasis should be counseled to follow up with a primary care physician given their higher risk for metabolic syndrome and adverse cardiovascular outcomes.

Gastrointestinal Conditions

Psoriasis and inflammatory bowel disease (IBD) have a bidirectional association, and patients with psoriasis are about 1.7 times more likely to have either Crohn disease or ulcerative colitis.^17,18 This association may be related to a shared pathogenesis with regard to immune dysregulation and overactivated inflammatory pathways, but there are some important differences to consider from a therapeutic standpoint. Given the increased expression of IL-17 in patients with IBD,¹⁹ a phase II trial of secukinumab yielded surprising results—not only was secukinumab ineffective in treating Crohn disease, but there also were higher rates of adverse events²⁰ (as noted on the product label for all IL-17 inhibitors). We have come to understand that there are regulatory subsets of IL-17 cells that are important in mucosal homeostasis and also regulate IL-10, which generally is considered an anti-inflammatory cytokine.²¹ Thus, while IL-17 inhibition can reduce some component of inflammatory signaling, it also can increase inflammatory signaling through indirect pathways while increasing intestinal permeability to microbes. Importantly, this process seems to occur via IL-23–independent pathways; as such, while direct inhibition of IL-17 can be deleterious, IL-23 inhibitors have become important therapeutics for IBD.²²

IL-17 family, IL-17A clearly is the culprit for worsening colitis as evidenced by both human and animal models. On the contrary, IL-17F blockade has been shown to ameliorate colitis in a murine model, whereas IL-17A inhibition worsens it.²³ Furthermore, dual blockade of IL-17A and IL-17F has a protective effect against colitis, suggesting that the IL-17F inhibition is dominant. This interesting finding has some mechanistic backing, since blockade of IL-17F induces Treg cells that serve to maintain gut epithelium homeostasis and integrity.²⁴

Overall, IL-17A inhibitors should be avoided in patients with a history of IBD—namely, secukinumab and ixekizumab. While there may be theoretical reasons that brodalumab or bimekizumab may confer a somewhat different risk for IBD exacerbation, there may be better choices that would be expected to effectively treat both the psoriasis and IBD manifestations. Given the US Food and Drug Administration approval of IL-23 inhibitors for IBD and their high levels of efficacy in treating psoriasis, these likely will be the best choice for most patients. Another mainstay of IBD treatment is TNF-α inhibitors, but they come with other risks such as increased immunosuppression and increased risk for nonmelanoma skin cancer.

An important question remains: What about patients who do not have known IBD? Do we proactively change our treatment choice due to fear of IBD development given the higher incidence of both Crohn disease and ulcerative colitis in patients with psoriasis? What about patients with a family history of IBD? First-degree relatives of patients with Crohn disease and ulcerative colitis have an 8- and 4-fold higher risk for those same conditions, respectively.²⁵ Postmarketing surveillance and database findings of low rates of IBD development with IL-17 inhibitors gives only modest reassurance, as dermatologists generally know to avoid these medications for patients with even questionable IBD symptoms. It is important to emphasize to our patients that in no case do we believe that a psoriasis medication actually will cause IBD—rather, someone with subclinical IBD could experience a flare and a first manifestation of colitis. The drug is not the culprit in inducing IBD but rather may serve to unmask existing disease.

One study suggested that for patients who move on to the IL-17 inhibitor secukinumab after being treated with TNF-α inhibitors for psoriasis, the rates of IBD development are higher (4.8%) than in those who start IL-17A inhibition without prior treatment (1%)(OR, 8.38; P=.018).²⁶ This begs the question of whether subclinical IBD in many patients with psoriasis who are treated with TNF-α inhibitors can be unmasked later when they are transitioned to a treatment that either does not treat the IBD or could worsen it. There may be a mechanistic drive behind this sequencing of treatments that predisposes patients to colitis, which would suggest selecting an IL-23 inhibitor after failing/trying a TNF-α inhibitor. However, the data are very preliminary, and in real practice, other concerns such as severe psoriatic arthritis may outweigh these considerations, as the IL-17 inhibitor class still is considered to be more effective than IL-23 inhibition at treating psoriatic arthritis overall. For most patients with no personal history of IBD and no strong family history of IBD (ie, first-degree relatives), the choice of biologic should not be affected by concern over gastrointestinal issues.

