Abrocitinib emerges as a potential treatment option for moderate-to-severe atopic dermatitis

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Key clinical point: Preliminary evidence from a meta-analysis suggests that abrocitinib was significantly beneficial with a tolerable adverse event profile in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At 12 weeks, patients treated with abrocitinib achieved a significantly higher Investigator’s Global Assessment response vs those treated with placebo (risk ratio [RR], 3.52; P less than .00001). Treatment-emergent adverse effects were mostly mild and manageable, with a higher risk in the abrocitinib vs placebo group (RR, 1.17; P = .002).

Study details: Findings are from a meta-analysis of 4 randomized controlled trials, which assessed clinical outcomes in 1,175 patients with moderate-to-severe AD with inadequate response to topical medications who received abrocitinib 100 or 200 mg and 334 control participants who received placebo.

Disclosures: The study did not receive any funding. No conflict of interests was reported.

Source: Meher BR et al. J Dermatol Treat. 2021 Jul 27. doi: 10.1080/09546634.2021.1961997.

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Key clinical point: Preliminary evidence from a meta-analysis suggests that abrocitinib was significantly beneficial with a tolerable adverse event profile in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At 12 weeks, patients treated with abrocitinib achieved a significantly higher Investigator’s Global Assessment response vs those treated with placebo (risk ratio [RR], 3.52; P less than .00001). Treatment-emergent adverse effects were mostly mild and manageable, with a higher risk in the abrocitinib vs placebo group (RR, 1.17; P = .002).

Study details: Findings are from a meta-analysis of 4 randomized controlled trials, which assessed clinical outcomes in 1,175 patients with moderate-to-severe AD with inadequate response to topical medications who received abrocitinib 100 or 200 mg and 334 control participants who received placebo.

Disclosures: The study did not receive any funding. No conflict of interests was reported.

Source: Meher BR et al. J Dermatol Treat. 2021 Jul 27. doi: 10.1080/09546634.2021.1961997.

Key clinical point: Preliminary evidence from a meta-analysis suggests that abrocitinib was significantly beneficial with a tolerable adverse event profile in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At 12 weeks, patients treated with abrocitinib achieved a significantly higher Investigator’s Global Assessment response vs those treated with placebo (risk ratio [RR], 3.52; P less than .00001). Treatment-emergent adverse effects were mostly mild and manageable, with a higher risk in the abrocitinib vs placebo group (RR, 1.17; P = .002).

Study details: Findings are from a meta-analysis of 4 randomized controlled trials, which assessed clinical outcomes in 1,175 patients with moderate-to-severe AD with inadequate response to topical medications who received abrocitinib 100 or 200 mg and 334 control participants who received placebo.

Disclosures: The study did not receive any funding. No conflict of interests was reported.

Source: Meher BR et al. J Dermatol Treat. 2021 Jul 27. doi: 10.1080/09546634.2021.1961997.

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Atopic dermatitis tied to increased risk for hypertension

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Key clinical point: Patients with atopic dermatitis (AD), particularly those with a moderate-to-severe form of the disease, had significantly higher odds of hypertension than healthy controls.

Major finding: Overall, odds of hypertension was significantly higher in patients with AD than healthy controls (odds ratio [OR], 1.16; 95% confidence interval [CI], 1.04-1.30), particularly in those with moderate-to-severe AD (OR, 2.33; 95% CI, 1.10-4.94). Hypertension was mainly reported as an adverse event from cyclosporine A (pooled prevalence, 7.8%).

Study details: Findings are from a meta-analysis of 19 studies involving 269,861 adults with AD and 718,873 healthy controls, including 52,530 children with AD and 340,356 children as healthy controls.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Yousaf M et al. Br J Dermatol. 2021 Jul 28. doi: 10.1111/bjd.20661.

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Key clinical point: Patients with atopic dermatitis (AD), particularly those with a moderate-to-severe form of the disease, had significantly higher odds of hypertension than healthy controls.

Major finding: Overall, odds of hypertension was significantly higher in patients with AD than healthy controls (odds ratio [OR], 1.16; 95% confidence interval [CI], 1.04-1.30), particularly in those with moderate-to-severe AD (OR, 2.33; 95% CI, 1.10-4.94). Hypertension was mainly reported as an adverse event from cyclosporine A (pooled prevalence, 7.8%).

Study details: Findings are from a meta-analysis of 19 studies involving 269,861 adults with AD and 718,873 healthy controls, including 52,530 children with AD and 340,356 children as healthy controls.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Yousaf M et al. Br J Dermatol. 2021 Jul 28. doi: 10.1111/bjd.20661.

Key clinical point: Patients with atopic dermatitis (AD), particularly those with a moderate-to-severe form of the disease, had significantly higher odds of hypertension than healthy controls.

Major finding: Overall, odds of hypertension was significantly higher in patients with AD than healthy controls (odds ratio [OR], 1.16; 95% confidence interval [CI], 1.04-1.30), particularly in those with moderate-to-severe AD (OR, 2.33; 95% CI, 1.10-4.94). Hypertension was mainly reported as an adverse event from cyclosporine A (pooled prevalence, 7.8%).

Study details: Findings are from a meta-analysis of 19 studies involving 269,861 adults with AD and 718,873 healthy controls, including 52,530 children with AD and 340,356 children as healthy controls.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Yousaf M et al. Br J Dermatol. 2021 Jul 28. doi: 10.1111/bjd.20661.

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Comorbidities account for higher incidence of hospitalization in patients with AD

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Key clinical point: Over 20 years of evidence indicates an increased incidence of hospitalizations among patients with atopic dermatitis (AD) in the United States, mainly attributed to increased burden of medical comorbidities rather than AD itself, highlighting the need for increased screening and management of comorbidities.

Major finding: The number of hospitalizations among patients with AD increased from 1.0 to 2.3 per 100,000 persons from 1998 to 2018 (adjusted P-trend less than .0001). However, the proportion of hospitalizations with AD as the principal diagnosis reduced from 11.5% in 1998 to 3.7% in 2018 (adjusted P-trend = .001). A higher proportion of patients reported Charlson Comorbidity Index score of 3 or higher in 2018 vs 1998 (27.8% vs 10.5%; adjusted P-trend less than .0001).

Study details: Findings are from a longitudinal study including 23,410 adults hospitalized with any form of AD between 1998 and 2018.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Edigin E et al. J Am Acad Dermatol. 2021 Jul 9. doi: 10.1016/j.jaad.2021.06.882.

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Key clinical point: Over 20 years of evidence indicates an increased incidence of hospitalizations among patients with atopic dermatitis (AD) in the United States, mainly attributed to increased burden of medical comorbidities rather than AD itself, highlighting the need for increased screening and management of comorbidities.

