Type 1 Diabetes Environmental Determinants Triggers
Abstract – Type 1 Diabetes Environmental Determinants Triggers
Type 1 diabetes is perceived as a chronic immune-mediated disease with a subclinical prodromal [non-specific precursor symptom] period characterized by selective loss of insulin-producing β-cells in the pancreatic islets in genetically susceptible subjects. A series of evidence supports a critical role of exogenous factors in the development of type 1 diabetes, such as 1) the fact that <10% of individuals with HLA-conferred diabetes susceptibility do progress to clinical disease, 2) a pairwise concordance of type 1 diabetes of <40% among monozygotic twins, 3) a more than 10-fold difference in the disease incidence among Caucasians living in Europe, 4) a several-fold increase in the incidence over the last 50 years, and 5) migration studies indicating that the disease incidence has increased in population groups who have moved from a low-incidence to a high-incidence region. This article discusses the trigger-booster hypothesis claiming that the diabetic disease process is triggered by an exogenous factor with definite seasonal variation and driven by one or several other environmental determinants. In addition, there are a series of modifying factors affecting the fate and pace of the process. Accordingly, progression to clinical type 1 diabetes typically requires the unfortunate combination of genetic disease susceptibility, a diabetogenic trigger, and a high exposure to a driving antigen.
Clinical type 1 diabetes represents end-stage insulitis, and it has been estimated that at the time of diagnosis, only 10–20% of the insulin-producing β-cells are still functioning. Environmental factors have been implicated in the pathogenesis of type 1 diabetes both as triggers and potentiators of β-cell destruction (1–3), although the contribution of any individual exogenous factor has not yet been definitely proven. Type 1 diabetes is considered to be a chronic immune-mediated disease with a subclinical prodrome of variable duration. It is characterized by selective loss of insulin-producing β-cells in the pancreatic islets in genetically susceptible subjects. The most important genes contributing to disease susceptibility are located in the HLA class II locus on the short arm of chromosome 6 (4). Nevertheless, only a relatively small proportion, i.e., <10%, of genetically susceptible individuals progress to clinical disease. This implies that additional factors are needed to trigger and drive β-cell destruction in genetically predisposed subjects.
It is important to note that by the time a person has clinically diagnosed type 1 diabetes, it is estimated that 80-90% of insulin-producing beta cells are no longer functioning. This would imply that early detection is vitally important to any prevention strategy. Since less than 10% of genetically susceptible individuals progress to clinical disease, it would be important for disease prevention to mitigate as early as possible the environmental triggers and potentiators involved. The Roman Diet and Health-e-Solutions lifestyle seeks to eliminate or minimize as many environmental trigger sand potentiators as possible in an effort to “deactivate” genes that may be involved in disease progression. Since the contribution of any individual exogenous factor has not yet been definitely proven, we cannot say for sure what the impact of eliminating or minimizing them has, but it sure does not hurt to try. After all, we are simply talking about a healthier overall lifestyle!
Until #CuringType1Diabetes is a reality within our reach, put your body in a position of strength to #MasterDiabetes the healthiest way possible. Lifestyle innovations as a priority over drug therapies may be the solution. Poor health feeds poor health in a vicious cycle, or negative feedback loop that is increasingly difficult to break the longer it continues. Promoting, supporting and creating health set in motion a positive feedback loop instead.
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