Psychiatric Conditions

It has been well established that psoriasis is linked to higher rates of depression, anxiety, and suicidality.²⁷ How do we take this into account when treating patients with psoriasis, especially when we have biologics with a warning label for suicidality and a Risk Evaluation and Mitigation Strategies program (brodalumab) and language around suicidal ideation in the label (bimekizumab)? While it is challenging to discuss mental health, it is not a conversation that we as dermatologists should shy away from. Appropriate treatment of psoriasis is an important tool to get our patients on the path to better mental health. A recent database study of more than 4000 patients showed that patients with psoriasis treated with biologics had a 17% lower risk for depression than those treated with conventional disease-modifying drugs such as methotrexate.²⁸ The comparator of the conventional disease-modifying drug class is important as it serves as a control for disease severity. Too often, a higher rate of depression, anxiety, or suicidality can be attributed to a medication when we in fact may just be capturing the background of higher incidence of all 3 in patients with severe psoriasis.

Indeed, even with the medication that many worry about on this front (brodalumab), multiple studies have confirmed that the effect on mental health generally is a positive one, with decreases in depressive symptoms.²⁹ In a cohort switched from TNF-α inhibitors to brodalumab, symptoms of depression actually improved,³⁰ so attributing a direct treatment effect to negative mental health outcomes does not seem to be justified, especially in light of the low number of suicide events in global postmarketing surveillance for brodalumab, comparable to or lower than other biologics for psoriasis.³¹ Similarly, bimekizumab has language in the label about discussing suicidality with patients, although the rates of suicidal ideation and behavior are no different from other biologics and rates of depression improved with its use.³²

Heightened awareness of our patients’ mental health is something that we as providers should embrace, even when it seems that we do not have much time to see each patient. The priority when a patient comes in with mental health symptoms should be to treat what is within our scope (ie, psoriasis) as quickly and effectively as possible— with a newer-generation biologic such as an IL-17 or IL-23 inhibitor—while encouraging the patient to seek care from a mental health professional. In these cases, one might even argue that the rapidity of action of IL-17 inhibitors may be of additional benefit.

Final Thoughts

We as dermatologists generally are tasked with seeing high volumes of patients, and an initial psoriasis consultation can be a lengthy visit; however, it is rewarding to establish this relationship with patients and a reminder of why we practice medicine to begin with. Psoriasis can be satisfying to treat, and we have so many highly effective medicines that can completely transform our patients’ lives. Applying an understanding of the interplay between psoriasis, its related comorbidities, and treatment choices can be a fulfilling exercise that captures the essence of shared decision-making, which can lead to better outcomes and satisfaction for both providers and patients.

In this video, Vasu Appalaneni, MD, a gastroenterologist at Dayton Gastroenterology in Beavercreek, Ohio, discusses what physicians and business leaders should be considering about the use of artificial intelligence in their practices.

In addition to her work at Dayton Gastroenterology, Dr. Appalaneni is executive vice president of clinical innovation at One GI, a gastroenterology management services organization that partners with gastroenterologists to help them manage and grow their independent gastroenterology practices. One GI is Dayton Gastroenterology’s parent company.

In this video, Vasu Appalaneni, MD, a gastroenterologist at Dayton Gastroenterology in Beavercreek, Ohio, discusses what physicians and business leaders should be considering about the use of artificial intelligence in their practices.

In addition to her work at Dayton Gastroenterology, Dr. Appalaneni is executive vice president of clinical innovation at One GI, a gastroenterology management services organization that partners with gastroenterologists to help them manage and grow their independent gastroenterology practices. One GI is Dayton Gastroenterology’s parent company.

In this video, Vasu Appalaneni, MD, a gastroenterologist at Dayton Gastroenterology in Beavercreek, Ohio, discusses what physicians and business leaders should be considering about the use of artificial intelligence in their practices.

In addition to her work at Dayton Gastroenterology, Dr. Appalaneni is executive vice president of clinical innovation at One GI, a gastroenterology management services organization that partners with gastroenterologists to help them manage and grow their independent gastroenterology practices. One GI is Dayton Gastroenterology’s parent company.

Artificial intelligence (AI) applications are expanding rapidly in healthcare. AI powered tools are increasingly used in everyday medical practice, assisting clinicians with tasks such as diagnosis, treatment planning, data analysis, and patient monitoring, effectively integrating AI into routine clinical decision making. Despite its potential to fundamentally transform the practice of medicine and healthcare delivery, AI in healthcare remains largely unregulated, with a lack of common standards to guide responsible design, development, and adoption of AI-based tools to guide clinical care.