Major finding: The number of hospitalizations among patients with AD increased from 1.0 to 2.3 per 100,000 persons from 1998 to 2018 (adjusted P-trend less than .0001). However, the proportion of hospitalizations with AD as the principal diagnosis reduced from 11.5% in 1998 to 3.7% in 2018 (adjusted P-trend = .001). A higher proportion of patients reported Charlson Comorbidity Index score of 3 or higher in 2018 vs 1998 (27.8% vs 10.5%; adjusted P-trend less than .0001).

Study details: Findings are from a longitudinal study including 23,410 adults hospitalized with any form of AD between 1998 and 2018.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Edigin E et al. J Am Acad Dermatol. 2021 Jul 9. doi: 10.1016/j.jaad.2021.06.882.

Key clinical point: Over 20 years of evidence indicates an increased incidence of hospitalizations among patients with atopic dermatitis (AD) in the United States, mainly attributed to increased burden of medical comorbidities rather than AD itself, highlighting the need for increased screening and management of comorbidities.

Major finding: The number of hospitalizations among patients with AD increased from 1.0 to 2.3 per 100,000 persons from 1998 to 2018 (adjusted P-trend less than .0001). However, the proportion of hospitalizations with AD as the principal diagnosis reduced from 11.5% in 1998 to 3.7% in 2018 (adjusted P-trend = .001). A higher proportion of patients reported Charlson Comorbidity Index score of 3 or higher in 2018 vs 1998 (27.8% vs 10.5%; adjusted P-trend less than .0001).

Study details: Findings are from a longitudinal study including 23,410 adults hospitalized with any form of AD between 1998 and 2018.

Disclosures: The study did not report any source of funding. No conflict of interests was reported.

Source: Edigin E et al. J Am Acad Dermatol. 2021 Jul 9. doi: 10.1016/j.jaad.2021.06.882.

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Methylation on golli-MBP locus serves as an indicator of atopic dermatitis severity in children

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Key clinical point: Reduced DNA methylation of golli-myelin basic protein (MBP) locus could serve as an important biomarker to determine the severity of atopic dermatitis (AD) in pediatric patients.

Major finding: Loss of DNA methylation and higher golli-MBP mRNA expression were observed in pediatric patients with AD (both P less than .0001). The score in the intensity of symptoms increased with decreasing methylation levels in cg27400313, the differentially methylated CpG cluster of MBP gene (P = .012).

Study details: The study used a discovery cohort of 24 pediatric patients with AD and 24 control participants to screen for DNA methylation. The results were further validated in an additional cohort of 224 pediatric patients with AD and 44 control participants.

Disclosures: The study was supported by grants from Ministry of Health and Welfare and Chang Gung Memorial Hospital. The authors declared no conflict of interests.

Source: Chen KD et al. J Invest Dermatol. 2021 Jul 19. doi: 10.1016/j.jid.2021.06.025.

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Key clinical point: Reduced DNA methylation of golli-myelin basic protein (MBP) locus could serve as an important biomarker to determine the severity of atopic dermatitis (AD) in pediatric patients.

Major finding: Loss of DNA methylation and higher golli-MBP mRNA expression were observed in pediatric patients with AD (both P less than .0001). The score in the intensity of symptoms increased with decreasing methylation levels in cg27400313, the differentially methylated CpG cluster of MBP gene (P = .012).

Study details: The study used a discovery cohort of 24 pediatric patients with AD and 24 control participants to screen for DNA methylation. The results were further validated in an additional cohort of 224 pediatric patients with AD and 44 control participants.

Disclosures: The study was supported by grants from Ministry of Health and Welfare and Chang Gung Memorial Hospital. The authors declared no conflict of interests.

Source: Chen KD et al. J Invest Dermatol. 2021 Jul 19. doi: 10.1016/j.jid.2021.06.025.

Key clinical point: Reduced DNA methylation of golli-myelin basic protein (MBP) locus could serve as an important biomarker to determine the severity of atopic dermatitis (AD) in pediatric patients.

Major finding: Loss of DNA methylation and higher golli-MBP mRNA expression were observed in pediatric patients with AD (both P less than .0001). The score in the intensity of symptoms increased with decreasing methylation levels in cg27400313, the differentially methylated CpG cluster of MBP gene (P = .012).

Study details: The study used a discovery cohort of 24 pediatric patients with AD and 24 control participants to screen for DNA methylation. The results were further validated in an additional cohort of 224 pediatric patients with AD and 44 control participants.

Disclosures: The study was supported by grants from Ministry of Health and Welfare and Chang Gung Memorial Hospital. The authors declared no conflict of interests.

Source: Chen KD et al. J Invest Dermatol. 2021 Jul 19. doi: 10.1016/j.jid.2021.06.025.

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Sleep disturbance and geriatric age in atopic dermatitis: Is there a link?

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Key clinical point: Geriatric patients experienced more profound sleep disturbance (SD) despite having similar severity of atopic dermatitis (AD) as younger adult patients with AD.

Major finding: Geriatric age was not associated with severity of AD as measured by Eczema Area and Severity Index score (adjusted odds ratio [aOR], 1.47; P = .3269). However, geriatric patients with AD spent an increased number of nights with SD from eczema (aOR, 2.14; P = .0142), experienced fatigue (aOR, 1.81; P = .0313), and had trouble staying asleep (aOR, 2.26; P = .0030).

Study details: Findings are from a cross-sectional, dermatology practice-based study conducted between 2014 and 2019 and included adults diagnosed with AD.

Disclosures: This study was supported by Agency for Healthcare Research and Quality, the Dermatology Foundation, and an unrestricted research grant from Galderma. The authors declared no conflict of interests.

Source: Manjunath J and Silverberg JI. J Am Acad Dermatol. 2021 Jul 29. doi: 10.1016/j.jaad.2021.07.039.

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Key clinical point: Geriatric patients experienced more profound sleep disturbance (SD) despite having similar severity of atopic dermatitis (AD) as younger adult patients with AD.

Major finding: Geriatric age was not associated with severity of AD as measured by Eczema Area and Severity Index score (adjusted odds ratio [aOR], 1.47; P = .3269). However, geriatric patients with AD spent an increased number of nights with SD from eczema (aOR, 2.14; P = .0142), experienced fatigue (aOR, 1.81; P = .0313), and had trouble staying asleep (aOR, 2.26; P = .0030).

Study details: Findings are from a cross-sectional, dermatology practice-based study conducted between 2014 and 2019 and included adults diagnosed with AD.

