Commentary

As physicians, we hold positions of power and privilege in society. With that power and privilege comes a sacred responsibility to serve as healthcare advocates, for our individual patients as well as for our larger communities in helping them navigate the complexities of the healthcare system and recognize and address barriers to care.

In addition to delivering high-quality, patient-centered care in our clinics and endoscopy units, it is imperative that gastroenterologists use our individual and collective voice in promoting policy reforms that improve healthcare access, affordability, and equity, and help the healthcare system work better for our patients.

 

University of Michigan

Particularly in the wake of Election Day, it is critical to realize the power of physician advocacy in informing rational policymaking relating to healthcare. In furtherance of this goal, AGA held its largest ever Advocacy Day this Fall, bringing together more than 100 members and patient advocates from 28 states to educate members of Congress and their staff about policies affecting GI patient care, including prior authorization, step therapy, federal research funding, and Medicare reimbursement. As a new slate of elected officials prepares to take office in January, I hope you will join me in considering how best to use your voice as a physician to promote systemic change, whether through participating in a future AGA Congressional Advocacy Day, or by meeting independently with your local, state, or federal elected officials to discuss the issues critical to the well-being of your patients and communities. Now more than ever, physician advocacy is critical to achieving a high-performing healthcare system.

In GIHN’s December issue, we highlight expert guidance on the use of noninvasive markers in prescribing resmetirom for MASH and summarize a recent systematic review revealing a link between environmental pollutant exposure and inflammatory bowel disease. In our Member Spotlight column, Dr. Jeffrey Lee (Kaiser Permanente N. California) updates us on his innovative research on colorectal cancer prevention. We hope you have a wonderful holiday season with your friends and family and look forward to seeing you again in 2025!

Megan A. Adams, MD, JD, MSc

Editor in Chief

As physicians, we hold positions of power and privilege in society. With that power and privilege comes a sacred responsibility to serve as healthcare advocates, for our individual patients as well as for our larger communities in helping them navigate the complexities of the healthcare system and recognize and address barriers to care.

In addition to delivering high-quality, patient-centered care in our clinics and endoscopy units, it is imperative that gastroenterologists use our individual and collective voice in promoting policy reforms that improve healthcare access, affordability, and equity, and help the healthcare system work better for our patients.

 

University of Michigan

Particularly in the wake of Election Day, it is critical to realize the power of physician advocacy in informing rational policymaking relating to healthcare. In furtherance of this goal, AGA held its largest ever Advocacy Day this Fall, bringing together more than 100 members and patient advocates from 28 states to educate members of Congress and their staff about policies affecting GI patient care, including prior authorization, step therapy, federal research funding, and Medicare reimbursement. As a new slate of elected officials prepares to take office in January, I hope you will join me in considering how best to use your voice as a physician to promote systemic change, whether through participating in a future AGA Congressional Advocacy Day, or by meeting independently with your local, state, or federal elected officials to discuss the issues critical to the well-being of your patients and communities. Now more than ever, physician advocacy is critical to achieving a high-performing healthcare system.

In GIHN’s December issue, we highlight expert guidance on the use of noninvasive markers in prescribing resmetirom for MASH and summarize a recent systematic review revealing a link between environmental pollutant exposure and inflammatory bowel disease. In our Member Spotlight column, Dr. Jeffrey Lee (Kaiser Permanente N. California) updates us on his innovative research on colorectal cancer prevention. We hope you have a wonderful holiday season with your friends and family and look forward to seeing you again in 2025!

Megan A. Adams, MD, JD, MSc

Editor in Chief

As physicians, we hold positions of power and privilege in society. With that power and privilege comes a sacred responsibility to serve as healthcare advocates, for our individual patients as well as for our larger communities in helping them navigate the complexities of the healthcare system and recognize and address barriers to care.

In addition to delivering high-quality, patient-centered care in our clinics and endoscopy units, it is imperative that gastroenterologists use our individual and collective voice in promoting policy reforms that improve healthcare access, affordability, and equity, and help the healthcare system work better for our patients.

 

University of Michigan

Particularly in the wake of Election Day, it is critical to realize the power of physician advocacy in informing rational policymaking relating to healthcare. In furtherance of this goal, AGA held its largest ever Advocacy Day this Fall, bringing together more than 100 members and patient advocates from 28 states to educate members of Congress and their staff about policies affecting GI patient care, including prior authorization, step therapy, federal research funding, and Medicare reimbursement. As a new slate of elected officials prepares to take office in January, I hope you will join me in considering how best to use your voice as a physician to promote systemic change, whether through participating in a future AGA Congressional Advocacy Day, or by meeting independently with your local, state, or federal elected officials to discuss the issues critical to the well-being of your patients and communities. Now more than ever, physician advocacy is critical to achieving a high-performing healthcare system.

In GIHN’s December issue, we highlight expert guidance on the use of noninvasive markers in prescribing resmetirom for MASH and summarize a recent systematic review revealing a link between environmental pollutant exposure and inflammatory bowel disease. In our Member Spotlight column, Dr. Jeffrey Lee (Kaiser Permanente N. California) updates us on his innovative research on colorectal cancer prevention. We hope you have a wonderful holiday season with your friends and family and look forward to seeing you again in 2025!

Megan A. Adams, MD, JD, MSc

Editor in Chief

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls. Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls. Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls. Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

• It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
• It’s easier to carry than many larger devices (though not the AUVI-Q).
• It cannot be injected incorrectly. 
• Expiration is 8 months longer than the EAI.
• There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

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

This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

• It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
• It’s easier to carry than many larger devices (though not the AUVI-Q).
• It cannot be injected incorrectly. 
• Expiration is 8 months longer than the EAI.
• There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

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

This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

• It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
• It’s easier to carry than many larger devices (though not the AUVI-Q).
• It cannot be injected incorrectly. 
• Expiration is 8 months longer than the EAI.
• There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

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

This transcript has been edited for clarity. 

As primary care doctors, lifestyle medicine is supposed to be a pillar of our practice. Per the evidence, lifestyle medicine can prevent up to 80% of chronic disease. It’s a real irony, then, that it’s the thing we’re least likely to be paid to do.

Thankfully, though, there are a few hacks to help you keep your patients healthy and yourself financially healthy at the same time.

No. 1: Be as accurate in your coding as possible. We all know working on things like sleep, exercise, and diet with patients takes time, so bill for it. With time-based billing, in particular, you can account for both the time spent in face-to-face encounters and the time spent afterward on documentation and care coordination. Make sure to capture that.

No. 2: Try group visits on for size. Group visit models are great for lifestyle medicine. They give you the flexibility to include longer conversations and deeper lessons on a range of subjects while still getting paid for what you do. Want to host a cooking class? Group visit. Want to bring in a personal trainer or hold a dance class or exercise dance class? Group visit. Meditation, yoga, or even a sleep hygiene class? Group visit. 

While there are a few tricks to getting paid for group visits, they’re the same things, such as documenting time and the various parts of the visit, that are key to getting paid for regular visits. They have the bonus of fighting burnout and making your own practice more meaningful as well.

No. 3: Think about joining a value-based care arrangement. While only accounting for 10% of the market right now, value-based care (VBC) is growing rapidly, and it’s easy to see why. By trading quality for the hamster wheel of billing widgets, physicians are freed up to think more about how best to take care of patients, including incorporating more lifestyle medicine. Some VBC models even have their own electronic medical records, freeing you from outdated structures when it comes to documenting patient visits.

No. 4: direct primary care. Direct primary care cuts out the middlemen of payers, letting patients pay physician practices directly for their own care. Like VBC, it opens up possibilities for practicing better medicine, including lifestyle medicine. In addition, it’s often very affordable, with a family of four often paying around $80 a month for a membership for the entire family. It’s a win-win for the doctor and the patient. 

Lifestyle medicine is a great way to improve both your patients’ and your own well-being. With a few flexes, it can improve your wallet’s well-being, too.

Tamaan K. Osbourne-Roberts, President/CEO, Happiness by the Numbers, Denver, Colorado, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

As primary care doctors, lifestyle medicine is supposed to be a pillar of our practice. Per the evidence, lifestyle medicine can prevent up to 80% of chronic disease. It’s a real irony, then, that it’s the thing we’re least likely to be paid to do.

Thankfully, though, there are a few hacks to help you keep your patients healthy and yourself financially healthy at the same time.

