📘 Nutritional factors and the risk of type 1 diabetes mellitus

Overall, the mother's nutrition during pregnancy does not appear to have a significant effect on the child's risk of type 1 diabetes mellitus. A low level of vitamin D in the mother obtained as a result of lifestyle, which also includes diet, can increase the risk of type 1 diabetes. Correcting the vitamin D level through supplements does not modify the risk of type 1 diabetes [1].

In other words, a spontaneously low level of vitamin D in the pregnant woman indicates a higher risk of T1DM in the child, which does not change if the woman starts taking vitamin D. The reason vitamin D was low is the cause of the higher risk of T1DM in the child, not the decrease in vitamin D itself. Changes in the pregnant woman's diet regarding the amount of gluten or the intake of omega-3 fatty acids did not significantly change the child's risk of type 1 diabetes [2].

Yes, high birth weight (over 4000 g) is associated with a slightly increased risk of type 1 diabetes. Birth weight over 4 kg has been associated with an increased risk of T1DM of approximately 10%, with a linear increase of 3% for every additional 500 g [3].

High birth weight is largely due to excess insulin in the fetal circulation, in response to the excess of available nutrients. The overloading of pancreatic beta cells increases their visibility to the immune system, thus increasing the risk of triggering autoimmunity after birth. It should be noted that the child's high birth weight is a modifiable factor through adequate glycemic control during pregnancy in the mother with diabetes [3].

Yes, it matters. Both too early (before 4 months) and too late (after 6–7 months) introduction seem to increase the risk of type 1 diabetes in the child. The optimal interval for cereal introduction is between 4 and 6 months, ideally while the child is still being breastfed. This recommendation coincides with the general recommended timing for food diversification [4].

In other words, not only what the infant eats matters, but also when they start eating. For too early introduction, the contact of cereals with the immature intestine, without the "protection" of breast milk, could increase the risk of the immune system reacting incorrectly [4].

Possibly, but the evidence is not firm. Introduction of fruits or root vegetables (carrot, potato, celery) before 4 months has been associated in some studies with a higher risk of autoimmunity, but this effect does not appear to be permanent and generally disappears after the age of 3 years. Autoimmunity that does not persist does not increase the risk of T1DM [5].

The likely explanation is that too early introduction of solid foods only accelerates the moment of triggering autoimmunity, without changing the overall long-term risk. The recommendation would be that food diversification begin between 4 and 6 months, without haste and without special avoidance of any healthy food [5].

Sugar consumption does not appear to be responsible for triggering autoimmunity specific to type 1 diabetes. Once autoimmunity has already started, sugar consumption can hasten the moment of clinical disease onset (progression to stage 3). The effect is stronger in children with increased genetic risk [6].

In patients with autoimmunity specific to T1DM, sugar forces the pancreas to produce larger amounts of insulin. This overloading stresses the beta cells and makes them "more visible" to the immune system, which attacks them more quickly. Avoidance of sugar-sweetened beverages in the first year of life is recommended, as well as limiting them afterwards, regardless of genetic risk [6].

The hypothesis that cow's milk proteins trigger type 1 diabetes was tested in a large dietary prevention study of the disease and was not confirmed. Replacing cow's milk with a formula with hydrolyzed proteins (infant powdered milk) did not reduce the risk of type 1 diabetes [7].

Later introduction of whole cow's milk (after 2–3 months) appears to have a protective effect, as does prolonged breastfeeding. There is no need to avoid cow's milk proteins with the aim of preventing type 1 diabetes (it does not work). Breastfeeding as long as possible and delaying the introduction of whole cow's milk are the current recommendations [7].

Yes. Children who gain weight faster than average have a higher risk of both autoimmunity and progression to clinical diabetes. Overweight in early childhood (2–10 years) can double the risk of developing type 1 diabetes [8].

The explanation is known as the "accelerator hypothesis". Excess weight causes the pancreas to produce more insulin (for the whole body), which overloads the beta cells and hastens their recognition and destruction by the immune system. Maintaining a healthy weight in the first years of life is one of the few modifiable factors demonstrated to be beneficial in this case [8].

The total number of calories does not appear to matter directly for triggering autoimmunity. However, they begin to matter more and more after the appearance of autoantibodies specific to T1DM. In general, the quality of calories matters more than their quantity [9].

Indirectly, however, caloric excess matters because it leads to weight gain in the absence of a corresponding caloric expenditure. Rapid weight gain accelerates progression to clinical diabetes (stage 3). The chain of consequences involves too many calories for your consumption → weight gain → insulin resistance → greater demand for insulin → overloading of beta cells → acceleration of their autoimmune destruction (very likely initiated by something else) [9].

Yes, but especially for children who already have autoantibodies. Foods with a high glycemic index (white bread, white rice, fried potatoes, sweets, juices) do not appear to trigger autoimmunity, but significantly accelerate the transition from autoimmunity to clinical diabetes (stage 3) [10].

Foods with a high glycemic index cause larger post-meal blood glucose peaks, and consequently the pancreas must respond with a greater amount of insulin. This repeated pressure on the beta cells makes them more vulnerable to immune attack, even if it was initially triggered by something else. Choosing foods with a low glycemic index (legumes, whole grains, whole fruits instead of juices) is a simple and accessible prevention strategy [10].

Yes. In children who already have autoantibodies, high sugar intake significantly increases the risk of developing clinical diabetes [6].

It should be noted that sugar does not trigger autoimmunity, but accelerates it once it has appeared. In short, sugar does not "cause" type 1 diabetes, but hastens its onset if the process has already started. Limiting added sugar is recommended for all children, not only for those at risk of developing T1DM [6].