Disclosures: This study was supported by Agency for Healthcare Research and Quality, the Dermatology Foundation, and an unrestricted research grant from Galderma. The authors declared no conflict of interests.

Source: Manjunath J and Silverberg JI. J Am Acad Dermatol. 2021 Jul 29. doi: 10.1016/j.jaad.2021.07.039.

Key clinical point: Geriatric patients experienced more profound sleep disturbance (SD) despite having similar severity of atopic dermatitis (AD) as younger adult patients with AD.

Major finding: Geriatric age was not associated with severity of AD as measured by Eczema Area and Severity Index score (adjusted odds ratio [aOR], 1.47; P = .3269). However, geriatric patients with AD spent an increased number of nights with SD from eczema (aOR, 2.14; P = .0142), experienced fatigue (aOR, 1.81; P = .0313), and had trouble staying asleep (aOR, 2.26; P = .0030).

Study details: Findings are from a cross-sectional, dermatology practice-based study conducted between 2014 and 2019 and included adults diagnosed with AD.

Disclosures: This study was supported by Agency for Healthcare Research and Quality, the Dermatology Foundation, and an unrestricted research grant from Galderma. The authors declared no conflict of interests.

Source: Manjunath J and Silverberg JI. J Am Acad Dermatol. 2021 Jul 29. doi: 10.1016/j.jaad.2021.07.039.

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Cold atmospheric plasma alleviates AD severity without any safety issues

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Key clinical point: Cold atmospheric plasma (CAP) can potentially improve the clinical severity of atopic dermatitis (AD) by recovering the diversity of skin microbiome and promoting wound healing for damaged skin barriers without any safety issues.

Major finding: At the end of treatment, reduction in Staphylococcus aureus count was significantly higher for the CAP vs sham group (10.14% vs 15.29%; P = .047). In the CAP group, mean modified AD antecubital severity score reduced significantly at week 4 vs baseline (13.12 vs 33.73; P less than .001), whereas reduction in the sham group was not statistically significant (P = .114). No severe adverse events were reported.

Study details: Findings are from a prospective analysis of 22 adults with mild-to-moderate AD having symmetric lesions. For each patient, the symmetric lesions were randomly assigned to either CAP or sham treatment.

Disclosures: The study did not report any source of funding. No conflicts of interest were reported.

Source: Kim YJ et al. Sci Rep. 2021 Jul 14. doi: 10.1038/s41598-021-93941-y.

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Key clinical point: Cold atmospheric plasma (CAP) can potentially improve the clinical severity of atopic dermatitis (AD) by recovering the diversity of skin microbiome and promoting wound healing for damaged skin barriers without any safety issues.

Major finding: At the end of treatment, reduction in Staphylococcus aureus count was significantly higher for the CAP vs sham group (10.14% vs 15.29%; P = .047). In the CAP group, mean modified AD antecubital severity score reduced significantly at week 4 vs baseline (13.12 vs 33.73; P less than .001), whereas reduction in the sham group was not statistically significant (P = .114). No severe adverse events were reported.

Study details: Findings are from a prospective analysis of 22 adults with mild-to-moderate AD having symmetric lesions. For each patient, the symmetric lesions were randomly assigned to either CAP or sham treatment.

Disclosures: The study did not report any source of funding. No conflicts of interest were reported.

Source: Kim YJ et al. Sci Rep. 2021 Jul 14. doi: 10.1038/s41598-021-93941-y.

Key clinical point: Cold atmospheric plasma (CAP) can potentially improve the clinical severity of atopic dermatitis (AD) by recovering the diversity of skin microbiome and promoting wound healing for damaged skin barriers without any safety issues.

Major finding: At the end of treatment, reduction in Staphylococcus aureus count was significantly higher for the CAP vs sham group (10.14% vs 15.29%; P = .047). In the CAP group, mean modified AD antecubital severity score reduced significantly at week 4 vs baseline (13.12 vs 33.73; P less than .001), whereas reduction in the sham group was not statistically significant (P = .114). No severe adverse events were reported.

Study details: Findings are from a prospective analysis of 22 adults with mild-to-moderate AD having symmetric lesions. For each patient, the symmetric lesions were randomly assigned to either CAP or sham treatment.

Disclosures: The study did not report any source of funding. No conflicts of interest were reported.

Source: Kim YJ et al. Sci Rep. 2021 Jul 14. doi: 10.1038/s41598-021-93941-y.

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Difamilast ointment shows promise for pediatric atopic dermatitis in phase 3

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Key clinical point: Difamilast 0.3% and 1% ointments demonstrated superiority over vehicle along with a favorable safety profile when applied twice daily for up to 4 weeks in pediatric patients with atopic dermatitis (AD).

Major finding: At week 4, the success rate in investigator global assessment score was significantly higher with difamilast 0.3% (44.6%; P = .0005) and 1% (47.1%; P less than .0001) vs vehicle (18.1%) group. Treatment-emergent adverse effects were mostly mild or moderate in severity, with adverse event profiles similar between treatment and vehicle groups.

Study details: Findings are from a double-blind phase 3 trial including 251 patients aged 2-14 years with mild-to-moderate AD who were randomly assigned to receive difamilast 0.3%, difamilast 1%, or vehicle ointment twice daily for 4 weeks.

Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Dr. Saeki and Dr. Baba declared receiving consultation fees from Otsuka Pharmaceutical Co., Ltd. Dr. Ito, Dr. Yokota, and Dr. Tsubouchi declared being employees of Otsuka Pharmaceutical Co., Ltd.

Source: Saeki H et al. Br J Dermatol. 2021 Jul 21. doi: 10.1111/bjd.20655.

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Key clinical point: Difamilast 0.3% and 1% ointments demonstrated superiority over vehicle along with a favorable safety profile when applied twice daily for up to 4 weeks in pediatric patients with atopic dermatitis (AD).

Major finding: At week 4, the success rate in investigator global assessment score was significantly higher with difamilast 0.3% (44.6%; P = .0005) and 1% (47.1%; P less than .0001) vs vehicle (18.1%) group. Treatment-emergent adverse effects were mostly mild or moderate in severity, with adverse event profiles similar between treatment and vehicle groups.

Study details: Findings are from a double-blind phase 3 trial including 251 patients aged 2-14 years with mild-to-moderate AD who were randomly assigned to receive difamilast 0.3%, difamilast 1%, or vehicle ointment twice daily for 4 weeks.

Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Dr. Saeki and Dr. Baba declared receiving consultation fees from Otsuka Pharmaceutical Co., Ltd. Dr. Ito, Dr. Yokota, and Dr. Tsubouchi declared being employees of Otsuka Pharmaceutical Co., Ltd.