No. 1: Be as accurate in your coding as possible. We all know working on things like sleep, exercise, and diet with patients takes time, so bill for it. With time-based billing, in particular, you can account for both the time spent in face-to-face encounters and the time spent afterward on documentation and care coordination. Make sure to capture that.

No. 2: Try group visits on for size. Group visit models are great for lifestyle medicine. They give you the flexibility to include longer conversations and deeper lessons on a range of subjects while still getting paid for what you do. Want to host a cooking class? Group visit. Want to bring in a personal trainer or hold a dance class or exercise dance class? Group visit. Meditation, yoga, or even a sleep hygiene class? Group visit. 

While there are a few tricks to getting paid for group visits, they’re the same things, such as documenting time and the various parts of the visit, that are key to getting paid for regular visits. They have the bonus of fighting burnout and making your own practice more meaningful as well.

No. 3: Think about joining a value-based care arrangement. While only accounting for 10% of the market right now, value-based care (VBC) is growing rapidly, and it’s easy to see why. By trading quality for the hamster wheel of billing widgets, physicians are freed up to think more about how best to take care of patients, including incorporating more lifestyle medicine. Some VBC models even have their own electronic medical records, freeing you from outdated structures when it comes to documenting patient visits.

No. 4: direct primary care. Direct primary care cuts out the middlemen of payers, letting patients pay physician practices directly for their own care. Like VBC, it opens up possibilities for practicing better medicine, including lifestyle medicine. In addition, it’s often very affordable, with a family of four often paying around $80 a month for a membership for the entire family. It’s a win-win for the doctor and the patient. 

Lifestyle medicine is a great way to improve both your patients’ and your own well-being. With a few flexes, it can improve your wallet’s well-being, too.

Tamaan K. Osbourne-Roberts, President/CEO, Happiness by the Numbers, Denver, Colorado, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

As primary care doctors, lifestyle medicine is supposed to be a pillar of our practice. Per the evidence, lifestyle medicine can prevent up to 80% of chronic disease. It’s a real irony, then, that it’s the thing we’re least likely to be paid to do.

Thankfully, though, there are a few hacks to help you keep your patients healthy and yourself financially healthy at the same time.

No. 1: Be as accurate in your coding as possible. We all know working on things like sleep, exercise, and diet with patients takes time, so bill for it. With time-based billing, in particular, you can account for both the time spent in face-to-face encounters and the time spent afterward on documentation and care coordination. Make sure to capture that.

No. 2: Try group visits on for size. Group visit models are great for lifestyle medicine. They give you the flexibility to include longer conversations and deeper lessons on a range of subjects while still getting paid for what you do. Want to host a cooking class? Group visit. Want to bring in a personal trainer or hold a dance class or exercise dance class? Group visit. Meditation, yoga, or even a sleep hygiene class? Group visit. 

While there are a few tricks to getting paid for group visits, they’re the same things, such as documenting time and the various parts of the visit, that are key to getting paid for regular visits. They have the bonus of fighting burnout and making your own practice more meaningful as well.

No. 3: Think about joining a value-based care arrangement. While only accounting for 10% of the market right now, value-based care (VBC) is growing rapidly, and it’s easy to see why. By trading quality for the hamster wheel of billing widgets, physicians are freed up to think more about how best to take care of patients, including incorporating more lifestyle medicine. Some VBC models even have their own electronic medical records, freeing you from outdated structures when it comes to documenting patient visits.

No. 4: direct primary care. Direct primary care cuts out the middlemen of payers, letting patients pay physician practices directly for their own care. Like VBC, it opens up possibilities for practicing better medicine, including lifestyle medicine. In addition, it’s often very affordable, with a family of four often paying around $80 a month for a membership for the entire family. It’s a win-win for the doctor and the patient. 

Lifestyle medicine is a great way to improve both your patients’ and your own well-being. With a few flexes, it can improve your wallet’s well-being, too.

Tamaan K. Osbourne-Roberts, President/CEO, Happiness by the Numbers, Denver, Colorado, has disclosed no relevant financial relationships.

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

How comfortable are you giving nutritional advice to your patients? When you offer it are you basing your advice on something you learned during medical school or your training? Was it included in a course devoted to nutrition? Did you learn it later as part of continuing medical education course (CME)? Or was it just something you just picked up from your experience seeing patients (osmosis)? It is very unlikely that a significant portion, or any part for that matter, of your medical training was devoted to nutrition. It certainly wasn’t during my training.

I recently read an interview with Emily M. Broad Leib, JD, faculty director of the Harvard School Center for Health Law and Policy Innovation, Cambridge, Massachusetts, who would like to correct that deficiency. She feels doctors need to know more about food and that acquiring that knowledge should be a significant component of their formal training.

In the interview, Leib said that “roughly 86% of physicians report they do not feel adequately trained to answer basic questions on diet or nutrition.” She also notes that while “72% of entering medical students report they believe food is important to health” less than 50% retained this belief after graduation.

Leib and associates feel they have recently reached a milestone in their efforts to include nutrition in the mainstream of medical education this fall by publishing a paper that demonstrates “consensus on doctor-approved nutritional standard for medical schools and residency programs.”
 

36 Recommended Competencies

Curious about what these nutrition experts chose to include in medical training, I decided to drill down into the list of 36 consensus-driven competencies they had agreed upon.

It was an interesting voyage into a forest of redundancies, many of which can be boiled down to having the student demonstrate that he/she understands that what we eat is important to our health and that there is a complex web of relationships connecting our society to the food consume.

Some of the recommended competencies I found make perfect sense. For example the student/trainee should be able to take a diet and food history and be able to interpret lab values and anthropometric measurements and be able to discuss the patient’s weight and diet with sensitivity while keeping in mind his/her own biases about food.

Some other recommendations are more problematic, for example, “performs a comprehensive nutrition-focused physical examination” or “demonstrates knowledge of how to create culinary nutrition SMART [Specific, Measurable, Achievable, Relevant, and Time-Bound] goals for personal use and for patient care” or “provides brief counseling interventions to help patients decrease visceral adiposity or reduce the risk of metabolic syndrome.” Including competencies like these demonstrates a lack of understanding of the time restraints and realities of a primary care physician’s life and training.

Instead of simply reinforcing the prospective physician’s preexisting assumption that food and health are entwined and discussing when and how to consult a nutrition expert, these 36 competencies seem to be an attempt to create fast-tracked part-time dietitians and nutrition advocates out of medical students and trainees who already believe that nutrition is important for health but also have a very full plate of clinical responsibilities ahead of them.

The study that Leib quotes — that 72% of medical students believed food was important in health while after graduation only 50% of agreed — doesn’t necessarily mean that professors are preaching that food was unimportant. It is more likely by the end of medical school the students have seen that food must share the spotlight with numerous other factors that influence their patients’ health.
 

‘A More Appropriate Focus’

In my experience, diet and lifestyle counseling done well is extremely time consuming and best done by people for whom that is their specialty. A more appropriate focus for a list of nutritional competencies for physicians in training would be for the student to achieve an understanding of when and how to consult a dietitian and then how to support and evaluate the dietitian’s recommendations to the patient.

Finally, I don’t think we can ignore a serious public relations problem that hangs like a cloud over the nutrition advocacy community. It is the same one that casts a shadow on the medical community as well. It is a common perception among the lay public that nutritionists (and physicians) are always changing their recommendations when it comes to food. What is believable? Just think about eggs, red wine, or introducing peanuts to infants, to name just a few. And what about the food pyramids that seem to have been rebuilt every several years? The problem is compounded when some “credentialed” nutritionists and physicians continue to make dietary pronouncements with only a shred of evidence or poorly documented anecdotal observations.

The first of the 36 competencies I reviewed reads: “Provide evidence-based, culturally sensitive nutrition and food recommendations for the prevention and treatment of disease.” When it comes to nutrition the “evidence” can be tough to come by. The natural experiments in which individuals and populations had extremely limited access to a certain nutrients (eg, scurvy) don’t occur very often. Animal studies don’t always extrapolate to humans. And, observational studies concerning diet often have co-factors that are difficult to control and must run over time courses that can tax even the most patient researchers.

I certainly applaud Leib and associates for promoting their primary goal of including more about of the relationship between food and health in the medical school and trainee curriculum. But I must voice a caution to be careful to keep it truly evidence-based and in a format that acknowledges the realities of the life and education of a primary care provider.

The best nutritional advice I ever received in my training was from an older pediatric professor who suggested that a healthy diet consisted of everything in moderation.