But this is changing. In mid-January, the US Department of Health & Human Services released its Strategic Plan for the Use of AI in Health, Human Services, and Public Health (available at www.healthit.gov), presenting an approach to catalyze innovation, promote trustworthy AI development, democratize technologies and resources, and cultivate AI-empowered workforces and organizational cultures. While there is no immediate regulatory impact, the plan does provide important insights into how the federal government thinks about AI, which will be a part of driving regulations in the future. As crucial stakeholders in the health AI universe and advocates for its responsible use in clinical practice, it is critical that we as clinicians keep abreast of developments in this rapidly evolving space. 

 

In this month’s issue of GI & Hepatology News, we summarize a recent systematic review and meta-analysis highlighting worsening health disparities for Hispanic adults with MASLD. We also report the results of an industry-sponsored study comparing the real-world clinical effectiveness of GI Genius (an AI-driven tool) with that of standard colonoscopy.

In February’s Member Spotlight, we introduce you to international AGA member Dr. Tossapol Kerdsirichairat (clinical associate professor of gastroenterology at Bumrungrad International Hospital in Bangkok, Thailand), who shares his insights regarding the challenges and rewards of practicing gastroenterology at one of the largest private hospitals in Southeast Asia. ‘Tos’ is one of roughly 25% of AGA members who live and work outside the United States.

Finally, this month’s In Focus column from The New Gastroenterologist focuses on management of chronic constipation, a highly prevalent condition that significantly impacts the quality of life of many of our patients. We hope you enjoy this and all the exciting content in our February issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

Artificial intelligence (AI) applications are expanding rapidly in healthcare. AI powered tools are increasingly used in everyday medical practice, assisting clinicians with tasks such as diagnosis, treatment planning, data analysis, and patient monitoring, effectively integrating AI into routine clinical decision making. Despite its potential to fundamentally transform the practice of medicine and healthcare delivery, AI in healthcare remains largely unregulated, with a lack of common standards to guide responsible design, development, and adoption of AI-based tools to guide clinical care.

But this is changing. In mid-January, the US Department of Health & Human Services released its Strategic Plan for the Use of AI in Health, Human Services, and Public Health (available at www.healthit.gov), presenting an approach to catalyze innovation, promote trustworthy AI development, democratize technologies and resources, and cultivate AI-empowered workforces and organizational cultures. While there is no immediate regulatory impact, the plan does provide important insights into how the federal government thinks about AI, which will be a part of driving regulations in the future. As crucial stakeholders in the health AI universe and advocates for its responsible use in clinical practice, it is critical that we as clinicians keep abreast of developments in this rapidly evolving space. 

 

In this month’s issue of GI & Hepatology News, we summarize a recent systematic review and meta-analysis highlighting worsening health disparities for Hispanic adults with MASLD. We also report the results of an industry-sponsored study comparing the real-world clinical effectiveness of GI Genius (an AI-driven tool) with that of standard colonoscopy.

In February’s Member Spotlight, we introduce you to international AGA member Dr. Tossapol Kerdsirichairat (clinical associate professor of gastroenterology at Bumrungrad International Hospital in Bangkok, Thailand), who shares his insights regarding the challenges and rewards of practicing gastroenterology at one of the largest private hospitals in Southeast Asia. ‘Tos’ is one of roughly 25% of AGA members who live and work outside the United States.

Finally, this month’s In Focus column from The New Gastroenterologist focuses on management of chronic constipation, a highly prevalent condition that significantly impacts the quality of life of many of our patients. We hope you enjoy this and all the exciting content in our February issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

Artificial intelligence (AI) applications are expanding rapidly in healthcare. AI powered tools are increasingly used in everyday medical practice, assisting clinicians with tasks such as diagnosis, treatment planning, data analysis, and patient monitoring, effectively integrating AI into routine clinical decision making. Despite its potential to fundamentally transform the practice of medicine and healthcare delivery, AI in healthcare remains largely unregulated, with a lack of common standards to guide responsible design, development, and adoption of AI-based tools to guide clinical care.

But this is changing. In mid-January, the US Department of Health & Human Services released its Strategic Plan for the Use of AI in Health, Human Services, and Public Health (available at www.healthit.gov), presenting an approach to catalyze innovation, promote trustworthy AI development, democratize technologies and resources, and cultivate AI-empowered workforces and organizational cultures. While there is no immediate regulatory impact, the plan does provide important insights into how the federal government thinks about AI, which will be a part of driving regulations in the future. As crucial stakeholders in the health AI universe and advocates for its responsible use in clinical practice, it is critical that we as clinicians keep abreast of developments in this rapidly evolving space. 