Source: Saeki H et al. Br J Dermatol. 2021 Jul 21. doi: 10.1111/bjd.20655.

Key clinical point: Difamilast 0.3% and 1% ointments demonstrated superiority over vehicle along with a favorable safety profile when applied twice daily for up to 4 weeks in pediatric patients with atopic dermatitis (AD).

Major finding: At week 4, the success rate in investigator global assessment score was significantly higher with difamilast 0.3% (44.6%; P = .0005) and 1% (47.1%; P less than .0001) vs vehicle (18.1%) group. Treatment-emergent adverse effects were mostly mild or moderate in severity, with adverse event profiles similar between treatment and vehicle groups.

Study details: Findings are from a double-blind phase 3 trial including 251 patients aged 2-14 years with mild-to-moderate AD who were randomly assigned to receive difamilast 0.3%, difamilast 1%, or vehicle ointment twice daily for 4 weeks.

Disclosures: This study was funded by Otsuka Pharmaceutical Co., Ltd. Dr. Saeki and Dr. Baba declared receiving consultation fees from Otsuka Pharmaceutical Co., Ltd. Dr. Ito, Dr. Yokota, and Dr. Tsubouchi declared being employees of Otsuka Pharmaceutical Co., Ltd.

Source: Saeki H et al. Br J Dermatol. 2021 Jul 21. doi: 10.1111/bjd.20655.

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Upadacitinib shows superior efficacy over dupilumab for moderate-to-severe atopic dermatitis in phase 3b

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Key clinical point: Upadacitinib demonstrated superior efficacy over dupilumab for treatment of adults with moderate-to-severe atopic dermatitis (AD) with no new safety signals identified.

Major finding: At week 16, a higher proportion of patients achieved 75% improvement in Eczema Area and Severity Index with upadacitinib vs dupilumab (71.0% vs 61.1%; P = .006). Rates of serious treatment-emergent adverse events leading to drug discontinuation in upadacitinib vs dupilumab were 2.9% vs 1.2%, with no new safety risks observed for upadacitinib.

Study details: Findings are 24-week results of Heads up, a phase 3b trial including 692 adults with moderate-to-severe AD who were randomly assigned to receive oral upadacitinib, 30 mg once daily, or subcutaneous dupilumab, 300 mg every alternate week.

Disclosures: This study was funded by AbbVie. The authors declared serving as speaker, consultant, scientific advisor, clinical study investigator, and/or receiving personal fees and grants from various sources including AbbVie. Four authors declared being employees and/or shareholders of AbbVie.

Source: Blauvelt A et al. JAMA Dermatol. 2021 Aug 4. doi: 10.1001/jamadermatol.2021.3023.

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Key clinical point: Upadacitinib demonstrated superior efficacy over dupilumab for treatment of adults with moderate-to-severe atopic dermatitis (AD) with no new safety signals identified.

Major finding: At week 16, a higher proportion of patients achieved 75% improvement in Eczema Area and Severity Index with upadacitinib vs dupilumab (71.0% vs 61.1%; P = .006). Rates of serious treatment-emergent adverse events leading to drug discontinuation in upadacitinib vs dupilumab were 2.9% vs 1.2%, with no new safety risks observed for upadacitinib.

Study details: Findings are 24-week results of Heads up, a phase 3b trial including 692 adults with moderate-to-severe AD who were randomly assigned to receive oral upadacitinib, 30 mg once daily, or subcutaneous dupilumab, 300 mg every alternate week.

Disclosures: This study was funded by AbbVie. The authors declared serving as speaker, consultant, scientific advisor, clinical study investigator, and/or receiving personal fees and grants from various sources including AbbVie. Four authors declared being employees and/or shareholders of AbbVie.

Source: Blauvelt A et al. JAMA Dermatol. 2021 Aug 4. doi: 10.1001/jamadermatol.2021.3023.

Key clinical point: Upadacitinib demonstrated superior efficacy over dupilumab for treatment of adults with moderate-to-severe atopic dermatitis (AD) with no new safety signals identified.

Major finding: At week 16, a higher proportion of patients achieved 75% improvement in Eczema Area and Severity Index with upadacitinib vs dupilumab (71.0% vs 61.1%; P = .006). Rates of serious treatment-emergent adverse events leading to drug discontinuation in upadacitinib vs dupilumab were 2.9% vs 1.2%, with no new safety risks observed for upadacitinib.

Study details: Findings are 24-week results of Heads up, a phase 3b trial including 692 adults with moderate-to-severe AD who were randomly assigned to receive oral upadacitinib, 30 mg once daily, or subcutaneous dupilumab, 300 mg every alternate week.

Disclosures: This study was funded by AbbVie. The authors declared serving as speaker, consultant, scientific advisor, clinical study investigator, and/or receiving personal fees and grants from various sources including AbbVie. Four authors declared being employees and/or shareholders of AbbVie.

Source: Blauvelt A et al. JAMA Dermatol. 2021 Aug 4. doi: 10.1001/jamadermatol.2021.3023.

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Better to binge drink than regularly tipple, suggests GI cancer study

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When weekly levels are similar

Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts – compared with higher amounts or binge drinking, given similar weekly levels.

“The novel finding of the current study is that frequent drinking may be more dangerous than binge drinking with regard to GI cancers. Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts -- compared with higher amounts or binge drinking, given similar weekly levels.” first author Jung Eun Yook, MD, of Seoul (South Korea) National University Hospital, and colleagues reported in an article published Aug. 18, 2021, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.20382).

“This finding suggests that repeated alcohol consumption events even at lower amounts of alcohol may have a greater carcinogenic effect on GI organs than the consumption of larger amounts of alcohol at a lower frequency,” the investigators wrote.

A possible reason behind the difference in risk may be that the chronic “carcinogenic insult” from regular alcohol use may promote cancer development, whereas less frequent, episodic alcohol exposures may allow physiologic recovery, said the authors.

The results are from a population-based study that involved 11,737,467 participants in the Korean National Health System database who did not have cancer and who took part in a national screening program between January 2009 and December 2010.

They were followed from the year after their screening until either they had received a diagnosis of a GI cancer, death occurred, or the end of December 2017.

During a median follow-up of 6.4 years, 319,202 (2.7%) of those in the study developed a GI cancer.

The increase in the risk associated with alcohol consumption was dose dependent.