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 pdnews@mdedge.com.

How comfortable are you giving nutritional advice to your patients? When you offer it are you basing your advice on something you learned during medical school or your training? Was it included in a course devoted to nutrition? Did you learn it later as part of continuing medical education course (CME)? Or was it just something you just picked up from your experience seeing patients (osmosis)? It is very unlikely that a significant portion, or any part for that matter, of your medical training was devoted to nutrition. It certainly wasn’t during my training.

I recently read an interview with Emily M. Broad Leib, JD, faculty director of the Harvard School Center for Health Law and Policy Innovation, Cambridge, Massachusetts, who would like to correct that deficiency. She feels doctors need to know more about food and that acquiring that knowledge should be a significant component of their formal training.

In the interview, Leib said that “roughly 86% of physicians report they do not feel adequately trained to answer basic questions on diet or nutrition.” She also notes that while “72% of entering medical students report they believe food is important to health” less than 50% retained this belief after graduation.

Leib and associates feel they have recently reached a milestone in their efforts to include nutrition in the mainstream of medical education this fall by publishing a paper that demonstrates “consensus on doctor-approved nutritional standard for medical schools and residency programs.”
 

36 Recommended Competencies

Curious about what these nutrition experts chose to include in medical training, I decided to drill down into the list of 36 consensus-driven competencies they had agreed upon.

It was an interesting voyage into a forest of redundancies, many of which can be boiled down to having the student demonstrate that he/she understands that what we eat is important to our health and that there is a complex web of relationships connecting our society to the food consume.

Some of the recommended competencies I found make perfect sense. For example the student/trainee should be able to take a diet and food history and be able to interpret lab values and anthropometric measurements and be able to discuss the patient’s weight and diet with sensitivity while keeping in mind his/her own biases about food.

Some other recommendations are more problematic, for example, “performs a comprehensive nutrition-focused physical examination” or “demonstrates knowledge of how to create culinary nutrition SMART [Specific, Measurable, Achievable, Relevant, and Time-Bound] goals for personal use and for patient care” or “provides brief counseling interventions to help patients decrease visceral adiposity or reduce the risk of metabolic syndrome.” Including competencies like these demonstrates a lack of understanding of the time restraints and realities of a primary care physician’s life and training.

Instead of simply reinforcing the prospective physician’s preexisting assumption that food and health are entwined and discussing when and how to consult a nutrition expert, these 36 competencies seem to be an attempt to create fast-tracked part-time dietitians and nutrition advocates out of medical students and trainees who already believe that nutrition is important for health but also have a very full plate of clinical responsibilities ahead of them.

The study that Leib quotes — that 72% of medical students believed food was important in health while after graduation only 50% of agreed — doesn’t necessarily mean that professors are preaching that food was unimportant. It is more likely by the end of medical school the students have seen that food must share the spotlight with numerous other factors that influence their patients’ health.
 

‘A More Appropriate Focus’

In my experience, diet and lifestyle counseling done well is extremely time consuming and best done by people for whom that is their specialty. A more appropriate focus for a list of nutritional competencies for physicians in training would be for the student to achieve an understanding of when and how to consult a dietitian and then how to support and evaluate the dietitian’s recommendations to the patient.

Finally, I don’t think we can ignore a serious public relations problem that hangs like a cloud over the nutrition advocacy community. It is the same one that casts a shadow on the medical community as well. It is a common perception among the lay public that nutritionists (and physicians) are always changing their recommendations when it comes to food. What is believable? Just think about eggs, red wine, or introducing peanuts to infants, to name just a few. And what about the food pyramids that seem to have been rebuilt every several years? The problem is compounded when some “credentialed” nutritionists and physicians continue to make dietary pronouncements with only a shred of evidence or poorly documented anecdotal observations.

The first of the 36 competencies I reviewed reads: “Provide evidence-based, culturally sensitive nutrition and food recommendations for the prevention and treatment of disease.” When it comes to nutrition the “evidence” can be tough to come by. The natural experiments in which individuals and populations had extremely limited access to a certain nutrients (eg, scurvy) don’t occur very often. Animal studies don’t always extrapolate to humans. And, observational studies concerning diet often have co-factors that are difficult to control and must run over time courses that can tax even the most patient researchers.

I certainly applaud Leib and associates for promoting their primary goal of including more about of the relationship between food and health in the medical school and trainee curriculum. But I must voice a caution to be careful to keep it truly evidence-based and in a format that acknowledges the realities of the life and education of a primary care provider.

The best nutritional advice I ever received in my training was from an older pediatric professor who suggested that a healthy diet consisted of everything in moderation.

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 pdnews@mdedge.com.

How comfortable are you giving nutritional advice to your patients? When you offer it are you basing your advice on something you learned during medical school or your training? Was it included in a course devoted to nutrition? Did you learn it later as part of continuing medical education course (CME)? Or was it just something you just picked up from your experience seeing patients (osmosis)? It is very unlikely that a significant portion, or any part for that matter, of your medical training was devoted to nutrition. It certainly wasn’t during my training.

I recently read an interview with Emily M. Broad Leib, JD, faculty director of the Harvard School Center for Health Law and Policy Innovation, Cambridge, Massachusetts, who would like to correct that deficiency. She feels doctors need to know more about food and that acquiring that knowledge should be a significant component of their formal training.

In the interview, Leib said that “roughly 86% of physicians report they do not feel adequately trained to answer basic questions on diet or nutrition.” She also notes that while “72% of entering medical students report they believe food is important to health” less than 50% retained this belief after graduation.

Leib and associates feel they have recently reached a milestone in their efforts to include nutrition in the mainstream of medical education this fall by publishing a paper that demonstrates “consensus on doctor-approved nutritional standard for medical schools and residency programs.”
 

36 Recommended Competencies

Curious about what these nutrition experts chose to include in medical training, I decided to drill down into the list of 36 consensus-driven competencies they had agreed upon.

It was an interesting voyage into a forest of redundancies, many of which can be boiled down to having the student demonstrate that he/she understands that what we eat is important to our health and that there is a complex web of relationships connecting our society to the food consume.

Some of the recommended competencies I found make perfect sense. For example the student/trainee should be able to take a diet and food history and be able to interpret lab values and anthropometric measurements and be able to discuss the patient’s weight and diet with sensitivity while keeping in mind his/her own biases about food.

Some other recommendations are more problematic, for example, “performs a comprehensive nutrition-focused physical examination” or “demonstrates knowledge of how to create culinary nutrition SMART [Specific, Measurable, Achievable, Relevant, and Time-Bound] goals for personal use and for patient care” or “provides brief counseling interventions to help patients decrease visceral adiposity or reduce the risk of metabolic syndrome.” Including competencies like these demonstrates a lack of understanding of the time restraints and realities of a primary care physician’s life and training.

Instead of simply reinforcing the prospective physician’s preexisting assumption that food and health are entwined and discussing when and how to consult a nutrition expert, these 36 competencies seem to be an attempt to create fast-tracked part-time dietitians and nutrition advocates out of medical students and trainees who already believe that nutrition is important for health but also have a very full plate of clinical responsibilities ahead of them.

The study that Leib quotes — that 72% of medical students believed food was important in health while after graduation only 50% of agreed — doesn’t necessarily mean that professors are preaching that food was unimportant. It is more likely by the end of medical school the students have seen that food must share the spotlight with numerous other factors that influence their patients’ health.
 

‘A More Appropriate Focus’

In my experience, diet and lifestyle counseling done well is extremely time consuming and best done by people for whom that is their specialty. A more appropriate focus for a list of nutritional competencies for physicians in training would be for the student to achieve an understanding of when and how to consult a dietitian and then how to support and evaluate the dietitian’s recommendations to the patient.

Finally, I don’t think we can ignore a serious public relations problem that hangs like a cloud over the nutrition advocacy community. It is the same one that casts a shadow on the medical community as well. It is a common perception among the lay public that nutritionists (and physicians) are always changing their recommendations when it comes to food. What is believable? Just think about eggs, red wine, or introducing peanuts to infants, to name just a few. And what about the food pyramids that seem to have been rebuilt every several years? The problem is compounded when some “credentialed” nutritionists and physicians continue to make dietary pronouncements with only a shred of evidence or poorly documented anecdotal observations.

