Type 2 diabetes is near entirely a condition caused by the presence of excess visceral fat tissue, by being overweight or obese. Even in relatively late stages, type 2 diabetes can be reversed by low calorie diets and the consequent loss of that excess visceral fat. Visceral fat is metabolically active, and directly provokes chronic inflammation through a range of mechanisms, such as by mimicking the signaling of cells infected by pathogens. Excess visceral fat also disrupts insulin metabolism and control of blood glucose. The abnormal, sugar-rich diabetic metabolism also directly provokes inflammation, such as via the interaction between molecules altered by sugars known as advanced glycation endproducts (AGEs) and the receptor for AGEs (RAGE) on cell surfaces.
However it is caused, unresolved inflammatory signaling is disruptive to tissue function and structure, changing the behavior of cells for the worse. This chronic inflammation accelerates the onset and progression of all of the common fatal age-related conditions. That outcome is well established, both the mechanisms and the epidemiology demonstrating correlations between inflammation and age-related diseases.
Today's research materials add to the existing mountain of epidemiological data that aims to quantify the harms done by type 2 diabetes. As one might expect, patients with type 2 diabetes have significantly worse outcomes in long-term health. Sadly we live in an era in which obesity is prevalent, for reasons that have yet to be concretely determined. Many factors may contribute, from lesser degrees of exercise to refined dietary components that were not common a century ago to microplastics in the environment. Whatever the hierarchy of causes, the outcome is clearly harmful to health, medical costs, and life expectancy.
Type 2 diabetes (T2D) is projected to become the biggest epidemic disease in the world, affecting an estimated 1.3 billion people by 2050. T2D frequently occurs with other chronic conditions, such as high blood pressure, heart failure, chronic kidney disease, and depression, contributing substantially to the global burden of multimorbidity. Researchers explored how T2D influenced the rate of chronic disease development in 502,368 UK Biobank participants. The average age of the participants at enrollment was 58 years, and around 46% were men. Researchers used health records to track health outcomes over 15 years on average.
To calculate the pace of chronic disease development, researchers used multistate models to compare transition rates between groups with equivalent total disease. For example, they compared how long it took someone with T2D and one additional chronic condition to acquire a third condition, versus how long it took someone with two non-T2D chronic conditions to develop another condition. This approach isolates the role of T2D by ensuring both groups start with the same total number of chronic conditions.
Individuals with T2D consistently experienced higher transition rates (more rapid progression) between multiple disease stages. For example, for individuals with two chronic conditions, those with T2D as one of them progressed to a third condition at a rate of 5.7% per year, compared to 3.5% per year for those with two non-T2D conditions. This corresponds to people with T2D continuously facing a 60% higher risk of a new disease being diagnosed compared to those without T2D.
We analyzed data from the UK Biobank, a prospective population-based cohort study (n=502,368, median age 58 years [range 37-73], 46% male at baseline) with a median follow-up 15.3 year. 9.5% of participants were diagnosed with T2D over the period. We counted the current number of morbidities (among 80 long-term chronic conditions) identified through hospital admission records using ICD-10 diagnosis codes.
The total follow-up time was 7.5 million person-years (PY), of which 0.33 million PY was in T2D. Individuals with T2D consistently experienced higher transition rates between morbidity transition stages. For example, the transition rate from 2 to 3 morbidities was 3.48 per 100 PY without the presence of T2D, compared to 5.68 per 100 PY once T2D was present (rate ratio=1.6). The disproportion of transition rates was most pronounced in early disease stages. Further, the transition rates were consistently influenced by T2D status and age, with younger individuals with T2D showing the most accelerated progression.
View the full article at FightAging