Compared with those who did not consume alcohol, the risk of developing GI cancer was higher for mild drinkers (adjusted hazard ratio, 1.04; 95% confidence interval, 1.03-1.05), moderate drinkers (aHR, 1.14; 95% CI, 1.12-1.15), and heavy drinkers (aHR, 1.28; 95% CI, 1.26-1.29), after adjusting for age, sex, income, smoking status with intensity, regular exercise, body mass index, diabetes, hypertension, and dyslipidemia.

There was a linear association between the frequency of drinking and GI cancer risk, with an aHR of 1.39 for individuals who reported drinking every day (95% CI, 1.36-1.41). The risk for GI cancer increased with consumption of five to seven units per occasion (aHR, 1.15). Notably, there were no similar increases with higher intake, including intake of 8-14 units per occasion (aHR, 1.11; 95% CI, 1.09-1.12), and even up to more than 14 units per occasion (aHR, 1.11; 95%CI, 1.08-1.14), in comparison with an intake of 5-7 units per occasion.

“Given similar weekly alcohol consumption levels, the risk of GI cancer increased with a higher frequency of drinking and decreased with a higher amount per occasion,” the authors write.

“Most previous studies just assess alcohol consumption as a total amount, [such as] drinks per occasion times occasion per week equals drinks per week [and] grams per week,” coauthor Dong Wook Shin, MD, DrPH, Samsung Medical Center, Sungkyunkwan University, Seoul, South Korea, said in an interview.

“But it was not known whether frequent drinking with small amount is more harmful than binge drinking, given a similar level of total drinking,” Dr. Shin said.

The increased risk associated with frequent drinking was generally similar with respect to esophageal, gastric, colorectal, biliary, and pancreatic cancer.

An exception was liver cancer, which showed a slightly decreased risk among mild drinkers (aHR, 0.91; 95% CI, 0.89-0.93).

Of note, the association between alcohol intake and the incidence of GI cancer was lower among women than men in terms of weekly consumption, frequency, and amount of alcohol consumed per occasion.

The associations between drinking and cancer type in terms of esophageal and liver cancers were similar between men and women. However, the alcohol-related risk for colorectal, biliary, and pancreatic cancers was less prominent for women.

 

 

Possible mechanisms related to regular drinking

A factor that might account for the increase in GI cancer risk with frequent drinking is that regular alcohol consumption “promotes the accumulation of cell divisions in the stem cells that maintain tissues in homeostasis,” the authors explained.

Another possible explanation is that long-term alcohol exposure may promote carcinogenesis, whereas less frequent exposure might allow “physiological homeostasis,” the authors wrote, adding that in vivo experiments have shown that duration and dose of alcohol exposure have been linked to cancer development.

Importantly, the findings support the importance of reducing the frequency of alcohol use to prevent cancer, the authors noted.

“Alcohol users who have a glass of wine or beer during dinner every day may develop more cancer than people who occasionally consume several drinks,” they cautioned.
 

Genetics, self-reporting considerations

In a related commentary, John D. Potter, MBBS, PhD, of the Research Center for Hauora and Health, Massey University, Wellington, New Zealand, noted that, in addition to supporting the known link between alcohol and cancers of the esophagus, colorectum, and liver, the study “strengthens evidence for a role of alcohol in stomach, biliary tract, and pancreas cancers.”

In comparison with nondrinkers, those who reported heavy drinking were much more likely to be smokers (51.6% vs. 9.0%); however, the study adjusted for smoking.

“Because the researchers were able to control for tobacco, this last finding [regarding the association with cancers of the stomach, biliary tract, and pancreas] is particularly informative,” Dr. Potter noted.

An important caveat is that more than a quarter of the Korean population is known to have an inactive form of the aldehyde dehydrogenase gene (ALDH2), which could have effects on alcohol metabolism as well as the risk for cancer, Dr. Potter wrote.

“This common polymorphism in ALDH2 (ALDH2 rs671 [c.1510G>A (Glu504Lys)]) has paradoxical effects,” he wrote.

“It increases the level of acetaldehyde in the blood of drinkers, which in turn increases the risk of cancer because acetaldehyde is a key player in the carcinogenicity of alcoholic beverages,” Dr. Potter explained. “On the other hand, the accumulation of acetaldehyde and the resultant flushing response are sufficiently unpleasant that they tend to reduce alcohol consumption among those with the Lys allele.”

The study results may therefore not be generalizable to a population in which the distribution of the variation in the ALDH2 enzyme differs, Dr. Potter added.

The lower prevalence of the inactive form (in North America, for instance) would mean that this lower prevalence was not a constraint on individuals’ drinking behavior as it is for some in Korea, Dr. Potter explained.

He noted another consideration: the underreporting of alcohol use is a well-known limitation of studies involving the assessment of alcohol consumption.

Dr. Shin agreed that underreporting is a limitation.

“People tend to underestimate their alcohol use,” Dr. Shin said in an interview.

However, he noted that “our study participants are health-screening participants aged 40 years and older, [and] people who participate in health screening tend to have higher awareness and better health behavior than nonparticipants.”

The authors and Dr. Potter disclosed no relevant financial relationships.

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

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When weekly levels are similar

When weekly levels are similar

Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts – compared with higher amounts or binge drinking, given similar weekly levels.

“The novel finding of the current study is that frequent drinking may be more dangerous than binge drinking with regard to GI cancers. Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts -- compared with higher amounts or binge drinking, given similar weekly levels.” first author Jung Eun Yook, MD, of Seoul (South Korea) National University Hospital, and colleagues reported in an article published Aug. 18, 2021, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.20382).

“This finding suggests that repeated alcohol consumption events even at lower amounts of alcohol may have a greater carcinogenic effect on GI organs than the consumption of larger amounts of alcohol at a lower frequency,” the investigators wrote.

A possible reason behind the difference in risk may be that the chronic “carcinogenic insult” from regular alcohol use may promote cancer development, whereas less frequent, episodic alcohol exposures may allow physiologic recovery, said the authors.

The results are from a population-based study that involved 11,737,467 participants in the Korean National Health System database who did not have cancer and who took part in a national screening program between January 2009 and December 2010.

They were followed from the year after their screening until either they had received a diagnosis of a GI cancer, death occurred, or the end of December 2017.

During a median follow-up of 6.4 years, 319,202 (2.7%) of those in the study developed a GI cancer.

The increase in the risk associated with alcohol consumption was dose dependent.

Compared with those who did not consume alcohol, the risk of developing GI cancer was higher for mild drinkers (adjusted hazard ratio, 1.04; 95% confidence interval, 1.03-1.05), moderate drinkers (aHR, 1.14; 95% CI, 1.12-1.15), and heavy drinkers (aHR, 1.28; 95% CI, 1.26-1.29), after adjusting for age, sex, income, smoking status with intensity, regular exercise, body mass index, diabetes, hypertension, and dyslipidemia.