The first of the 36 competencies I reviewed reads: “Provide evidence-based, culturally sensitive nutrition and food recommendations for the prevention and treatment of disease.” When it comes to nutrition the “evidence” can be tough to come by. The natural experiments in which individuals and populations had extremely limited access to a certain nutrients (eg, scurvy) don’t occur very often. Animal studies don’t always extrapolate to humans. And, observational studies concerning diet often have co-factors that are difficult to control and must run over time courses that can tax even the most patient researchers.

I certainly applaud Leib and associates for promoting their primary goal of including more about of the relationship between food and health in the medical school and trainee curriculum. But I must voice a caution to be careful to keep it truly evidence-based and in a format that acknowledges the realities of the life and education of a primary care provider.

The best nutritional advice I ever received in my training was from an older pediatric professor who suggested that a healthy diet consisted of everything in moderation.

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 pdnews@mdedge.com.

A member of the Elaeagnaceae family, Hippophae rhamnoides, better known as sea buckthorn, is a high-altitude wild shrub endemic to Europe and Asia with edible fruits and a lengthy record of use in traditional Chinese medicine.^1-6 Used as a health supplement and consumed in the diet throughout the world,⁵ sea buckthorn berries, seeds, and leaves have been used in traditional medicine to treat burns/injuries, edema, hypertension, inflammation, skin grafts, ulcers, and wounds.^4,7

This hardy plant is associated with a wide range of biologic activities, including anti-atherogenic, anti-atopic dermatitis, antibacterial, anticancer, antifungal, anti-inflammatory, antimicrobial, antioxidant, anti-psoriasis, anti-sebum, anti-stress, anti-tumor, cytoprotective, hepatoprotective, immunomodulatory, neuroprotective, radioprotective, and tissue regenerative functions.^4,5,8-11 Sea buckthorn has also been included in several cosmeceutical formulations to treat wrinkles, scars, pigmentary conditions, and hair disorders, as well as to rejuvenate, even, and smooth the skin.⁴

Indre Brazauskaite/EyeEm/Getty Images

Key Constituents

Functional constituents identified in sea buckthorn include alkaloids, carotenoids, flavonoids, lignans, organic acids, phenolic acids, proanthocyanidins, polyunsaturated acids (including omega-3, -6, -7, and -9), steroids, tannins, terpenoids, and volatile oils, as well as nutritional compounds such as minerals, proteins, and vitamins.^4,5,11 Sea buckthorn pericarp oil contains copious amounts of saturated palmitic acid (29%-36%) and omega-7 unsaturated palmitoleic acid (36%-48%), which fosters cutaneous and mucosal epithelialization, as well as linoleic (10%-12%) and oleic (4%-6%) acids.^12,6 Significant amounts of carotenoids as well as alpha‐linolenic fatty acid (38%), linoleic (36%), oleic (13%), and palmitic (7%) acids are present in sea buckthorn seed oil.⁶

Polysaccharides

In an expansive review on the pharmacological activities of sea buckthorn polysaccharides, Teng and colleagues reported in April 2024 that 20 diverse polysaccharides have been culled from sea buckthorn and exhibited various healthy activities, including antioxidant, anti-fatigue, anti-inflammatory, anti-obesity, anti-tumor, hepatoprotective, hypoglycemic, and immunoregulation, and regulation of intestinal flora activities.¹

Proanthocyanidins and Anti-Aging

In 2023, Liu and colleagues investigated the anti–skin aging impact of sea buckthorn proanthocyanidins in D-galactose-induced aging in mice given the known free radical scavenging activity of these compounds. They found the proanthocyanidins mitigated D-galactose-induced aging and can augment the total antioxidant capacity of the body. Sea buckthorn proanthocyanidins can further attenuate the effects of skin aging by regulating the TGF-beta¹/Smads pathway and MMPs/TIMP system, thus amplifying collagen I and tropoelastin content.¹³

Baumann Cosmetic &amp; Research Institute

A year earlier, many of the same investigators assessed the possible protective activity of sea buckthorn proanthocyanidins against cutaneous aging engendered by oxidative stress from hydrogen peroxide. The compounds amplified superoxide dismutase and glutathione antioxidant functions. The extracts also fostered collagen I production in aging human skin fibroblasts via the TGF-beta1/Smads pathway and hindered collagen I degradation by regulating the MMPs/TIMPs system, which maintained extracellular matrix integrity. Senescent cell migration was also promoted with 100 mcg/mL of sea buckthorn proanthocyanidins. The researchers concluded that this sets the stage for investigating how sea buckthorn proanthocyanidins can be incorporated in cosmetic formulations.14 In a separate study, Liu and colleagues demonstrated that sea buckthorn proanthocyanidins can attenuate oxidative damage and protect mitochondrial function.⁹

Acne and Barrier Functions

The extracts of H rhamnoides and Cassia fistula in a combined formulation were found to be effective in lowering skin sebum content in humans with grade I and grade II acne vulgaris in a 2014 single-blind, randomized, placebo-controlled, split-face study with two groups of 25 patients each (aged 18-37 years).¹⁵ Khan and colleagues have also reported that a sea buckthorn oil-in-water emulsion improved barrier function in human skin as tested by a tewameter and corneometer (noninvasive probes) in 13 healthy males with a mean age of 27 ± 4.8 years.¹⁶

Anti-Aging, Antioxidant, Antibacterial, Skin-Whitening Activity

Zaman and colleagues reported in 2011 that results from an in vivo study of the effects of a sea buckthorn fruit extract topical cream on stratum corneum water content and transepidermal water loss indicated that the formulation enhanced cell surface integrin expression thus facilitating collagen contraction.¹⁷

In 2012, Khan and colleagues reported amelioration in skin elasticity, thus achieving an anti-aging result, from the use of a water-in-oil–based hydroalcoholic cream loaded with fruit extract of H rhamnoides, as measured with a Cutometer.¹⁸ The previous year, some of the same researchers reported that the antioxidants and flavonoids found in a topical sea buckthorn formulation could decrease cutaneous melanin and erythema levels.

More recently, Gęgotek and colleagues found that sea buckthorn seed oil prevented redox balance and lipid metabolism disturbances in skin fibroblasts and keratinocytes caused by UVA or UVB. They suggested that such findings point to the potential of this natural agent to confer anti-inflammatory properties and photoprotection to the skin.¹⁹

In 2020, Ivanišová and colleagues investigated the antioxidant and antimicrobial activities of H rhamnoides 100% oil, 100% juice, dry berries, and tea (dry berries, leaves, and twigs). They found that all of the studied sea buckthorn products displayed high antioxidant activity (identified through DPPH radical scavenging and molybdenum reducing antioxidant power tests). Sea buckthorn juice contained the highest total content of polyphenols, flavonoids, and carotenoids. All of the tested products also exhibited substantial antibacterial activity against the tested microbes.²⁰

Burns and Wound Healing

In a preclinical study of the effects of sea buckthorn leaf extracts on wound healing in albino rats using an excision-punch wound model in 2005, Gupta and colleagues found that twice daily topical application of the aqueous leaf extract fostered wound healing. This was indicated by higher hydroxyproline and protein levels, a diminished wound area, and lower lipid peroxide levels. The investigators suggested that sea buckthorn may facilitate wound healing at least in part because of elevated antioxidant activity in the granulation tissue.³

A year later, Wang and colleagues reported on observations of using H rhamnoides oil, a traditional Chinese herbal medicine derived from sea buckthorn fruit, as a burn treatment. In the study, 151 burn patients received an H rhamnoides oil dressing (changed every other day until wound healing) that was covered with a disinfecting dressing. The dressing reduced swelling and effusion, and alleviated pain, with patients receiving the sea buckthorn dressing experiencing greater apparent exudation reduction, pain reduction, and more rapid epithelial cell growth and wound healing than controls (treated only with Vaseline gauze). The difference between the two groups was statistically significant.²¹

Conclusion

Sea buckthorn has been used for hundreds if not thousands of years in traditional medical applications, including for dermatologic purposes. Emerging data appear to support the use of this dynamic plant for consideration in dermatologic applications. As is often the case, much more work is necessary in the form of randomized controlled trials to determine the effectiveness of sea buckthorn formulations as well as the most appropriate avenues of research or uses for dermatologic application of this traditionally used botanical agent.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at dermnews@mdedge.com.