No. Although type 1 diabetes and celiac disease share common genetic factors, gluten avoidance does not prevent diabetes. The only caveat is cereal introduction in the infant within the optimal window of 4-6 months of life, ideally while the child is still being breastfed [11].

The prevalence of celiac disease in children with type 1 diabetes is nevertheless 5–6% (compared to 1% in the general population), which justifies periodic screening for celiac disease in all children with T1DM. There are no current recommendations for avoiding gluten for the purpose of preventing type 1 diabetes. A gluten-free diet is necessary only if celiac disease is diagnosed [11].

Probably yes, but only in the autoimmunity triggering phase and especially through marine forms. Children with higher intake of omega-3 fatty acids (from fatty fish, fish oil, cod liver oil) appear to have a significantly lower risk of developing autoantibodies. The protective mechanism probably involves reducing general inflammation and balancing the immune response [12].

Whatever protective effect omega-3 fatty acids might have, it disappears completely after autoimmunity has appeared. Once autoimmunity has started, omega-3 fatty acids cannot slow progression to clinical diabetes. Regular inclusion of fatty fish (salmon, sardines, mackerel) in children's diet is a good idea anyway [12].

Fibers have a possible positive indirect effect, through the intestinal bacteria. When fibers reach the colon, the good bacteria ferment them and produce short-chain fatty acids (acetate and butyrate), which have anti-inflammatory effects and modulate (help) the immune system [13].

The microbiome of healthy children (the bacterial colonies in the intestine) contains more bacteria capable of producing these fatty acids than that of children who develop type 1 diabetes. However, simply increasing fiber intake does not guarantee a favorable microbiome. The relationship between fibers, bacteria and immunity is complex. Adequate fiber intake is recommended for all patients, but not specifically for the prevention of type 1 diabetes [13].

The evidence is mixed and sometimes surprising. Some studies suggest that moderate dietary intake of saturated fats may even be protective against type 1 diabetes, while an elevated blood level of saturated fats is associated with increased risk [14].

The explanation is that saturated fats in the blood reflect more the body's own production than what you eat. Their elevated blood level may therefore be a sign of inappropriate metabolism, not necessarily a direct consequence of diet. Currently, limitation of saturated fats is recommended for the prevention of cardiovascular disease, but not specifically for type 1 diabetes [14].

Possibly. Some studies have found a higher incidence of type 1 diabetes in areas with nitrates in drinking water, and children with diabetes had on average higher intake of nitrites from food (cold cuts, processed meat) [15].

Biological plausibility exists. Streptozotocin, the compound used in the laboratory to induce diabetes in mice, is an N-nitroso compound similar to those in processed meat. However, studies conducted in humans are not yet sufficient for a firm conclusion. Limiting processed meat consumption remains a general health recommendation [15].

Probably, but direct evidence in humans is limited. Studies in animals (not in humans) clearly show that dietary emulsifiers (additives that bind water and fats in processed products) and products formed at high temperatures (frying, charred grilling) increase the risk of type 1 diabetes [16].

The presumed mechanisms include alteration of intestinal bacteria, increased intestinal permeability ("leaky gut syndrome"), systemic inflammation and overloading of beta cells. A diet based on foods as little processed as possible, prepared at moderate temperatures (boiling, steam cooking, medium-temperature oven), instead of frying or grilling, is recommendable not only for diabetes prevention, but also for health in general [16].

We don't know. There are no studies that have directly examined whether a vegetarian diet prevents type 1 diabetes. Existing studies show a lower risk of diabetes in vegans, but this effect mainly refers to type 2 diabetes, not type 1 [17].

Theoretically, a well-planned vegetarian diet could help by reducing inflammation, improving the intestinal microbiome, and avoiding processed meat. The vegetarian diet is an accepted dietary model for people with diabetes, but without recommending it specifically for prevention. If chosen, the diet must be varied and balanced, with attention to intake of vitamin B12, iron and protein [17].

There is no evidence that the Mediterranean diet prevents the onset of type 1 diabetes, but there is clear evidence that it improves glycemic control in children and adolescents who already have the disease. Better adherence to this dietary model is associated with lower glycated hemoglobin (HbA1c) and more time in the target range of blood glucose [18].

The principles of the Mediterranean diet are based on more vegetables and fruits, whole grains, fish (especially fatty), extra virgin olive oil, nuts and seeds, moderate amounts of dairy and little red meat. The Mediterranean diet is recommended for people with diabetes, especially for reducing cardiovascular risk [18].

Zinc has a central role in pancreatic beta cells, and one of the major autoantibodies in type 1 diabetes attacks precisely the zinc transporter from these cells (ZnT8). However, there are no studies showing that zinc supplementation prevents type 1 diabetes [19].

Vitamin C, obtained from natural sources, possibly has a positive effect. Children with higher intake of vitamin C in their diet have a significantly lower risk of autoimmunity and type 1 diabetes. The practical solution is not supplements, but regular consumption of fruits and vegetables rich in vitamin C, such as bell pepper, citrus, kiwi, strawberries, cabbage, fresh parsley [19].

Possibly, but not through supplements. Observational studies show that a higher level of vitamin E in the blood, obtained from diet, is associated with a reduced risk of type 1 diabetes. The effect is modest but present [20].

However, supplementation with antioxidant vitamins (E, C, beta-carotene) is not recommended because of the lack of clear evidence of efficacy and some possible long-term safety problems (especially for beta-carotene). The best source of antioxidants remains a diversified diet, rich in fruits, vegetables, nuts and seeds [20].