There was a linear association between the frequency of drinking and GI cancer risk, with an aHR of 1.39 for individuals who reported drinking every day (95% CI, 1.36-1.41). The risk for GI cancer increased with consumption of five to seven units per occasion (aHR, 1.15). Notably, there were no similar increases with higher intake, including intake of 8-14 units per occasion (aHR, 1.11; 95% CI, 1.09-1.12), and even up to more than 14 units per occasion (aHR, 1.11; 95%CI, 1.08-1.14), in comparison with an intake of 5-7 units per occasion.

“Given similar weekly alcohol consumption levels, the risk of GI cancer increased with a higher frequency of drinking and decreased with a higher amount per occasion,” the authors write.

“Most previous studies just assess alcohol consumption as a total amount, [such as] drinks per occasion times occasion per week equals drinks per week [and] grams per week,” coauthor Dong Wook Shin, MD, DrPH, Samsung Medical Center, Sungkyunkwan University, Seoul, South Korea, said in an interview.

“But it was not known whether frequent drinking with small amount is more harmful than binge drinking, given a similar level of total drinking,” Dr. Shin said.

The increased risk associated with frequent drinking was generally similar with respect to esophageal, gastric, colorectal, biliary, and pancreatic cancer.

An exception was liver cancer, which showed a slightly decreased risk among mild drinkers (aHR, 0.91; 95% CI, 0.89-0.93).

Of note, the association between alcohol intake and the incidence of GI cancer was lower among women than men in terms of weekly consumption, frequency, and amount of alcohol consumed per occasion.

The associations between drinking and cancer type in terms of esophageal and liver cancers were similar between men and women. However, the alcohol-related risk for colorectal, biliary, and pancreatic cancers was less prominent for women.

 

 

Possible mechanisms related to regular drinking

A factor that might account for the increase in GI cancer risk with frequent drinking is that regular alcohol consumption “promotes the accumulation of cell divisions in the stem cells that maintain tissues in homeostasis,” the authors explained.

Another possible explanation is that long-term alcohol exposure may promote carcinogenesis, whereas less frequent exposure might allow “physiological homeostasis,” the authors wrote, adding that in vivo experiments have shown that duration and dose of alcohol exposure have been linked to cancer development.

Importantly, the findings support the importance of reducing the frequency of alcohol use to prevent cancer, the authors noted.

“Alcohol users who have a glass of wine or beer during dinner every day may develop more cancer than people who occasionally consume several drinks,” they cautioned.
 

Genetics, self-reporting considerations

In a related commentary, John D. Potter, MBBS, PhD, of the Research Center for Hauora and Health, Massey University, Wellington, New Zealand, noted that, in addition to supporting the known link between alcohol and cancers of the esophagus, colorectum, and liver, the study “strengthens evidence for a role of alcohol in stomach, biliary tract, and pancreas cancers.”

In comparison with nondrinkers, those who reported heavy drinking were much more likely to be smokers (51.6% vs. 9.0%); however, the study adjusted for smoking.

“Because the researchers were able to control for tobacco, this last finding [regarding the association with cancers of the stomach, biliary tract, and pancreas] is particularly informative,” Dr. Potter noted.

An important caveat is that more than a quarter of the Korean population is known to have an inactive form of the aldehyde dehydrogenase gene (ALDH2), which could have effects on alcohol metabolism as well as the risk for cancer, Dr. Potter wrote.

“This common polymorphism in ALDH2 (ALDH2 rs671 [c.1510G>A (Glu504Lys)]) has paradoxical effects,” he wrote.

“It increases the level of acetaldehyde in the blood of drinkers, which in turn increases the risk of cancer because acetaldehyde is a key player in the carcinogenicity of alcoholic beverages,” Dr. Potter explained. “On the other hand, the accumulation of acetaldehyde and the resultant flushing response are sufficiently unpleasant that they tend to reduce alcohol consumption among those with the Lys allele.”

The study results may therefore not be generalizable to a population in which the distribution of the variation in the ALDH2 enzyme differs, Dr. Potter added.

The lower prevalence of the inactive form (in North America, for instance) would mean that this lower prevalence was not a constraint on individuals’ drinking behavior as it is for some in Korea, Dr. Potter explained.

He noted another consideration: the underreporting of alcohol use is a well-known limitation of studies involving the assessment of alcohol consumption.

Dr. Shin agreed that underreporting is a limitation.

“People tend to underestimate their alcohol use,” Dr. Shin said in an interview.

However, he noted that “our study participants are health-screening participants aged 40 years and older, [and] people who participate in health screening tend to have higher awareness and better health behavior than nonparticipants.”

The authors and Dr. Potter disclosed no relevant financial relationships.

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

Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts – compared with higher amounts or binge drinking, given similar weekly levels.

“The novel finding of the current study is that frequent drinking may be more dangerous than binge drinking with regard to GI cancers. Alcohol use is a known risk factor for gastrointestinal (GI) cancers. Now, new research indicates that this risk is more associated with frequent drinking – even in smaller amounts -- compared with higher amounts or binge drinking, given similar weekly levels.” first author Jung Eun Yook, MD, of Seoul (South Korea) National University Hospital, and colleagues reported in an article published Aug. 18, 2021, in JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.20382).

“This finding suggests that repeated alcohol consumption events even at lower amounts of alcohol may have a greater carcinogenic effect on GI organs than the consumption of larger amounts of alcohol at a lower frequency,” the investigators wrote.

A possible reason behind the difference in risk may be that the chronic “carcinogenic insult” from regular alcohol use may promote cancer development, whereas less frequent, episodic alcohol exposures may allow physiologic recovery, said the authors.

The results are from a population-based study that involved 11,737,467 participants in the Korean National Health System database who did not have cancer and who took part in a national screening program between January 2009 and December 2010.

They were followed from the year after their screening until either they had received a diagnosis of a GI cancer, death occurred, or the end of December 2017.

During a median follow-up of 6.4 years, 319,202 (2.7%) of those in the study developed a GI cancer.

The increase in the risk associated with alcohol consumption was dose dependent.

Compared with those who did not consume alcohol, the risk of developing GI cancer was higher for mild drinkers (adjusted hazard ratio, 1.04; 95% confidence interval, 1.03-1.05), moderate drinkers (aHR, 1.14; 95% CI, 1.12-1.15), and heavy drinkers (aHR, 1.28; 95% CI, 1.26-1.29), after adjusting for age, sex, income, smoking status with intensity, regular exercise, body mass index, diabetes, hypertension, and dyslipidemia.