References

1. Teng H et al. J Ethnopharmacol. 2024 Apr 24;324:117809. doi: 10.1016/j.jep.2024.117809.

2. Wang Z et al. Int J Biol Macromol. 2024 Apr;263(Pt 1):130206. doi: 10.1016/j.ijbiomac.2024.130206.

3. Gupta A et al. Int J Low Extrem Wounds. 2005 Jun;4(2):88-92. doi: 10.1177/1534734605277401.

4. Pundir S et al. J Ethnopharmacol. 2021 Feb 10;266:113434. doi: 10.1016/j.jep.2020.113434.

5. Ma QG et al. J Agric Food Chem. 2023 Mar 29;71(12):4769-4788. doi: 10.1021/acs.jafc.2c06916.

6. Poljšak N et al. Phytother Res. 2020 Feb;34(2):254-269. doi: 10.1002/ptr.6524. doi: 10.1002/ptr.6524.

7. Upadhyay NK et al. Evid Based Complement Alternat Med. 2011;2011:659705. doi: 10.1093/ecam/nep189.

8. Suryakumar G, Gupta A. J Ethnopharmacol. 2011 Nov 18;138(2):268-78. doi: 10.1016/j.jep.2011.09.024.

9. Liu K et al. Front Pharmacol. 2022 Jul 8;13:914146. doi: 10.3389/fphar.2022.914146.

10. Akhtar N et al. J Pharm Bioallied Sci. 2010 Jan;2(1):13-7. doi: 10.4103/0975-7406.62698.

11. Ren R et al. RSC Adv. 2020 Dec 17;10(73):44654-44671. doi: 10.1039/d0ra06488b.

12. Ito H et al. Burns. 2014 May;40(3):511-9. doi: 10.1016/j.burns.2013.08.011.

13. Liu X et al. Food Sci Nutr. 2023 Dec 7;12(2):1082-1094. doi: 10.1002/fsn3.3823.

14. Liu X at al. Antioxidants (Basel). 2022 Sep 25;11(10):1900. doi: 10.3390/antiox11101900.

15. Khan BA, Akhtar N. Postepy Dermatol Alergol. 2014 Aug;31(4):229-234. doi: 10.5114/pdia.2014.40934.

16. Khan BA, Akhtar N. Pak J Pharm Sci. 2014 Nov;27(6):1919-22.

17. Khan AB et al. African J Pharm Pharmacol. 2011 Aug;5(8):1092-5.

18. Khan BA, Akhtar N, Braga VA. Trop J Pharm Res. 2012;11(6):955-62.

19. Gęgotek A et al. Antioxidants (Basel). 2018 Aug 23;7(9):110. doi: 10.3390/antiox7090110.

20. Ivanišová E et al. Acta Sci Pol Technol Aliment. 2020 Apr-Jun;19(2):195-205. doi: 10.17306/J.AFS.0809.

21. Wang ZY, Luo XL, He CP. Nan Fang Yi Ke Da Xue Xue Bao. 2006 Jan;26(1):124-5.

A member of the Elaeagnaceae family, Hippophae rhamnoides, better known as sea buckthorn, is a high-altitude wild shrub endemic to Europe and Asia with edible fruits and a lengthy record of use in traditional Chinese medicine.^1-6 Used as a health supplement and consumed in the diet throughout the world,⁵ sea buckthorn berries, seeds, and leaves have been used in traditional medicine to treat burns/injuries, edema, hypertension, inflammation, skin grafts, ulcers, and wounds.^4,7

This hardy plant is associated with a wide range of biologic activities, including anti-atherogenic, anti-atopic dermatitis, antibacterial, anticancer, antifungal, anti-inflammatory, antimicrobial, antioxidant, anti-psoriasis, anti-sebum, anti-stress, anti-tumor, cytoprotective, hepatoprotective, immunomodulatory, neuroprotective, radioprotective, and tissue regenerative functions.^4,5,8-11 Sea buckthorn has also been included in several cosmeceutical formulations to treat wrinkles, scars, pigmentary conditions, and hair disorders, as well as to rejuvenate, even, and smooth the skin.⁴

Indre Brazauskaite/EyeEm/Getty Images

Key Constituents

Functional constituents identified in sea buckthorn include alkaloids, carotenoids, flavonoids, lignans, organic acids, phenolic acids, proanthocyanidins, polyunsaturated acids (including omega-3, -6, -7, and -9), steroids, tannins, terpenoids, and volatile oils, as well as nutritional compounds such as minerals, proteins, and vitamins.^4,5,11 Sea buckthorn pericarp oil contains copious amounts of saturated palmitic acid (29%-36%) and omega-7 unsaturated palmitoleic acid (36%-48%), which fosters cutaneous and mucosal epithelialization, as well as linoleic (10%-12%) and oleic (4%-6%) acids.^12,6 Significant amounts of carotenoids as well as alpha‐linolenic fatty acid (38%), linoleic (36%), oleic (13%), and palmitic (7%) acids are present in sea buckthorn seed oil.⁶

Polysaccharides

In an expansive review on the pharmacological activities of sea buckthorn polysaccharides, Teng and colleagues reported in April 2024 that 20 diverse polysaccharides have been culled from sea buckthorn and exhibited various healthy activities, including antioxidant, anti-fatigue, anti-inflammatory, anti-obesity, anti-tumor, hepatoprotective, hypoglycemic, and immunoregulation, and regulation of intestinal flora activities.¹

Proanthocyanidins and Anti-Aging

In 2023, Liu and colleagues investigated the anti–skin aging impact of sea buckthorn proanthocyanidins in D-galactose-induced aging in mice given the known free radical scavenging activity of these compounds. They found the proanthocyanidins mitigated D-galactose-induced aging and can augment the total antioxidant capacity of the body. Sea buckthorn proanthocyanidins can further attenuate the effects of skin aging by regulating the TGF-beta¹/Smads pathway and MMPs/TIMP system, thus amplifying collagen I and tropoelastin content.¹³

Baumann Cosmetic &amp; Research Institute

A year earlier, many of the same investigators assessed the possible protective activity of sea buckthorn proanthocyanidins against cutaneous aging engendered by oxidative stress from hydrogen peroxide. The compounds amplified superoxide dismutase and glutathione antioxidant functions. The extracts also fostered collagen I production in aging human skin fibroblasts via the TGF-beta1/Smads pathway and hindered collagen I degradation by regulating the MMPs/TIMPs system, which maintained extracellular matrix integrity. Senescent cell migration was also promoted with 100 mcg/mL of sea buckthorn proanthocyanidins. The researchers concluded that this sets the stage for investigating how sea buckthorn proanthocyanidins can be incorporated in cosmetic formulations.14 In a separate study, Liu and colleagues demonstrated that sea buckthorn proanthocyanidins can attenuate oxidative damage and protect mitochondrial function.⁹

Acne and Barrier Functions

The extracts of H rhamnoides and Cassia fistula in a combined formulation were found to be effective in lowering skin sebum content in humans with grade I and grade II acne vulgaris in a 2014 single-blind, randomized, placebo-controlled, split-face study with two groups of 25 patients each (aged 18-37 years).¹⁵ Khan and colleagues have also reported that a sea buckthorn oil-in-water emulsion improved barrier function in human skin as tested by a tewameter and corneometer (noninvasive probes) in 13 healthy males with a mean age of 27 ± 4.8 years.¹⁶

Anti-Aging, Antioxidant, Antibacterial, Skin-Whitening Activity

Zaman and colleagues reported in 2011 that results from an in vivo study of the effects of a sea buckthorn fruit extract topical cream on stratum corneum water content and transepidermal water loss indicated that the formulation enhanced cell surface integrin expression thus facilitating collagen contraction.¹⁷

In 2012, Khan and colleagues reported amelioration in skin elasticity, thus achieving an anti-aging result, from the use of a water-in-oil–based hydroalcoholic cream loaded with fruit extract of H rhamnoides, as measured with a Cutometer.¹⁸ The previous year, some of the same researchers reported that the antioxidants and flavonoids found in a topical sea buckthorn formulation could decrease cutaneous melanin and erythema levels.

