Classen John B
Classen Immunotherapies, Inc. 3637 Rockdale Road, Manchester, MD 21102, USA.
Curr Diabetes Rev. 2012 Nov;8(6):413-8. doi: 10.2174/157339912803529869.
There is an epidemic in children of metabolic syndrome, obesity, type 2 diabetes and other individual diseases that form the components of metabolic syndrome. Poor diet and low exercise can not explain many facets of the epidemic including the onset in children 6 month of age, the protective effect of obesity on the incidence of type 1 diabetes and the epidemic of type 2 diabetes/metabolic syndrome in grass fed horses. Poor diet and exercise also do not explain the epidemic of type 1 diabetes in children that resembles the epidemic of type 2 diabetes/metabolic syndrome. Several papers have been published to indicate that the epidemics of type 1 and type 2 diabetes/metabolic syndrome in children are linked and are polar opposite responses to iatrogenic inflammation. Several lines of research support this. Data from different races indicates that there is an inverse relationship between developing type 1 diabetes and type 2 diabetes. Races with high risk of developing type 2 diabetes have a decreased risk of developing type 1 diabetes. Data from Italy confirmed an inverse association between obesity and type 1 diabetes. Further studies indicate the inverse relationship between type 1 diabetes and type 2 diabetes/obesity is due to cortisol production. Data indicates those with low cortisol responses have a predilection for type 1 diabetes and other autoimmune disorders following inflammation, while those with high cortisol/ immune suppressive responses develop type 2 diabetes/metabolic syndrome/obesity which resembles a Cushingoid state but are spared in the autoimmune disorders. Japanese children produce much more cortisol following immunization than Caucasian children. The later explains why discontinuation of BCG vaccination was associated with a decrease in type 1 diabetes in European children and a decrease in type 2 diabetes in Japanese children. Both the epidemics of type 1 diabetes and metabolic syndrome correlate with an increase in immunization. Finally, there is a strong mechanism data that macrophage produced interleukin 1, tumor necrosis factor and interleukin 6, which are released following inflammation, causing destruction of insulin secreting islet cells and increase cortisol release, and thus have the ability to cause both type 1 and type 2 diabetes/metabolic syndrome (which resembles a Cushingoid state). The propensity to develop type 1 diabetes or type 2 diabetes/metabolic syndrome depends on the propensity to release of cortisol which correlates with race.
儿童中存在代谢综合征、肥胖症、2型糖尿病以及构成代谢综合征各成分的其他个别疾病的流行情况。不良饮食和缺乏运动无法解释该流行情况的诸多方面，包括6个月大儿童的发病情况、肥胖对1型糖尿病发病率的保护作用以及草饲马中2型糖尿病/代谢综合征的流行情况。不良饮食和运动也无法解释儿童中1型糖尿病的流行情况，而这种流行情况与2型糖尿病/代谢综合征的流行情况相似。已有多篇论文表明，儿童中1型糖尿病和2型糖尿病/代谢综合征的流行情况相互关联，且是对医源性炎症的截然相反的反应。多项研究支持这一观点。来自不同种族的数据表明，患1型糖尿病和2型糖尿病之间存在负相关关系。患2型糖尿病风险高的种族患1型糖尿病的风险降低。来自意大利的数据证实肥胖与1型糖尿病之间存在负相关。进一步的研究表明，1型糖尿病与2型糖尿病/肥胖症之间的负相关关系是由于皮质醇的产生。数据表明，皮质醇反应低的人在炎症后易患1型糖尿病和其他自身免疫性疾病，而皮质醇/免疫抑制反应高的人则会发展为2型糖尿病/代谢综合征/肥胖症，这类似于库欣样状态，但不会患自身免疫性疾病。日本儿童在接种疫苗后产生的皮质醇比白种儿童多得多。后者解释了为什么停止接种卡介苗与欧洲儿童1型糖尿病发病率的降低以及日本儿童2型糖尿病发病率的降低有关。1型糖尿病和代谢综合征的流行情况均与免疫接种的增加相关。最后，有强有力的机制数据表明，巨噬细胞产生的白细胞介素1、肿瘤坏死因子和白细胞介素6在炎症后释放，会导致分泌胰岛素的胰岛细胞遭到破坏，并增加皮质醇的释放，从而有能力引发1型糖尿病和2型糖尿病/代谢综合征（类似于库欣样状态）。患1型糖尿病或2型糖尿病/代谢综合征的倾向取决于皮质醇的释放倾向，而这与种族相关。