There was a linear association between the frequency of drinking and GI cancer risk, with an aHR of 1.39 for individuals who reported drinking every day (95% CI, 1.36-1.41). The risk for GI cancer increased with consumption of five to seven units per occasion (aHR, 1.15). Notably, there were no similar increases with higher intake, including intake of 8-14 units per occasion (aHR, 1.11; 95% CI, 1.09-1.12), and even up to more than 14 units per occasion (aHR, 1.11; 95%CI, 1.08-1.14), in comparison with an intake of 5-7 units per occasion.

“Given similar weekly alcohol consumption levels, the risk of GI cancer increased with a higher frequency of drinking and decreased with a higher amount per occasion,” the authors write.

“Most previous studies just assess alcohol consumption as a total amount, [such as] drinks per occasion times occasion per week equals drinks per week [and] grams per week,” coauthor Dong Wook Shin, MD, DrPH, Samsung Medical Center, Sungkyunkwan University, Seoul, South Korea, said in an interview.

“But it was not known whether frequent drinking with small amount is more harmful than binge drinking, given a similar level of total drinking,” Dr. Shin said.

The increased risk associated with frequent drinking was generally similar with respect to esophageal, gastric, colorectal, biliary, and pancreatic cancer.

An exception was liver cancer, which showed a slightly decreased risk among mild drinkers (aHR, 0.91; 95% CI, 0.89-0.93).

Of note, the association between alcohol intake and the incidence of GI cancer was lower among women than men in terms of weekly consumption, frequency, and amount of alcohol consumed per occasion.

The associations between drinking and cancer type in terms of esophageal and liver cancers were similar between men and women. However, the alcohol-related risk for colorectal, biliary, and pancreatic cancers was less prominent for women.

 

 

Possible mechanisms related to regular drinking

A factor that might account for the increase in GI cancer risk with frequent drinking is that regular alcohol consumption “promotes the accumulation of cell divisions in the stem cells that maintain tissues in homeostasis,” the authors explained.

Another possible explanation is that long-term alcohol exposure may promote carcinogenesis, whereas less frequent exposure might allow “physiological homeostasis,” the authors wrote, adding that in vivo experiments have shown that duration and dose of alcohol exposure have been linked to cancer development.

Importantly, the findings support the importance of reducing the frequency of alcohol use to prevent cancer, the authors noted.

“Alcohol users who have a glass of wine or beer during dinner every day may develop more cancer than people who occasionally consume several drinks,” they cautioned.
 

Genetics, self-reporting considerations

In a related commentary, John D. Potter, MBBS, PhD, of the Research Center for Hauora and Health, Massey University, Wellington, New Zealand, noted that, in addition to supporting the known link between alcohol and cancers of the esophagus, colorectum, and liver, the study “strengthens evidence for a role of alcohol in stomach, biliary tract, and pancreas cancers.”

In comparison with nondrinkers, those who reported heavy drinking were much more likely to be smokers (51.6% vs. 9.0%); however, the study adjusted for smoking.

“Because the researchers were able to control for tobacco, this last finding [regarding the association with cancers of the stomach, biliary tract, and pancreas] is particularly informative,” Dr. Potter noted.

An important caveat is that more than a quarter of the Korean population is known to have an inactive form of the aldehyde dehydrogenase gene (ALDH2), which could have effects on alcohol metabolism as well as the risk for cancer, Dr. Potter wrote.

“This common polymorphism in ALDH2 (ALDH2 rs671 [c.1510G>A (Glu504Lys)]) has paradoxical effects,” he wrote.

“It increases the level of acetaldehyde in the blood of drinkers, which in turn increases the risk of cancer because acetaldehyde is a key player in the carcinogenicity of alcoholic beverages,” Dr. Potter explained. “On the other hand, the accumulation of acetaldehyde and the resultant flushing response are sufficiently unpleasant that they tend to reduce alcohol consumption among those with the Lys allele.”

The study results may therefore not be generalizable to a population in which the distribution of the variation in the ALDH2 enzyme differs, Dr. Potter added.

The lower prevalence of the inactive form (in North America, for instance) would mean that this lower prevalence was not a constraint on individuals’ drinking behavior as it is for some in Korea, Dr. Potter explained.

He noted another consideration: the underreporting of alcohol use is a well-known limitation of studies involving the assessment of alcohol consumption.

Dr. Shin agreed that underreporting is a limitation.

“People tend to underestimate their alcohol use,” Dr. Shin said in an interview.

However, he noted that “our study participants are health-screening participants aged 40 years and older, [and] people who participate in health screening tend to have higher awareness and better health behavior than nonparticipants.”

The authors and Dr. Potter disclosed no relevant financial relationships.

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

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Journal retracts more articles for being ‘unethical, scientifically flawed, and based on racist ideas and agenda’

Article Type
Changed
Thu, 08/26/2021 - 12:07

Eight months after a psychology journal retracted a pair of articles that were “unethical, scientifically flawed, and based on racist ideas and agenda,” the publication has pulled three more papers – all at least a quarter century old – for the same reason.

All five papers were written by J. Philippe Rushton, formerly of the University of Western Ontario, who died in 2012. As we wrote in December 2020, Rushton published dubious studies that promoted tropes of white supremacy, including that Blacks are less intelligent than Whites and that:

East Asians and their descendants average a larger brain size, greater intelligence, more sexual restraint, slower rates of maturation, and greater law abidingness and social organization than do Europeans and their descendants, who average higher scores on these dimensions than Africans and their descendants.

Here’s the new notice, whose language mirrors that of the earlier retraction statement:

The following articles have been retracted from Psychological Reports:

Rushton, J. P. (1987). An Evolutionary Theory of Health, Longevity, and Personality: Sociobiology and r/K Reproductive Strategies . Psychological Reports, 60, 539-49.

Rushton, J. P. (1992). Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits (with Reference to Oriental-White-Black Differences): The 1989 AAAS Paper . Psychological Reports, 71, 811-21.

Rushton, J. P. (1995). Race and Crime: International Data 1989-1990 . Psychological Reports, 76, 207-312.

This retraction is following a review that found that the research was unethical, scientifically flawed, and based on racist ideas and agenda. Specifically, these publications authored by Philippe Rushton on the subject of intelligence and race have been rejected based on the following findings:

A better understanding of the human genome (Yudell et al., 2016)

An inappropriately applied ecological theory that explains differences between species’ reproductive strategies to humans (Allen et al., 1992 ; Anderson, 1991)

A misuse of population genetic measures and misconceptions about heritability (Bailey, 1997)

Ignoring alternative explanations or evidence that did not support the racist theories being presented (Cain & Vanderwolf, 1990)

Rushton’s findings have not been replicated (Peregrine, Ember, & Ember, 2003)

Together, the papers have been cited 48 times, according to Clarivate Analytics’ Web of Science. At the time of this writing, none of the original abstracts include a link to the retraction notice.