 

In this month’s issue of GI & Hepatology News, we summarize a recent systematic review and meta-analysis highlighting worsening health disparities for Hispanic adults with MASLD. We also report the results of an industry-sponsored study comparing the real-world clinical effectiveness of GI Genius (an AI-driven tool) with that of standard colonoscopy.

In February’s Member Spotlight, we introduce you to international AGA member Dr. Tossapol Kerdsirichairat (clinical associate professor of gastroenterology at Bumrungrad International Hospital in Bangkok, Thailand), who shares his insights regarding the challenges and rewards of practicing gastroenterology at one of the largest private hospitals in Southeast Asia. ‘Tos’ is one of roughly 25% of AGA members who live and work outside the United States.

Finally, this month’s In Focus column from The New Gastroenterologist focuses on management of chronic constipation, a highly prevalent condition that significantly impacts the quality of life of many of our patients. We hope you enjoy this and all the exciting content in our February issue.

Megan A. Adams, MD, JD, MSc

Editor in Chief

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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].

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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].

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

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].

You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.

The Brain Benefits of BP Lowering

It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.

In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.

Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.

 

Potential Harms of Lowering BP

All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions. 

When it comes to dementia, there is also a concern that overtreating high BP could make things worse. Hypotension and decreased cerebral perfusion could hasten cognitive decline by depriving the brain of that all too necessary oxygen. 

A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.

A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.

 

Deprescribing, Yes or No? 

However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.

Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress. 

Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.

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

You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.

The Brain Benefits of BP Lowering

It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.

In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.

Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.

 

Potential Harms of Lowering BP

All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions. 

When it comes to dementia, there is also a concern that overtreating high BP could make things worse. Hypotension and decreased cerebral perfusion could hasten cognitive decline by depriving the brain of that all too necessary oxygen. 

A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.

A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.

 

Deprescribing, Yes or No? 

However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.

Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress. 

Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.

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

You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.

The Brain Benefits of BP Lowering

It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.

In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.

Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.

 

Potential Harms of Lowering BP

All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions. 

When it comes to dementia, there is also a concern that overtreating high BP could make things worse. Hypotension and decreased cerebral perfusion could hasten cognitive decline by depriving the brain of that all too necessary oxygen. 

A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.

A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.

 

Deprescribing, Yes or No? 

However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.

Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress. 

Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.

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

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

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].

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

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].

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

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].

This transcript has been edited for clarity. 

I want to talk about something that’s extremely controversial, but something that needs public discussion, in my view, as sometimes it doesn’t get the attention it deserves. That is: Are you ever too old to become a parent? 

In my experience, this topic comes up when women — often, single women — decide that they haven’t had a child and they consider pursuing fertility services using in vitro fertilization, donor sperm, a younger woman’s egg, or an egg they’ve preserved, and they say they’d like to have a child. 

I don’t have any huge objection to a younger woman with good health and energy trying to pursue parenting, but we’ve seen women try to do this in their 60s. It does seem to me, biologically, that is a high risk for anyone to undertake a pregnancy at that age. I think there’s agreement from obstetricians that they’re high risk. 

I think it’s dangerous, if you’re going to be the single parent at that age, that you may wind up entering a nursing home by the time your child enters, say, high school. In thinking about parenting, sure, we want to think about our own values and what we want, and normally, people don’t tell us what to do. I’m not calling for any legislation here. I’m calling for an ethical discussion about the rights and wrongs of parenting at older age. 

In response to the case I made against single women over age 60 trying to have children, it’s often brought up to me that men do it. Recently, there was a story about Al Pacino, who had a kid — I think he’s now 84, so he must have had the child at 83.

In an interview with Newsweek, he said he had this child with his ex, who was 30, a woman named Noor Alfallah. He also said he doesn’t see the child very much. He communicates mainly with that child as a co-parent through digital texting and internet contact. He said he uses video basically as a parent.

Why that is, I’m not sure. Did he have a falling out with his ex and has he been excluded? Is he in poor health such that he can’t really do parenting anymore? 

I cite his case, and there are many other celebrities that we’ve heard about over the years who’ve had kids in their 80s, such as the former talk show host Larry King and, I believe, Clint Eastwood. There are cases that hit the news all the time about older men.

I think the same question should apply ethically. Again, I’m not saying we’re going to ban it or outlaw it, but it’s something we have to discuss and think through. I think doctors involved in helping a very old parent should raise the questions so that people can at least discuss them.

