Toshihide Tsuda

Background/Objectives: Obesity is a risk factor for chronic kidney disease (CKD) in Asians. The Asia-Pacific body mass index (BMI) classification sets lower obesity cutoffs than the conventional BMI classification for all races, generally reflecting the lower BMIs in Asians. This longitudinal study evaluated the association between BMI, as classified by the Asia-Pacific BMI system, and CKD development in non-diabetic Asian adults. Methods: A population-based longitudinal study (1998–2023) was conducted in non-diabetic Japanese adults (hemoglobin A1c < 6.5%) in Zentsuji City (Kagawa Prefecture, Japan). The generalized gamma model was used to assess the relationship between time-varying BMI categories and CKD development, stratified by sex. CKD was defined as an estimated glomerular filtration rate of 2. BMI was calculated as weight (kg) divided by the square of height (m²) and categorized per the Asia-Pacific classification as overweight (23.0–24.9 kg/m²), obesity class I (25.0–29.9 kg/m²), and obesity class II (≥30.0 kg/m²). Results: CKD developed in 34.2% of 3098 men and 34.8% of 4391 women. The mean follow-up times were 7.41 years for men and 8.25 years for women. During follow-up, the BMI distributions for men were 5.0% underweight, 43.3% normal weight, 25.6% overweight, 24.1% obesity class I, and 2.0% obesity class II; those for women were 7.7%, 50.5%, 20.5%, 18.3%, and 2.9%, respectively. Compared with normal weight, obesity class I was associated with a 6% (95% confidence interval [CI]: 2–10%) shorter time to CKD onset in men and 5% (95% CI: 2–7%) in women. In both sexes, obesity class II showed shorter survival times than normal weight by point estimates, although all 95% CIs crossed the null value. Conclusions: Obesity, as classified by the Asia-Pacific BMI system, shortened the time to CKD onset in non-diabetic Asians. The conventional BMI cutoff for obesity (≥30.0 kg/m²) may be too high to identify CKD risk in this population. The findings of this study may be useful for public health professionals in designing interventions to prevent CKD.

Background/Objectives: Obesity is a risk factor for chronic kidney disease (CKD) in Asians. The Asia-Pacific body mass index (BMI) classification sets lower obesity cutoffs than the conventional BMI classification for all races, generally reflecting the lower BMIs in Asians. This longitudinal study evaluated the association between BMI, as classified by the Asia-Pacific BMI system, and CKD development in non-diabetic Asian adults. Methods: A population-based longitudinal study (1998–2023) was conducted in non-diabetic Japanese adults (hemoglobin A1c < 6.5%) in Zentsuji City (Kagawa Prefecture, Japan). The generalized gamma model was used to assess the relationship between time-varying BMI categories and CKD development, stratified by sex. CKD was defined as an estimated glomerular filtration rate of 2 . BMI was calculated as weight (kg) divided by the square of height (m ² ) and categorized per the Asia-Pacific classification as overweight (23.0–24.9 kg/m ² ), obesity class I (25.0–29.9 kg/m ² ), and obesity class II (≥30.0 kg/m ² ). Results: CKD developed in 34.2% of 3,098 men and 34.8% of 4,391 women. The mean follow-up times were 7.41 years for men and 8.25 years for women. During follow-up, the BMI distributions for men were 5.0% underweight, 43.3% normal weight, 25.6% overweight, 24.1% obesity class I, and 2.0% obesity class II; those for women were 7.7%, 50.5%, 20.5%, 18.3%, and 2.9%, respectively. Compared with normal weight, obesity class I was associated with a 6% (95% confidence interval [CI]: 2%–10%) shorter time to CKD onset in men and 5% (95% CI: 2%–7%) in women. In both sexes, obesity class II showed shorter survival times than normal weight by point estimates, although all 95% CIs crossed the null value. Conclusions: Obesity, as classified by the Asia-Pacific BMI system, shortened the time to CKD onset in non-diabetic Asians. The conventional BMI cutoff for obesity (≥30.0 kg/m ² ) may be too high to identify CKD risk in this population. The findings of this study may be useful for public health professionals in designing interventions to prevent CKD.