More recently, Gęgotek and colleagues found that sea buckthorn seed oil prevented redox balance and lipid metabolism disturbances in skin fibroblasts and keratinocytes caused by UVA or UVB. They suggested that such findings point to the potential of this natural agent to confer anti-inflammatory properties and photoprotection to the skin.¹⁹

In 2020, Ivanišová and colleagues investigated the antioxidant and antimicrobial activities of H rhamnoides 100% oil, 100% juice, dry berries, and tea (dry berries, leaves, and twigs). They found that all of the studied sea buckthorn products displayed high antioxidant activity (identified through DPPH radical scavenging and molybdenum reducing antioxidant power tests). Sea buckthorn juice contained the highest total content of polyphenols, flavonoids, and carotenoids. All of the tested products also exhibited substantial antibacterial activity against the tested microbes.²⁰

Burns and Wound Healing

In a preclinical study of the effects of sea buckthorn leaf extracts on wound healing in albino rats using an excision-punch wound model in 2005, Gupta and colleagues found that twice daily topical application of the aqueous leaf extract fostered wound healing. This was indicated by higher hydroxyproline and protein levels, a diminished wound area, and lower lipid peroxide levels. The investigators suggested that sea buckthorn may facilitate wound healing at least in part because of elevated antioxidant activity in the granulation tissue.³

A year later, Wang and colleagues reported on observations of using H rhamnoides oil, a traditional Chinese herbal medicine derived from sea buckthorn fruit, as a burn treatment. In the study, 151 burn patients received an H rhamnoides oil dressing (changed every other day until wound healing) that was covered with a disinfecting dressing. The dressing reduced swelling and effusion, and alleviated pain, with patients receiving the sea buckthorn dressing experiencing greater apparent exudation reduction, pain reduction, and more rapid epithelial cell growth and wound healing than controls (treated only with Vaseline gauze). The difference between the two groups was statistically significant.²¹

Conclusion

Sea buckthorn has been used for hundreds if not thousands of years in traditional medical applications, including for dermatologic purposes. Emerging data appear to support the use of this dynamic plant for consideration in dermatologic applications. As is often the case, much more work is necessary in the form of randomized controlled trials to determine the effectiveness of sea buckthorn formulations as well as the most appropriate avenues of research or uses for dermatologic application of this traditionally used botanical agent.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at dermnews@mdedge.com.

References

1. Teng H et al. J Ethnopharmacol. 2024 Apr 24;324:117809. doi: 10.1016/j.jep.2024.117809.

2. Wang Z et al. Int J Biol Macromol. 2024 Apr;263(Pt 1):130206. doi: 10.1016/j.ijbiomac.2024.130206.

3. Gupta A et al. Int J Low Extrem Wounds. 2005 Jun;4(2):88-92. doi: 10.1177/1534734605277401.

4. Pundir S et al. J Ethnopharmacol. 2021 Feb 10;266:113434. doi: 10.1016/j.jep.2020.113434.

5. Ma QG et al. J Agric Food Chem. 2023 Mar 29;71(12):4769-4788. doi: 10.1021/acs.jafc.2c06916.

6. Poljšak N et al. Phytother Res. 2020 Feb;34(2):254-269. doi: 10.1002/ptr.6524. doi: 10.1002/ptr.6524.

7. Upadhyay NK et al. Evid Based Complement Alternat Med. 2011;2011:659705. doi: 10.1093/ecam/nep189.

8. Suryakumar G, Gupta A. J Ethnopharmacol. 2011 Nov 18;138(2):268-78. doi: 10.1016/j.jep.2011.09.024.

9. Liu K et al. Front Pharmacol. 2022 Jul 8;13:914146. doi: 10.3389/fphar.2022.914146.

10. Akhtar N et al. J Pharm Bioallied Sci. 2010 Jan;2(1):13-7. doi: 10.4103/0975-7406.62698.

11. Ren R et al. RSC Adv. 2020 Dec 17;10(73):44654-44671. doi: 10.1039/d0ra06488b.

12. Ito H et al. Burns. 2014 May;40(3):511-9. doi: 10.1016/j.burns.2013.08.011.

13. Liu X et al. Food Sci Nutr. 2023 Dec 7;12(2):1082-1094. doi: 10.1002/fsn3.3823.

14. Liu X at al. Antioxidants (Basel). 2022 Sep 25;11(10):1900. doi: 10.3390/antiox11101900.

15. Khan BA, Akhtar N. Postepy Dermatol Alergol. 2014 Aug;31(4):229-234. doi: 10.5114/pdia.2014.40934.

16. Khan BA, Akhtar N. Pak J Pharm Sci. 2014 Nov;27(6):1919-22.

17. Khan AB et al. African J Pharm Pharmacol. 2011 Aug;5(8):1092-5.

18. Khan BA, Akhtar N, Braga VA. Trop J Pharm Res. 2012;11(6):955-62.

19. Gęgotek A et al. Antioxidants (Basel). 2018 Aug 23;7(9):110. doi: 10.3390/antiox7090110.

20. Ivanišová E et al. Acta Sci Pol Technol Aliment. 2020 Apr-Jun;19(2):195-205. doi: 10.17306/J.AFS.0809.

21. Wang ZY, Luo XL, He CP. Nan Fang Yi Ke Da Xue Xue Bao. 2006 Jan;26(1):124-5.

A member of the Elaeagnaceae family, Hippophae rhamnoides, better known as sea buckthorn, is a high-altitude wild shrub endemic to Europe and Asia with edible fruits and a lengthy record of use in traditional Chinese medicine.^1-6 Used as a health supplement and consumed in the diet throughout the world,⁵ sea buckthorn berries, seeds, and leaves have been used in traditional medicine to treat burns/injuries, edema, hypertension, inflammation, skin grafts, ulcers, and wounds.^4,7

This hardy plant is associated with a wide range of biologic activities, including anti-atherogenic, anti-atopic dermatitis, antibacterial, anticancer, antifungal, anti-inflammatory, antimicrobial, antioxidant, anti-psoriasis, anti-sebum, anti-stress, anti-tumor, cytoprotective, hepatoprotective, immunomodulatory, neuroprotective, radioprotective, and tissue regenerative functions.^4,5,8-11 Sea buckthorn has also been included in several cosmeceutical formulations to treat wrinkles, scars, pigmentary conditions, and hair disorders, as well as to rejuvenate, even, and smooth the skin.⁴

Indre Brazauskaite/EyeEm/Getty Images

Key Constituents

Functional constituents identified in sea buckthorn include alkaloids, carotenoids, flavonoids, lignans, organic acids, phenolic acids, proanthocyanidins, polyunsaturated acids (including omega-3, -6, -7, and -9), steroids, tannins, terpenoids, and volatile oils, as well as nutritional compounds such as minerals, proteins, and vitamins.^4,5,11 Sea buckthorn pericarp oil contains copious amounts of saturated palmitic acid (29%-36%) and omega-7 unsaturated palmitoleic acid (36%-48%), which fosters cutaneous and mucosal epithelialization, as well as linoleic (10%-12%) and oleic (4%-6%) acids.^12,6 Significant amounts of carotenoids as well as alpha‐linolenic fatty acid (38%), linoleic (36%), oleic (13%), and palmitic (7%) acids are present in sea buckthorn seed oil.⁶

Polysaccharides

In an expansive review on the pharmacological activities of sea buckthorn polysaccharides, Teng and colleagues reported in April 2024 that 20 diverse polysaccharides have been culled from sea buckthorn and exhibited various healthy activities, including antioxidant, anti-fatigue, anti-inflammatory, anti-obesity, anti-tumor, hepatoprotective, hypoglycemic, and immunoregulation, and regulation of intestinal flora activities.¹

Proanthocyanidins and Anti-Aging

In 2023, Liu and colleagues investigated the anti–skin aging impact of sea buckthorn proanthocyanidins in D-galactose-induced aging in mice given the known free radical scavenging activity of these compounds. They found the proanthocyanidins mitigated D-galactose-induced aging and can augment the total antioxidant capacity of the body. Sea buckthorn proanthocyanidins can further attenuate the effects of skin aging by regulating the TGF-beta¹/Smads pathway and MMPs/TIMP system, thus amplifying collagen I and tropoelastin content.¹³

Baumann Cosmetic &amp; Research Institute

A year earlier, many of the same investigators assessed the possible protective activity of sea buckthorn proanthocyanidins against cutaneous aging engendered by oxidative stress from hydrogen peroxide. The compounds amplified superoxide dismutase and glutathione antioxidant functions. The extracts also fostered collagen I production in aging human skin fibroblasts via the TGF-beta1/Smads pathway and hindered collagen I degradation by regulating the MMPs/TIMPs system, which maintained extracellular matrix integrity. Senescent cell migration was also promoted with 100 mcg/mL of sea buckthorn proanthocyanidins. The researchers concluded that this sets the stage for investigating how sea buckthorn proanthocyanidins can be incorporated in cosmetic formulations.14 In a separate study, Liu and colleagues demonstrated that sea buckthorn proanthocyanidins can attenuate oxidative damage and protect mitochondrial function.⁹