If you’re going to have a kid at 84, it means you’re not going to be around in any competent way by the time the kid hits high school. I’m not sure that’s in the child’s best interest. Certainly, there is the case that a younger woman could adequately raise the kid, but if something happens to her, you’re not going to be around in that age category to parent at all. 

It’s also the case that older parents, if you’re using your sperm, may have the same issues as women, whose eggs age in their late 30s into their 40s; you’re more likely to transmit a genetic disease. We don’t talk about it often, but it is a fact that someone who’s thinking about parenting either naturally or using infertility techniques really should be responsible and think about it.

Bottom line: Am I going to say we should let Congress or a state legislature step in and say, you’re going to go to jail if you have a kid at age X? No. Ethics is there for a reason; it’s trying to make sure that you don’t do things that harm or hurt the interests of a kid. 

If two older people have a child and they’re not likely to be there for a crucial period — say, the teenage years — and they haven’t made provisions for the care of the child, if both die, that’s a problem. 

If one person who’s very old tries to do it, they’re not likely to be alive and/or in good health when the kid enters puberty or into the teenage years; that’s something that you have to think about. Am I doing this because I’m just going to do what I want to do, or am I going to really look out for the best interests of any child I might create? 

This is food for thought about the question of when anyone is too old to parent. I know that’s partly determined by partner, resources, and many other variables, but I don’t believe that we should ignore the discussion of the ethics of the decision just out of respect for the idea that we’re not going to legislate.

Dr. Caplan is with the Division of Medical Ethics at New York University’s Grossman School of Medicine. He has disclosed relevant financial relationships with Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position) and Medscape.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

I want to talk about something that’s extremely controversial, but something that needs public discussion, in my view, as sometimes it doesn’t get the attention it deserves. That is: Are you ever too old to become a parent? 

In my experience, this topic comes up when women — often, single women — decide that they haven’t had a child and they consider pursuing fertility services using in vitro fertilization, donor sperm, a younger woman’s egg, or an egg they’ve preserved, and they say they’d like to have a child. 

I don’t have any huge objection to a younger woman with good health and energy trying to pursue parenting, but we’ve seen women try to do this in their 60s. It does seem to me, biologically, that is a high risk for anyone to undertake a pregnancy at that age. I think there’s agreement from obstetricians that they’re high risk. 

I think it’s dangerous, if you’re going to be the single parent at that age, that you may wind up entering a nursing home by the time your child enters, say, high school. In thinking about parenting, sure, we want to think about our own values and what we want, and normally, people don’t tell us what to do. I’m not calling for any legislation here. I’m calling for an ethical discussion about the rights and wrongs of parenting at older age. 

In response to the case I made against single women over age 60 trying to have children, it’s often brought up to me that men do it. Recently, there was a story about Al Pacino, who had a kid — I think he’s now 84, so he must have had the child at 83.

In an interview with Newsweek, he said he had this child with his ex, who was 30, a woman named Noor Alfallah. He also said he doesn’t see the child very much. He communicates mainly with that child as a co-parent through digital texting and internet contact. He said he uses video basically as a parent.

Why that is, I’m not sure. Did he have a falling out with his ex and has he been excluded? Is he in poor health such that he can’t really do parenting anymore? 

I cite his case, and there are many other celebrities that we’ve heard about over the years who’ve had kids in their 80s, such as the former talk show host Larry King and, I believe, Clint Eastwood. There are cases that hit the news all the time about older men.

I think the same question should apply ethically. Again, I’m not saying we’re going to ban it or outlaw it, but it’s something we have to discuss and think through. I think doctors involved in helping a very old parent should raise the questions so that people can at least discuss them.

If you’re going to have a kid at 84, it means you’re not going to be around in any competent way by the time the kid hits high school. I’m not sure that’s in the child’s best interest. Certainly, there is the case that a younger woman could adequately raise the kid, but if something happens to her, you’re not going to be around in that age category to parent at all. 

It’s also the case that older parents, if you’re using your sperm, may have the same issues as women, whose eggs age in their late 30s into their 40s; you’re more likely to transmit a genetic disease. We don’t talk about it often, but it is a fact that someone who’s thinking about parenting either naturally or using infertility techniques really should be responsible and think about it.

Bottom line: Am I going to say we should let Congress or a state legislature step in and say, you’re going to go to jail if you have a kid at age X? No. Ethics is there for a reason; it’s trying to make sure that you don’t do things that harm or hurt the interests of a kid. 

If two older people have a child and they’re not likely to be there for a crucial period — say, the teenage years — and they haven’t made provisions for the care of the child, if both die, that’s a problem. 