Background After reviewing selected scientific evidence, Schuz et al. made two recommendations in the 2018 International Agency for Research on Cancer (IARC) Technical Publication No. 46. Their first recommendation was against population thyroid screening after a nuclear accident, and the second was that consideration be given to offering a long-term thyroid monitoring program for higher-risk individuals (100-500 mGy or more radiation) after a nuclear accident. However, their review of the scientific evidence was inadequate and misrepresented the information from both Chernobyl and Fukushima. We wrote a review article published in Environmental Health in 2022 using the "Toolkit for detecting misused epidemiological methods." Schuz et al. critiqued our 2022 review article in 2023; their critique, based also on their 2018 IARC Technical Publication No. 46, was so fraught with problems that we developed this response. Main bodySchuz et al. suggest that hundreds of thyroid cancer cases in children and adolescents, detected through population thyroid examinations using ultrasound echo and conducted since October 2011 in Fukushima, were not caused by the 2011 Fukushima Daiichi Nuclear Power Plant accident. Schuz et al. compared thyroid cancers in Fukushima directly with those in Chernobyl after April 1986 and listed up to five reasons to deny a causal relationship between radiation and thyroid cancers in Fukushima; however, those reasons we dismiss based on available evidence. No new scientific evidence was presented in their response to our commentary in which we pointed out that misinformation and biased scientific evidence had formed the basis of their arguments. Their published article provided erroneous information on Fukushima. The article implied overdiagnosis in adults and suggested that overdiagnosis would apply to current Fukushima cases. The IARC report did not validate the secondary confirmatory examination in the program which obscures the fact that overdiagnosis may not have occurred as much in Fukushima. The report consequently precluded the provision of important information and measures. ConclusionInformation provided in the IARC Technical Publication No. 46 was based on selected scientific evidence resulting in both public and policy-maker confusion regarding past and present nuclear accidents, especially in Japan. It should be withdrawn.

It is well known that science can be misused to hinder the resolution (i.e., the elimination and/or control) of a health problem. To recognize distorted and misapplied epidemiological science, a 33-item “Toolkit for detecting misused epidemiological methods” (hereinafter, the Toolkit) was published in 2021. Applying the Toolkit, we critically evaluated a review paper entitled, “Lessons learned from Chernobyl and Fukushima on thyroid cancer screening and recommendations in the case of a future nuclear accident” in Environment International in 2021, published by the SHAMISEN (Nuclear Emergency Situations - Improvement of Medical and Health Surveillance) international expert consortium. The article highlighted the claim that overdiagnosis of childhood thyroid cancers greatly increased the number of cases detected in ultrasound thyroid screening following the 2011 Fukushima nuclear accident. However, the reasons cited in the SHAMISEN review paper for overdiagnosis in mass screening lacked important information about the high incidence of thyroid cancers after the accident. The SHAMISEN review paper ignored published studies of screening results in unexposed areas, and included an invalid comparison of screenings among children with screenings among adults. The review omitted the actual state of screening in Fukushima after the nuclear accident, in which only nodules > 5 mm in diameter were examined. The growth rate of thyroid cancers was not slow, as emphasized in the SHAMISEN review paper; evidence shows that cancers detected in second-round screening grew to more than 5 mm in diameter over a 2-year period. The SHAMISEN consortium used an unfounded overdiagnosis hypothesis and misguided evidence to refute that the excess incidence of thyroid cancer was attributable to the nuclear accident, despite the findings of ongoing ultrasound screening for thyroid cancer in Fukushima and around Chernobyl. By our evaluation, the SHAMISEN review paper includes 20 of the 33 items in the Toolkit that demonstrate the misuse of epidemiology. The International Agency for Research on Cancer meeting in 2017 and its publication cited in the SHAMISEN review paper includes 12 of the 33 items in the Toolkit. Finally, we recommend a few enhancements to the Toolkit to increase its utility.