New breakthroughs in diabetes may aid in preventing and potentially curing the condition. New trials and insights may provide the answer. Diabetes is a condition of the body in which the effectiveness of insulin is either decreased or inexistent. How it develops is a complex process and has two different trajectories dependent on it being either type 1 or type 2. The contemporary understanding of type 2 is it may be caused by lifestyle factors particularly in relation to exercise and diet, adiposity is a common predisposing causative factor. Insulin resistance develops under inferior diet conditions and exhaustion of the insulin producing beta cells in the pancreas.
Type 1 differs to type 2 diabetes when the ability to produce insulin is inexistent, an individual may need insulin injections from this point forward and has been described as irreversible, new treatments however aim to derail this belief. Recently it has been strongly suggested diabetes type 1 has many environmental triggers, which seem to be gaining more attention and significance including; the fact under 5% of individuals with genetic susceptibility develop the condition, as high as a 15-fold difference in geographic variation, a substantial increase in the prevalence of the condition over the past few decades especially in Europe, increasing prevalence in migrating populations and those with high prospect and reduced prospect genotypes has altered. It is believed it requires a genetic susceptibility, an importantly timed trigger and an ongoing exposure to an unknown antigen.
It has also been suggested how certain pathogens may have an affinity for pancreas beta cells leading to lesions and an expected autoimmune response, to clear atrophied cells. Maternal protection from these specific viruses may have also decreased as a result of more hygienic conditions, meaning relevant antibodies evade transferral from mother to baby, leading the individual to be more vulnerable if the pathogen is contracted. Specific triggering pathogens are rare in countries even where type 1 is high in prevalence, although probably still present this paradox may be explained by an absence of inherited immunity.
Diabetes progression may be associated to insulitis suggesting the beta cells may be saved from an end stage cascade into diabetes. This progression of the condition is similar to the progression seen in the liver condition cirrhosis, when the cells have been exposed to antigens long term (part of an autoimmune response) these cells go into protective mode, from this point the cells are unable to duplicate or regenerate leading to the deleterious effects of both conditions.
Studies in the past have revealed how some of these beta cells are only dormant, particularly in older individuals, possibly hinting how these cells may be reactivated as has been demonstrated in vitro. Presently, trials using immunotherapy may prevent the progression to diabetes type 1 by stopping the deleterious immune response and reversing it to a protective response. The drawback with this approach may be it only saves cells which have somehow evaded mortality and may compel cells tagged for clearing to bypass this process, a more effective strategy in the future for those actually diagnosed with type1 may be to utilise stem cells which might reactivate dormant or expired cells.
If these cells evade lesions of any type and source they may then abstain from an autoimmune response on its existence and give beta cells a new lease of life. As the processes which induce diabetes are long term, the likelihood of cells surviving may be high especially if an individual has acquired antibody protection from a pathogenic diabetes activating virus earlier in life.
This knowledge allows a different mentality to prevail especially in relation to type 1 diabetes. An individual may now prevent the condition from cascading into diabetes by understanding the signs of an autoimmune response; antibodies associated with diabetes are seen when the condition is activated consistently in autumn or winter and viruses or nutrients highly likely to contribute to its progression. Optimism exists for those already experiencing the condition in the form of immunotherapy and possibly stem cell treatment in the future.
Why does the understanding of certain conditions vary between different eras?