Type 1 diabetes (T1D) is an autoimmune disease, where the immune system attacks its own pancreas and destroys insulin producing β-cells. This results in the inability to produce insulin and the need for external insulin administration.
Over 90% of people diagnosed with T1D make autoantibodies against specific β-cell proteins, including: insulin, glutamate decarboxylase, islet antigen-2, zinc transporter-8, and tetraspanin-7. People with T1D also risk developing other autoimmune diseases.
Genetics or Environment?
Traditionally, T1D was classified as 'juvenile onset' however, the disease can occur at any age, with up to 50% of cases occurring in adulthood.
More than 50 susceptibility genes have been identified for T1D. Approximately 70% of T1D patients carry the Human Leukocyte Antigens (HLA) risk genes.
The incidence of T1D is increasing at a rate of 3-5% per year. Genetics alone is not sufficient to explain this increase. This increase can only be explained by changes in environment or lifestyle, especially since:
T1D has become more common in developed countries where eating habits and lifestyle have changed profoundly.
T1D in monozygotic twin sets is estimated at only 40%, suggesting a role for non-genetic influences.
Less than 10% of genetically susceptible people develop clinical T1D.
Many people who are diagnosed with T1D do not have a relative with the disease.
Environmental factors may alter gene 'expression' via epigenetic mechanisms. T1D is now understood to result from a complex interplay between environmental factors, microbiome, genome, metabolism, and immune system which varies between individuals.
Conventional treatment for T1D is effective, but gaining a better understanding of the mechanisms involved in the pathogenesis of T1D may help individuals manage the disease.
Environmental factors that may increase the risk of T1D
Exposure to viruses (eg Coxsackie B virus, enterovirus, CMV), especially in early life.
Vitamin D insufficiency.
Decreased gut microbiome diversity, dysbiosis and intestinal permeability.
Early exposure to cow's milk proteins, possibly because albumin in cow's milk is a molecular mimic of ICA-1, a surface protein on βcells. Breast milk may be protective.
Overuse of antibiotics, especially in early age.
Processed foods may be related to a greater risk since they contain higher amounts of advanced glycation end-products. Nitrites in processed meat products increase risk.
Toxic chemicals - levels of anti-GAD antibodies were 4 times higher in factory workers heavily exposed to toxic matter without protective wear vs non-factory workers.
Air pollution - In a small case-control study of 69 children with T1D, ozone and particulate matter less than 10 μm in diameter, were associated with increased T1D.
Caesarean delivery, older maternal age, introduction of solid foods at an early age and early childhood diet may increase risk.
In non-obese diabetic mice, a gluten-free diet delayed diabetes.
Psychological stress may induce T1D-associated autoimmunity and β cell stress.
What can I eat?
Knowing what to eat if you have T1D can be challenging since your diet needs to:
effectively manage blood sugar levels (since hypoglycaemia can be very inflammatory and hyperglycaemia can be dangerous)
be anti-inflammatory to control the autoimmune process
eliminate food groups that may be triggering the autoimmune process
be nutrient dense to prevent further autoimmune destruction
nurture your gut microbiome
This is where personalised nutritional therapy comes into its own and can be very beneficial. Without favouring any diets, a cross between a Mediterranean, Paleo and Elimination diet may be needed together with the correct nutrient supplementations, tailored to the individual's needs.
Without a doubt, processed and sugary foods, sugary drinks (including fruit juice), alcohol and refined carbohydrates should all be avoided. Nutrient dense, wholefoods, high in fibre and non-starchy carbohydrates, good quality protein and healthy fats should be the baseline. Exercise, stress levels, vitamin D levels, reducing toxic exposure and optimising sleep should also be considered as a priority.
The use of the glycaemic index and glycaemic load to rank carbohydrate foods according to their effects on glycemia may be useful when understanding carbohydrates.
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