If one person who’s very old tries to do it, they’re not likely to be alive and/or in good health when the kid enters puberty or into the teenage years; that’s something that you have to think about. Am I doing this because I’m just going to do what I want to do, or am I going to really look out for the best interests of any child I might create? 

This is food for thought about the question of when anyone is too old to parent. I know that’s partly determined by partner, resources, and many other variables, but I don’t believe that we should ignore the discussion of the ethics of the decision just out of respect for the idea that we’re not going to legislate.

Dr. Caplan is with the Division of Medical Ethics at New York University’s Grossman School of Medicine. He has disclosed relevant financial relationships with Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position) and Medscape.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

I want to talk about something that’s extremely controversial, but something that needs public discussion, in my view, as sometimes it doesn’t get the attention it deserves. That is: Are you ever too old to become a parent? 

In my experience, this topic comes up when women — often, single women — decide that they haven’t had a child and they consider pursuing fertility services using in vitro fertilization, donor sperm, a younger woman’s egg, or an egg they’ve preserved, and they say they’d like to have a child. 

I don’t have any huge objection to a younger woman with good health and energy trying to pursue parenting, but we’ve seen women try to do this in their 60s. It does seem to me, biologically, that is a high risk for anyone to undertake a pregnancy at that age. I think there’s agreement from obstetricians that they’re high risk. 

I think it’s dangerous, if you’re going to be the single parent at that age, that you may wind up entering a nursing home by the time your child enters, say, high school. In thinking about parenting, sure, we want to think about our own values and what we want, and normally, people don’t tell us what to do. I’m not calling for any legislation here. I’m calling for an ethical discussion about the rights and wrongs of parenting at older age. 

In response to the case I made against single women over age 60 trying to have children, it’s often brought up to me that men do it. Recently, there was a story about Al Pacino, who had a kid — I think he’s now 84, so he must have had the child at 83.

In an interview with Newsweek, he said he had this child with his ex, who was 30, a woman named Noor Alfallah. He also said he doesn’t see the child very much. He communicates mainly with that child as a co-parent through digital texting and internet contact. He said he uses video basically as a parent.

Why that is, I’m not sure. Did he have a falling out with his ex and has he been excluded? Is he in poor health such that he can’t really do parenting anymore? 

I cite his case, and there are many other celebrities that we’ve heard about over the years who’ve had kids in their 80s, such as the former talk show host Larry King and, I believe, Clint Eastwood. There are cases that hit the news all the time about older men.

I think the same question should apply ethically. Again, I’m not saying we’re going to ban it or outlaw it, but it’s something we have to discuss and think through. I think doctors involved in helping a very old parent should raise the questions so that people can at least discuss them.

If you’re going to have a kid at 84, it means you’re not going to be around in any competent way by the time the kid hits high school. I’m not sure that’s in the child’s best interest. Certainly, there is the case that a younger woman could adequately raise the kid, but if something happens to her, you’re not going to be around in that age category to parent at all. 

It’s also the case that older parents, if you’re using your sperm, may have the same issues as women, whose eggs age in their late 30s into their 40s; you’re more likely to transmit a genetic disease. We don’t talk about it often, but it is a fact that someone who’s thinking about parenting either naturally or using infertility techniques really should be responsible and think about it.

Bottom line: Am I going to say we should let Congress or a state legislature step in and say, you’re going to go to jail if you have a kid at age X? No. Ethics is there for a reason; it’s trying to make sure that you don’t do things that harm or hurt the interests of a kid. 

If two older people have a child and they’re not likely to be there for a crucial period — say, the teenage years — and they haven’t made provisions for the care of the child, if both die, that’s a problem. 

If one person who’s very old tries to do it, they’re not likely to be alive and/or in good health when the kid enters puberty or into the teenage years; that’s something that you have to think about. Am I doing this because I’m just going to do what I want to do, or am I going to really look out for the best interests of any child I might create? 

This is food for thought about the question of when anyone is too old to parent. I know that’s partly determined by partner, resources, and many other variables, but I don’t believe that we should ignore the discussion of the ethics of the decision just out of respect for the idea that we’re not going to legislate.

Dr. Caplan is with the Division of Medical Ethics at New York University’s Grossman School of Medicine. He has disclosed relevant financial relationships with Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position) and Medscape.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

I would like to briefly discuss a very interesting paper that appeared in Nature:“Megastudy Shows That Reminders Boost Vaccination but Adding Free Rides Does Not.” 

