PDF(Pubmed)
Abstract：
LADA is a common form of diabetes described as a mix between type 1 and type 2 diabetes. Understanding of how genes and environmental factors interact in the development of LADA is central for future efforts to prevent the disease. This review aims to synthesize the literature on lifestyle factors linked to LADA risk and discuss their potential interaction with genetic susceptibility.
Current knowledge on environmental risk factors for LADA is primarily based on observational data from Scandinavian populations. Increasing evidence suggest that lifestyle factors promoting type 2 diabetes such as obesity, sedentariness, low birth weight and smoking, is implicated in the risk of LADA. Data from mendelian randomization studies support that the link between LADA and obesity, low birth weight and smoking is causal. Limited evidence indicates that dietary factors including consumption of red meat, coffee and sweetened beverages may increase the risk while consumption of alcohol and omega-3 fatty acids may reduce the risk. Several lifestyle factors, including smoking and obesity, seem to interact with human leukocyte antigen genes associated with autoimmunity, conferring much stronger effects on disease risk among those exposed to both factors.
Available studies suggest that lifestyle modification has the potential for prevention of LADA, particularly for individuals with high risk of disease such as those with genetic susceptibility. Research into risk factors of LADA is however limited, confirmations are warranted, many factors remain to be explored, and there is a need for intervention studies to assess causality.
Current knowledge on environmental risk factors for LADA is primarily based on observational data from Scandinavian populations. Increasing evidence suggest that lifestyle factors promoting type 2 diabetes such as obesity, sedentariness, low birth weight and smoking, is implicated in the risk of LADA. Data from mendelian randomization studies support that the link between LADA and obesity, low birth weight and smoking is causal. Limited evidence indicates that dietary factors including consumption of red meat, coffee and sweetened beverages may increase the risk while consumption of alcohol and omega-3 fatty acids may reduce the risk. Several lifestyle factors, including smoking and obesity, seem to interact with human leukocyte antigen genes associated with autoimmunity, conferring much stronger effects on disease risk among those exposed to both factors.
Available studies suggest that lifestyle modification has the potential for prevention of LADA, particularly for individuals with high risk of disease such as those with genetic susceptibility. Research into risk factors of LADA is however limited, confirmations are warranted, many factors remain to be explored, and there is a need for intervention studies to assess causality.
摘要：
LADA是一种常见的糖尿病形式，被描述为1型和2型糖尿病之间的混合物。了解基因和环境因素在LADA发展中的相互作用是未来预防疾病的核心。这篇综述旨在综合与LADA风险相关的生活方式因素的文献，并讨论它们与遗传易感性的潜在相互作用。
目前对LADA环境风险因素的了解主要基于斯堪的纳维亚人口的观测数据。越来越多的证据表明，生活方式因素促进2型糖尿病，如肥胖，镇静，低出生体重和吸烟，与LADA的风险有关。孟德尔随机化研究的数据支持LADA与肥胖之间的联系，低出生体重和吸烟是因果关系。有限的证据表明，包括食用红肉在内的饮食因素，咖啡和甜味饮料可能会增加风险，而酒精和omega-3脂肪酸的消费可能会降低风险。几个生活方式因素，包括吸烟和肥胖，似乎与自身免疫相关的人类白细胞抗原基因相互作用，在暴露于这两种因素的人群中，对疾病风险的影响要大得多。
现有研究表明，改变生活方式有可能预防LADA，特别是对于患有疾病的高风险个体，如具有遗传易感性的个体。然而，对LADA风险因素的研究有限，确认是有保证的，许多因素仍有待探索，并且有必要进行干预研究来评估因果关系。
目前对LADA环境风险因素的了解主要基于斯堪的纳维亚人口的观测数据。越来越多的证据表明，生活方式因素促进2型糖尿病，如肥胖，镇静，低出生体重和吸烟，与LADA的风险有关。孟德尔随机化研究的数据支持LADA与肥胖之间的联系，低出生体重和吸烟是因果关系。有限的证据表明，包括食用红肉在内的饮食因素，咖啡和甜味饮料可能会增加风险，而酒精和omega-3脂肪酸的消费可能会降低风险。几个生活方式因素，包括吸烟和肥胖，似乎与自身免疫相关的人类白细胞抗原基因相互作用，在暴露于这两种因素的人群中，对疾病风险的影响要大得多。
现有研究表明，改变生活方式有可能预防LADA，特别是对于患有疾病的高风险个体，如具有遗传易感性的个体。然而，对LADA风险因素的研究有限，确认是有保证的，许多因素仍有待探索，并且有必要进行干预研究来评估因果关系。