When we wrote about the Rushton case last year, we received a copy of an email from the journal saying that it would be retracting Rushton’s 1992 paper, “Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits” along with the other two articles. That didn’t happen at the time.

We asked Cory Scherer, the editor of Psychological Reports, about the eight-month gap between retractions. He told us:

I got an email from a researcher who brought these articles to our attention and when I read them I moved fast on the first retraction and the rest were found when that retraction was already written and in press. I didn’t want to add them to the original retraction until I did my due diligence about the second set found.

Our search of the journal’s website turned up eight articles in total by Rushton in the journal, of which three remain unretracted. Mr. Scherer said he has created a committee to review the remnant papers to see if they require retraction.

 

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Eight months after a psychology journal retracted a pair of articles that were “unethical, scientifically flawed, and based on racist ideas and agenda,” the publication has pulled three more papers – all at least a quarter century old – for the same reason.

All five papers were written by J. Philippe Rushton, formerly of the University of Western Ontario, who died in 2012. As we wrote in December 2020, Rushton published dubious studies that promoted tropes of white supremacy, including that Blacks are less intelligent than Whites and that:

East Asians and their descendants average a larger brain size, greater intelligence, more sexual restraint, slower rates of maturation, and greater law abidingness and social organization than do Europeans and their descendants, who average higher scores on these dimensions than Africans and their descendants.

Here’s the new notice, whose language mirrors that of the earlier retraction statement:

The following articles have been retracted from Psychological Reports:

Rushton, J. P. (1987). An Evolutionary Theory of Health, Longevity, and Personality: Sociobiology and r/K Reproductive Strategies . Psychological Reports, 60, 539-49.

Rushton, J. P. (1992). Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits (with Reference to Oriental-White-Black Differences): The 1989 AAAS Paper . Psychological Reports, 71, 811-21.

Rushton, J. P. (1995). Race and Crime: International Data 1989-1990 . Psychological Reports, 76, 207-312.

This retraction is following a review that found that the research was unethical, scientifically flawed, and based on racist ideas and agenda. Specifically, these publications authored by Philippe Rushton on the subject of intelligence and race have been rejected based on the following findings:

A better understanding of the human genome (Yudell et al., 2016)

An inappropriately applied ecological theory that explains differences between species’ reproductive strategies to humans (Allen et al., 1992 ; Anderson, 1991)

A misuse of population genetic measures and misconceptions about heritability (Bailey, 1997)

Ignoring alternative explanations or evidence that did not support the racist theories being presented (Cain & Vanderwolf, 1990)

Rushton’s findings have not been replicated (Peregrine, Ember, & Ember, 2003)

Together, the papers have been cited 48 times, according to Clarivate Analytics’ Web of Science. At the time of this writing, none of the original abstracts include a link to the retraction notice.

When we wrote about the Rushton case last year, we received a copy of an email from the journal saying that it would be retracting Rushton’s 1992 paper, “Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits” along with the other two articles. That didn’t happen at the time.

We asked Cory Scherer, the editor of Psychological Reports, about the eight-month gap between retractions. He told us:

I got an email from a researcher who brought these articles to our attention and when I read them I moved fast on the first retraction and the rest were found when that retraction was already written and in press. I didn’t want to add them to the original retraction until I did my due diligence about the second set found.

Our search of the journal’s website turned up eight articles in total by Rushton in the journal, of which three remain unretracted. Mr. Scherer said he has created a committee to review the remnant papers to see if they require retraction.

 

Eight months after a psychology journal retracted a pair of articles that were “unethical, scientifically flawed, and based on racist ideas and agenda,” the publication has pulled three more papers – all at least a quarter century old – for the same reason.

All five papers were written by J. Philippe Rushton, formerly of the University of Western Ontario, who died in 2012. As we wrote in December 2020, Rushton published dubious studies that promoted tropes of white supremacy, including that Blacks are less intelligent than Whites and that:

East Asians and their descendants average a larger brain size, greater intelligence, more sexual restraint, slower rates of maturation, and greater law abidingness and social organization than do Europeans and their descendants, who average higher scores on these dimensions than Africans and their descendants.

Here’s the new notice, whose language mirrors that of the earlier retraction statement:

The following articles have been retracted from Psychological Reports:

Rushton, J. P. (1987). An Evolutionary Theory of Health, Longevity, and Personality: Sociobiology and r/K Reproductive Strategies . Psychological Reports, 60, 539-49.

Rushton, J. P. (1992). Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits (with Reference to Oriental-White-Black Differences): The 1989 AAAS Paper . Psychological Reports, 71, 811-21.

Rushton, J. P. (1995). Race and Crime: International Data 1989-1990 . Psychological Reports, 76, 207-312.

This retraction is following a review that found that the research was unethical, scientifically flawed, and based on racist ideas and agenda. Specifically, these publications authored by Philippe Rushton on the subject of intelligence and race have been rejected based on the following findings:

A better understanding of the human genome (Yudell et al., 2016)

An inappropriately applied ecological theory that explains differences between species’ reproductive strategies to humans (Allen et al., 1992 ; Anderson, 1991)

A misuse of population genetic measures and misconceptions about heritability (Bailey, 1997)

Ignoring alternative explanations or evidence that did not support the racist theories being presented (Cain & Vanderwolf, 1990)

Rushton’s findings have not been replicated (Peregrine, Ember, & Ember, 2003)

Together, the papers have been cited 48 times, according to Clarivate Analytics’ Web of Science. At the time of this writing, none of the original abstracts include a link to the retraction notice.

When we wrote about the Rushton case last year, we received a copy of an email from the journal saying that it would be retracting Rushton’s 1992 paper, “Contributions to the History of Psychology: XC. Evolutionary Biology and Heritable Traits” along with the other two articles. That didn’t happen at the time.

We asked Cory Scherer, the editor of Psychological Reports, about the eight-month gap between retractions. He told us:

I got an email from a researcher who brought these articles to our attention and when I read them I moved fast on the first retraction and the rest were found when that retraction was already written and in press. I didn’t want to add them to the original retraction until I did my due diligence about the second set found.

Our search of the journal’s website turned up eight articles in total by Rushton in the journal, of which three remain unretracted. Mr. Scherer said he has created a committee to review the remnant papers to see if they require retraction.

 

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