Obviously, the paper has a provocative title. This is really an excellent example of what one might call implementation research, or quite frankly, what might work and what might not work in terms of having a very pragmatic goal. In this case, it was how do we get people to receive vaccinations. 

This specific study looked at individuals who were scheduled to receive or were candidates to receive COVID-19 booster vaccinations. The question came up: If you gave them free rides to the location — this is obviously a high-risk population — would that increase the vaccination rate vs the other item that they were looking at here, which was potentially texting them to remind them?

The study very importantly and relevantly demonstrated, quite nicely, that offering free rides did not make a difference, but sending texts to remind them increased the 30-day vaccination rate in this population by 21%. 

Again, it was a very pragmatic question that the trial addressed, and one might use this information in the future to increase the vaccination rate of a population where it is critical to do so. This type of research, which involves looking at very pragmatic questions and answering what is the optimal and most cost-effective way of doing it, should be encouraged. 

I encourage you to look at this paper if you’re interested in this topic.

Markman, Professor of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center; President, Medicine & Science, City of Hope Atlanta, Chicago, Phoenix, has disclosed ties with GlaxoSmithKline and AstraZeneca.

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

This transcript has been edited for clarity. 

I would like to briefly discuss a very interesting paper that appeared in Nature:“Megastudy Shows That Reminders Boost Vaccination but Adding Free Rides Does Not.” 

Obviously, the paper has a provocative title. This is really an excellent example of what one might call implementation research, or quite frankly, what might work and what might not work in terms of having a very pragmatic goal. In this case, it was how do we get people to receive vaccinations. 

This specific study looked at individuals who were scheduled to receive or were candidates to receive COVID-19 booster vaccinations. The question came up: If you gave them free rides to the location — this is obviously a high-risk population — would that increase the vaccination rate vs the other item that they were looking at here, which was potentially texting them to remind them?

The study very importantly and relevantly demonstrated, quite nicely, that offering free rides did not make a difference, but sending texts to remind them increased the 30-day vaccination rate in this population by 21%. 

Again, it was a very pragmatic question that the trial addressed, and one might use this information in the future to increase the vaccination rate of a population where it is critical to do so. This type of research, which involves looking at very pragmatic questions and answering what is the optimal and most cost-effective way of doing it, should be encouraged. 

I encourage you to look at this paper if you’re interested in this topic.

Markman, Professor of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center; President, Medicine & Science, City of Hope Atlanta, Chicago, Phoenix, has disclosed ties with GlaxoSmithKline and AstraZeneca.

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

This transcript has been edited for clarity. 

I would like to briefly discuss a very interesting paper that appeared in Nature:“Megastudy Shows That Reminders Boost Vaccination but Adding Free Rides Does Not.” 

Obviously, the paper has a provocative title. This is really an excellent example of what one might call implementation research, or quite frankly, what might work and what might not work in terms of having a very pragmatic goal. In this case, it was how do we get people to receive vaccinations. 

This specific study looked at individuals who were scheduled to receive or were candidates to receive COVID-19 booster vaccinations. The question came up: If you gave them free rides to the location — this is obviously a high-risk population — would that increase the vaccination rate vs the other item that they were looking at here, which was potentially texting them to remind them?

The study very importantly and relevantly demonstrated, quite nicely, that offering free rides did not make a difference, but sending texts to remind them increased the 30-day vaccination rate in this population by 21%. 

Again, it was a very pragmatic question that the trial addressed, and one might use this information in the future to increase the vaccination rate of a population where it is critical to do so. This type of research, which involves looking at very pragmatic questions and answering what is the optimal and most cost-effective way of doing it, should be encouraged. 

I encourage you to look at this paper if you’re interested in this topic.

Markman, Professor of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center; President, Medicine & Science, City of Hope Atlanta, Chicago, Phoenix, has disclosed ties with GlaxoSmithKline and AstraZeneca.

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

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Matthew F. Watto, MD: Welcome back to The Curbsiders. I’m Dr Matthew Frank Watto, here with my great friend and America’s primary care physician, Dr Paul Nelson Williams. Paul, how are you feeling about sports injuries? 

Paul N. Williams, MD: I’m feeling great, Matt.

Watto: You had a sports injury of the hip. Maybe that’s an overshare, Paul, but we talked about it on a podcast with Dr Carlin Senter (part 1 and part 2).

Williams: I think I’ve shared more than my hip injury, for sure. 

