Nutritional factors and the risk of type 1 diabetes

Overall, the mother's diet during pregnancy does not appear to have a significant effect on the child's risk of type 1 diabetes. A low level of vitamin D in the mother, resulting from her lifestyle, which also includes her 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 points to a higher risk of type 1 diabetes 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 type 1 diabetes in the child, not the low 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. A birth weight over 4 kg has been linked to an increased risk of type 1 diabetes of about 10%, with a linear rise of 3% for every additional 500 g [3].

High birth weight is largely caused by an excess of insulin in the foetal circulation, in response to the abundance of available nutrients. Overloading the pancreatic beta cells makes them more visible to the immune system, which raises the risk of autoimmunity being triggered after birth. It is worth remembering that the child's high birth weight is a modifiable factor, through good glucose control during pregnancy in mothers who have diabetes [3].

Yes, it matters. Both introducing cereals too early (before 4 months) and too late (after 6–7 months) appears to increase the child's risk of type 1 diabetes. The optimal window for introducing cereals is between 4 and 6 months, ideally while the child is still being breastfed. This advice coincides with the generally recommended timing for weaning [4].

In other words, it is not only what your baby eats that matters, but also when they start eating it. With introduction that is too early, the contact between cereals and an immature gut, without the "protection" of breast milk, may increase the risk of the immune system reacting in the wrong way [4].

Possibly, but the evidence is not firm. Introducing fruit or root vegetables (carrot, potato, celeriac) before 4 months has been linked in some studies to a higher risk of autoimmunity, but this effect does not appear to be permanent and generally disappears after the age of 3. Autoimmunity that does not persist does not increase the risk of type 1 diabetes [5].

The likely explanation is that introducing solid foods too early simply brings forward the moment autoimmunity is triggered, without changing the overall long-term risk. The recommendation would be for weaning to begin between 4 and 6 months, without rushing and without specifically avoiding any healthy food [5].

Sugar intake does not appear to be responsible for triggering the autoimmunity specific to type 1 diabetes. Once autoimmunity has already begun, however, sugar intake can bring forward the appearance of clinical disease (progression to stage 3). The effect is stronger in children at high genetic risk [6].

In children with autoimmunity specific to type 1 diabetes, sugar forces the pancreas to produce larger amounts of insulin. This extra demand stresses the beta cells and makes them "more visible" to the immune system, which then attacks them more quickly. It is recommended to avoid sugar-sweetened drinks in the first year of life and to limit them afterwards, whatever the genetic risk [6].

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

Introducing whole cow's milk later (after 2–3 months) appears to have a protective effect, as does prolonged breastfeeding. There is no need to avoid cow's milk proteins in order to prevent type 1 diabetes (it does not work). Breastfeeding for 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. Being 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 makes the pancreas produce more insulin (for the whole body), which overloads the beta cells and hastens their recognition and destruction by the immune system. Keeping to a healthy weight in the first years of life is one of the few modifiable factors shown to be helpful here [8].

The total number of calories does not appear to matter directly for triggering autoimmunity. They do, however, start to matter more and more once the autoantibodies specific to type 1 diabetes have appeared. In general, the quality of the calories matters more than their quantity [9].

Indirectly, though, a calorie excess does matter, because it leads to weight gain when it is not matched by a corresponding energy expenditure. Rapid weight gain accelerates progression to clinical diabetes (stage 3). The chain of consequences runs: too many calories for your needs → weight gain → insulin resistance → greater demand for insulin → overloading of the beta cells → faster autoimmune destruction (very likely set off by something else) [9].

Yes, but mainly for children who already have autoantibodies. High-glycaemic-index foods (white bread, white rice, chips, sweets, juices) do not appear to trigger autoimmunity, but they significantly speed up the move from autoimmunity to clinical diabetes (stage 3) [10].

High-glycaemic-index foods cause larger blood glucose peaks after meals, so the pancreas has to respond with a greater amount of insulin. This repeated pressure on the beta cells makes them more vulnerable to immune attack, even if that attack was initially set off by something else. Choosing low-glycaemic-index foods (pulses, wholegrains, whole fruit instead of juice) is a simple and accessible prevention strategy [10].

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

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

No. Although type 1 diabetes and coeliac disease share some common genetic factors, avoiding gluten does not prevent diabetes. The only caveat is to introduce cereals to your baby within the optimal window of 4–6 months of life, ideally while the child is still being breastfed [11].

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

Probably yes, but only in the phase when autoimmunity is being triggered, and especially through the marine forms. Children with a higher intake of omega-3 fatty acids (from oily 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 may have, it disappears completely once autoimmunity has appeared. Once autoimmunity has begun, omega-3 fatty acids cannot slow progression to clinical diabetes. Including oily fish regularly (salmon, sardines, mackerel) in children's diet is a good idea anyway [12].

Fibre may have a positive indirect effect, through the gut bacteria. When fibre reaches the colon, the good bacteria ferment it 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 gut) contains more bacteria able to produce these fatty acids than that of children who go on to develop type 1 diabetes. However, simply increasing fibre intake is no guarantee of a favourable microbiome. The relationship between fibre, bacteria and immunity is complex. An adequate fibre intake is recommended for all patients, but not specifically to prevent type 1 diabetes [13].

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

The explanation is that saturated fats in the blood reflect the body's own production more than what you eat. A high blood level may therefore be a sign of an unhealthy metabolism, rather than a direct consequence of the diet. At present, limiting saturated fat is recommended to prevent cardiovascular disease, but not specifically for type 1 diabetes [14].

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

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

Probably, but direct evidence in humans is limited. Animal studies (not human ones) clearly show that food emulsifiers (additives that bind water and fat in processed products) and compounds formed at high temperatures (frying, charred grilling) increase the risk of type 1 diabetes [16].

The presumed mechanisms include disruption of the gut bacteria, increased gut permeability ("leaky gut syndrome"), systemic inflammation and overloading of the beta cells. A diet based on foods that are as little processed as possible, cooked at moderate temperatures (boiling, steaming, a medium-temperature oven) rather than fried or grilled, is advisable not only to prevent diabetes but also for health in general [16].

We don't know. No studies have directly examined whether a vegetarian diet prevents type 1 diabetes. The existing studies show a lower risk of diabetes in vegans, but this mainly concerns type 2 diabetes, not type 1 [17].

In theory, a well-planned vegetarian diet could help by reducing inflammation, improving the gut microbiome and avoiding processed meat. A vegetarian diet is an accepted dietary pattern for people with diabetes, but it is not recommended specifically for prevention. If it is chosen, the diet must be varied and balanced, with attention paid to the 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 glucose control in children and adolescents who already have the disease. Better adherence to this dietary pattern is associated with a lower glycated haemoglobin (HbA1c) and more time in the target blood glucose range [18].

The principles of the Mediterranean diet are based on more vegetables and fruit, wholegrains, fish (especially oily fish), 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 to reduce cardiovascular risk [18].

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

Vitamin C, obtained from natural sources, may have a positive effect. Children with a higher intake of vitamin C in their diet have a significantly lower risk of autoimmunity and of type 1 diabetes. The practical answer is not supplements, but eating fruit and vegetables rich in vitamin C regularly, such as bell peppers, citrus fruit, kiwi, strawberries, cabbage and fresh parsley [19].

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

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