Acne and Barrier Functions

The extracts of H rhamnoides and Cassia fistula in a combined formulation were found to be effective in lowering skin sebum content in humans with grade I and grade II acne vulgaris in a 2014 single-blind, randomized, placebo-controlled, split-face study with two groups of 25 patients each (aged 18-37 years).¹⁵ Khan and colleagues have also reported that a sea buckthorn oil-in-water emulsion improved barrier function in human skin as tested by a tewameter and corneometer (noninvasive probes) in 13 healthy males with a mean age of 27 ± 4.8 years.¹⁶

Anti-Aging, Antioxidant, Antibacterial, Skin-Whitening Activity

Zaman and colleagues reported in 2011 that results from an in vivo study of the effects of a sea buckthorn fruit extract topical cream on stratum corneum water content and transepidermal water loss indicated that the formulation enhanced cell surface integrin expression thus facilitating collagen contraction.¹⁷

In 2012, Khan and colleagues reported amelioration in skin elasticity, thus achieving an anti-aging result, from the use of a water-in-oil–based hydroalcoholic cream loaded with fruit extract of H rhamnoides, as measured with a Cutometer.¹⁸ The previous year, some of the same researchers reported that the antioxidants and flavonoids found in a topical sea buckthorn formulation could decrease cutaneous melanin and erythema levels.

More recently, Gęgotek and colleagues found that sea buckthorn seed oil prevented redox balance and lipid metabolism disturbances in skin fibroblasts and keratinocytes caused by UVA or UVB. They suggested that such findings point to the potential of this natural agent to confer anti-inflammatory properties and photoprotection to the skin.¹⁹

In 2020, Ivanišová and colleagues investigated the antioxidant and antimicrobial activities of H rhamnoides 100% oil, 100% juice, dry berries, and tea (dry berries, leaves, and twigs). They found that all of the studied sea buckthorn products displayed high antioxidant activity (identified through DPPH radical scavenging and molybdenum reducing antioxidant power tests). Sea buckthorn juice contained the highest total content of polyphenols, flavonoids, and carotenoids. All of the tested products also exhibited substantial antibacterial activity against the tested microbes.²⁰

Burns and Wound Healing

In a preclinical study of the effects of sea buckthorn leaf extracts on wound healing in albino rats using an excision-punch wound model in 2005, Gupta and colleagues found that twice daily topical application of the aqueous leaf extract fostered wound healing. This was indicated by higher hydroxyproline and protein levels, a diminished wound area, and lower lipid peroxide levels. The investigators suggested that sea buckthorn may facilitate wound healing at least in part because of elevated antioxidant activity in the granulation tissue.³

A year later, Wang and colleagues reported on observations of using H rhamnoides oil, a traditional Chinese herbal medicine derived from sea buckthorn fruit, as a burn treatment. In the study, 151 burn patients received an H rhamnoides oil dressing (changed every other day until wound healing) that was covered with a disinfecting dressing. The dressing reduced swelling and effusion, and alleviated pain, with patients receiving the sea buckthorn dressing experiencing greater apparent exudation reduction, pain reduction, and more rapid epithelial cell growth and wound healing than controls (treated only with Vaseline gauze). The difference between the two groups was statistically significant.²¹

Conclusion

Sea buckthorn has been used for hundreds if not thousands of years in traditional medical applications, including for dermatologic purposes. Emerging data appear to support the use of this dynamic plant for consideration in dermatologic applications. As is often the case, much more work is necessary in the form of randomized controlled trials to determine the effectiveness of sea buckthorn formulations as well as the most appropriate avenues of research or uses for dermatologic application of this traditionally used botanical agent.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions, a SaaS company used to generate skin care routines in office and as a e-commerce solution. Write to her at dermnews@mdedge.com.

References

1. Teng H et al. J Ethnopharmacol. 2024 Apr 24;324:117809. doi: 10.1016/j.jep.2024.117809.

2. Wang Z et al. Int J Biol Macromol. 2024 Apr;263(Pt 1):130206. doi: 10.1016/j.ijbiomac.2024.130206.

3. Gupta A et al. Int J Low Extrem Wounds. 2005 Jun;4(2):88-92. doi: 10.1177/1534734605277401.

4. Pundir S et al. J Ethnopharmacol. 2021 Feb 10;266:113434. doi: 10.1016/j.jep.2020.113434.

5. Ma QG et al. J Agric Food Chem. 2023 Mar 29;71(12):4769-4788. doi: 10.1021/acs.jafc.2c06916.

6. Poljšak N et al. Phytother Res. 2020 Feb;34(2):254-269. doi: 10.1002/ptr.6524. doi: 10.1002/ptr.6524.

7. Upadhyay NK et al. Evid Based Complement Alternat Med. 2011;2011:659705. doi: 10.1093/ecam/nep189.

8. Suryakumar G, Gupta A. J Ethnopharmacol. 2011 Nov 18;138(2):268-78. doi: 10.1016/j.jep.2011.09.024.

9. Liu K et al. Front Pharmacol. 2022 Jul 8;13:914146. doi: 10.3389/fphar.2022.914146.

10. Akhtar N et al. J Pharm Bioallied Sci. 2010 Jan;2(1):13-7. doi: 10.4103/0975-7406.62698.

11. Ren R et al. RSC Adv. 2020 Dec 17;10(73):44654-44671. doi: 10.1039/d0ra06488b.

12. Ito H et al. Burns. 2014 May;40(3):511-9. doi: 10.1016/j.burns.2013.08.011.

13. Liu X et al. Food Sci Nutr. 2023 Dec 7;12(2):1082-1094. doi: 10.1002/fsn3.3823.

14. Liu X at al. Antioxidants (Basel). 2022 Sep 25;11(10):1900. doi: 10.3390/antiox11101900.

15. Khan BA, Akhtar N. Postepy Dermatol Alergol. 2014 Aug;31(4):229-234. doi: 10.5114/pdia.2014.40934.

16. Khan BA, Akhtar N. Pak J Pharm Sci. 2014 Nov;27(6):1919-22.

17. Khan AB et al. African J Pharm Pharmacol. 2011 Aug;5(8):1092-5.

18. Khan BA, Akhtar N, Braga VA. Trop J Pharm Res. 2012;11(6):955-62.

19. Gęgotek A et al. Antioxidants (Basel). 2018 Aug 23;7(9):110. doi: 10.3390/antiox7090110.

20. Ivanišová E et al. Acta Sci Pol Technol Aliment. 2020 Apr-Jun;19(2):195-205. doi: 10.17306/J.AFS.0809.

21. Wang ZY, Luo XL, He CP. Nan Fang Yi Ke Da Xue Xue Bao. 2006 Jan;26(1):124-5.

Hi, everyone. I’m Dr. Kenny Lin. I am a family physician and associate director of the Lancaster General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.

For the past 4 years, primary care clinicians have labored under a seemingly endless onslaught of bad news. A recent report estimated that there were over 1.3 million excess deaths in the United States from March 2020 to May 2023, including nearly half a million Americans younger than age 65. Social isolation and an ailing economy accelerated preexisting rises in drug overdoses and obesity, while teenage vaping threatened to hook a new generation on tobacco products even as adult smoking plummeted. Meanwhile, more than half of the nation’s physicians now report feelings of burnout, pay for family doctors appears to be stagnating, and our interactions with an increasing number of patients are fraught with suspicions about the value of vaccines— not just against COVID-19 but against flu and other viruses, too — and the medical system as a whole, doctors included. 

Now, for the good news.

A year and a half since the end of the pandemic emergency, we are seeing gains on several fronts, and physicians deserve much of the credit. Preliminary data from the Centers for Disease Control and Prevention show that 10,000 fewer people died from drug overdoses than in the previous year. Although multiple factors contributed to this change, the elimination of the X-waiver, which had previously been required for physicians to prescribe buprenorphine for opioid use disorder, in January 2023 has improved access to medications for addiction treatment. In addition, the expansion of state requirements to check prescription drug monitoring programs when opioids or benzodiazepines are prescribed, and to prescribe naloxone to patients taking more than a certain number of morphine milligram equivalents per day, has probably reduced the harms of hazardous drug use.