Watto: Whenever a patient presented with hip pain, I used to pray it was trochanteric bursitis, which now I know is not really the right thing to think about. Intra-articular hip pain presents as anterior hip pain, usually in the crease of the hip. Depending on the patient’s age and history, the differential for that type of pain includes iliopsoas tendonitis, FAI syndrome, a labral tear, a bone stress injury of the femoral neck, or osteoarthritis. 

So, what exactly is FAI and how might we diagnose it? 

Williams: FAI is what the cool kids call femoral acetabular impingement, and it’s exactly what it sounds like.

 

Something is pinching or impinging upon the joint itself and preventing full range of motion. This is a ball-and-socket joint, so it should have tremendous range of motion, able to move in all planes. If it’s impinged, then pain will occur with certain movements. There’s a cam type, which is characterized by enlargement of the femoral head neck junction, or a pincer type, which has more to do with overhang of the acetabulum, and it can also be mixed. In any case, impingement upon the patient’s full range of motion results in pain. 

You evaluate this with a couple of tests — the FABER and the FADIR. 

The FABER is flexion, abduction, and external rotation, and the FADIR is flexion, adduction, and internal rotation. If you elicit anterior pain with either of those tests, it’s probably one of the intra-articular pathologies, although it is hard to know for sure which one it is because these tests are fairly sensitive but not very specific. 

Watto: You can get x-rays to help with the diagnosis. You would order two views of the hip: an AP of the pelvis, which is just a straight-on shot to look for arthritis or fracture. Is there a healthy joint line there? The second is the Dunn view, in which the hip is flexed 90 degrees and abducted about 20 degrees. You are looking for fracture or impingement. You can diagnose FAI based on that view, and you might be able to diagnose a hip stress injury or osteoarthritis.

Unfortunately, you’re not going to see a labral tear, but Dr Senter said that both FAI and labral tears are treated the same way, with physical therapy. Patients with FAI who aren’t getting better might end up going for surgery, so at some point I would refer them to orthopedic surgery. But I feel much more comfortable now diagnosing these conditions with these tests.

Let’s talk a little bit about trochanteric pain syndrome. I used to think it was all bursitis. Why is that not correct? 

Williams: It’s nice of you to feign ignorance for the purpose of education. It used to be thought of as bursitis, but these days we know it is probably more likely a tendinopathy. 

 

Trochanteric pain syndrome was formerly known as trochanteric bursitis, but the bursa is not typically involved. Trochanteric pain syndrome is a tendinopathy of the surrounding structures: the gluteus medius, the iliotibial band, and the tensor fascia latae. The way these structures relate looks a bit like the face of a clock, as you can see on the infographic. In general, you manage this condition the same way you do with bursitis — physical therapy. You can also give corticosteroid injections. Physical therapy is probably more durable in terms of pain relief and functionality, but in the short term, corticosteroids might provide some degree of analgesia as well. 

Watto: The last thing we wanted to mention is bone stress injury, which can occur in high-mileage runners (20 miles or more per week). Patients with bone stress injury need to rest, usually non‒weight bearing, for a period of time. 

 

Treatment of a bone stress fracture depends on which side it’s on (top or bottom). If it’s on the top of the femoral neck (the tension side), it has to be fixed. If it’s on the compression side (the bottom side of the femoral neck), it might be able to be managed conservatively, but many patients are going to need surgery. This is a big deal. But it’s a spectrum; in some cases the bone is merely irritated and unhappy, without a break in the cortex. Those patients might not need surgery. 

In patients with a fracture of the femoral neck — especially younger, healthier patients — you should think about getting a bone density test and screening for relative energy deficiency in sport. This used to be called the female athlete triad, which includes disrupted menstrual cycles, being underweight, and fracture. We should be screening patients, asking them in a nonjudgmental way about their relationship with food, to make sure they are getting an appropriate number of calories.

They are actually in an energy deficit. They’re not eating enough to maintain a healthy body with so much activity. 

Williams: If you’re interested in this topic, you should refer to the full podcast with Dr Senter which is chock-full of helpful information.

Dr Watto, Clinical Assistant Professor, Department of Medicine, Perelman School of Medicine at University of Pennsylvania; Internist, Department of Medicine, Hospital Medicine Section, Pennsylvania Hospital, Philadelphia, Pennsylvania, has disclosed no relevant financial relationships. Dr Williams, Associate Professor of Clinical Medicine, Department of General Internal Medicine, Lewis Katz School of Medicine; Staff Physician, Department of General Internal Medicine, Temple Internal Medicine Associates, Philadelphia, Pennsylvania, disclosed ties with The Curbsiders.

A version of this article appeared on Medscape.com.