On the obesity front, recent data from the National Health and Nutrition Examination Survey found that the prevalence of obesity in adults fell for the first time in more than a decade, from 41.9% to 40.3%. To be sure, obesity remains far too common, and this finding could be the result of statistical chance rather than representing a true decline. But the widespread prescribing of GLP-1 receptor agonists by primary care physicians, in particular, could have played a role in the encouraging trend.

Although more research is needed to prove causality, one analysis suggests that these drugs could easily have lowered the body mass index (BMI) of more than enough patients to account for the observed decline. What’s more, the rise in prevalence of BMIs above 40 (from 7.7% to 9.7%) could be explained by the mortality benefit of the drugs: More people remained in this severe obesity category because they didn’t die from complications of their weight. Whether future studies support keeping people on GLP-1s for life or eventually “off-ramping” them to other weight control strategies, family physicians are well positioned to help.

Finally, with little fanfare, the youth smoking rate has fallen precipitously. In 2023, 1.9% of high school students and 1.1% of middle-schoolers reported smoking cigarettes in the past 30 days. And they didn’t simply swap one form of nicotine delivery device for another. The 30-day prevalence of vaping among high school students fell from 27.5% in 2019 to 7.8% this year. Changing social norms and stricter federal regulation of tobacco products are probably more responsible for this positive trend than medical care, though the US Preventive Services Task Force recommends education or brief counseling to prevent initiation of tobacco use among school-aged children and adolescents. Should tobacco use in youth remain at these historically low levels, millions of premature deaths from lung cancer and heart disease will have been prevented.

America’s doctors have earned the right to take a bow. We have much more work to do, but our efforts are making a meaningful difference in three seemingly intractable health problems.

Dr. Lin, Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania, has disclosed no relevant financial relationships.

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

Hi, everyone. I’m Dr. Kenny Lin. I am a family physician and associate director of the Lancaster General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.

For the past 4 years, primary care clinicians have labored under a seemingly endless onslaught of bad news. A recent report estimated that there were over 1.3 million excess deaths in the United States from March 2020 to May 2023, including nearly half a million Americans younger than age 65. Social isolation and an ailing economy accelerated preexisting rises in drug overdoses and obesity, while teenage vaping threatened to hook a new generation on tobacco products even as adult smoking plummeted. Meanwhile, more than half of the nation’s physicians now report feelings of burnout, pay for family doctors appears to be stagnating, and our interactions with an increasing number of patients are fraught with suspicions about the value of vaccines— not just against COVID-19 but against flu and other viruses, too — and the medical system as a whole, doctors included. 

Now, for the good news.

A year and a half since the end of the pandemic emergency, we are seeing gains on several fronts, and physicians deserve much of the credit. Preliminary data from the Centers for Disease Control and Prevention show that 10,000 fewer people died from drug overdoses than in the previous year. Although multiple factors contributed to this change, the elimination of the X-waiver, which had previously been required for physicians to prescribe buprenorphine for opioid use disorder, in January 2023 has improved access to medications for addiction treatment. In addition, the expansion of state requirements to check prescription drug monitoring programs when opioids or benzodiazepines are prescribed, and to prescribe naloxone to patients taking more than a certain number of morphine milligram equivalents per day, has probably reduced the harms of hazardous drug use.

On the obesity front, recent data from the National Health and Nutrition Examination Survey found that the prevalence of obesity in adults fell for the first time in more than a decade, from 41.9% to 40.3%. To be sure, obesity remains far too common, and this finding could be the result of statistical chance rather than representing a true decline. But the widespread prescribing of GLP-1 receptor agonists by primary care physicians, in particular, could have played a role in the encouraging trend.

Although more research is needed to prove causality, one analysis suggests that these drugs could easily have lowered the body mass index (BMI) of more than enough patients to account for the observed decline. What’s more, the rise in prevalence of BMIs above 40 (from 7.7% to 9.7%) could be explained by the mortality benefit of the drugs: More people remained in this severe obesity category because they didn’t die from complications of their weight. Whether future studies support keeping people on GLP-1s for life or eventually “off-ramping” them to other weight control strategies, family physicians are well positioned to help.

Finally, with little fanfare, the youth smoking rate has fallen precipitously. In 2023, 1.9% of high school students and 1.1% of middle-schoolers reported smoking cigarettes in the past 30 days. And they didn’t simply swap one form of nicotine delivery device for another. The 30-day prevalence of vaping among high school students fell from 27.5% in 2019 to 7.8% this year. Changing social norms and stricter federal regulation of tobacco products are probably more responsible for this positive trend than medical care, though the US Preventive Services Task Force recommends education or brief counseling to prevent initiation of tobacco use among school-aged children and adolescents. Should tobacco use in youth remain at these historically low levels, millions of premature deaths from lung cancer and heart disease will have been prevented.

America’s doctors have earned the right to take a bow. We have much more work to do, but our efforts are making a meaningful difference in three seemingly intractable health problems.

Dr. Lin, Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania, has disclosed no relevant financial relationships.

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

Hi, everyone. I’m Dr. Kenny Lin. I am a family physician and associate director of the Lancaster General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.

For the past 4 years, primary care clinicians have labored under a seemingly endless onslaught of bad news. A recent report estimated that there were over 1.3 million excess deaths in the United States from March 2020 to May 2023, including nearly half a million Americans younger than age 65. Social isolation and an ailing economy accelerated preexisting rises in drug overdoses and obesity, while teenage vaping threatened to hook a new generation on tobacco products even as adult smoking plummeted. Meanwhile, more than half of the nation’s physicians now report feelings of burnout, pay for family doctors appears to be stagnating, and our interactions with an increasing number of patients are fraught with suspicions about the value of vaccines— not just against COVID-19 but against flu and other viruses, too — and the medical system as a whole, doctors included. 

Now, for the good news.

A year and a half since the end of the pandemic emergency, we are seeing gains on several fronts, and physicians deserve much of the credit. Preliminary data from the Centers for Disease Control and Prevention show that 10,000 fewer people died from drug overdoses than in the previous year. Although multiple factors contributed to this change, the elimination of the X-waiver, which had previously been required for physicians to prescribe buprenorphine for opioid use disorder, in January 2023 has improved access to medications for addiction treatment. In addition, the expansion of state requirements to check prescription drug monitoring programs when opioids or benzodiazepines are prescribed, and to prescribe naloxone to patients taking more than a certain number of morphine milligram equivalents per day, has probably reduced the harms of hazardous drug use.

On the obesity front, recent data from the National Health and Nutrition Examination Survey found that the prevalence of obesity in adults fell for the first time in more than a decade, from 41.9% to 40.3%. To be sure, obesity remains far too common, and this finding could be the result of statistical chance rather than representing a true decline. But the widespread prescribing of GLP-1 receptor agonists by primary care physicians, in particular, could have played a role in the encouraging trend.

Although more research is needed to prove causality, one analysis suggests that these drugs could easily have lowered the body mass index (BMI) of more than enough patients to account for the observed decline. What’s more, the rise in prevalence of BMIs above 40 (from 7.7% to 9.7%) could be explained by the mortality benefit of the drugs: More people remained in this severe obesity category because they didn’t die from complications of their weight. Whether future studies support keeping people on GLP-1s for life or eventually “off-ramping” them to other weight control strategies, family physicians are well positioned to help.

Finally, with little fanfare, the youth smoking rate has fallen precipitously. In 2023, 1.9% of high school students and 1.1% of middle-schoolers reported smoking cigarettes in the past 30 days. And they didn’t simply swap one form of nicotine delivery device for another. The 30-day prevalence of vaping among high school students fell from 27.5% in 2019 to 7.8% this year. Changing social norms and stricter federal regulation of tobacco products are probably more responsible for this positive trend than medical care, though the US Preventive Services Task Force recommends education or brief counseling to prevent initiation of tobacco use among school-aged children and adolescents. Should tobacco use in youth remain at these historically low levels, millions of premature deaths from lung cancer and heart disease will have been prevented.

America’s doctors have earned the right to take a bow. We have much more work to do, but our efforts are making a meaningful difference in three seemingly intractable health problems.

Dr. Lin, Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Aspirin. Once upon a time, everybody over age 50 years was supposed to take a baby aspirin. Now we make it a point to tell people to stop. What is going on?  

Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients. 

That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).

Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy. 

For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal. 

People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day. 

Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.

Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell. 

More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.

We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does. 

If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing. 

The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead. 

The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine. 

That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.

But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?

Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.