 Flax seeds are one source of omega-3 fatty acids. Refined fish oil is another source, but unrefined fish oil may contain higher levels of chemicals. Omega-3 fatty acidsNorris et al. (2007) found that dietary intake of omega-3 fatty acids, found in fish, flax seeds, walnuts, soy, canola, and greens, is protective against the development of type 1 diabetes-related autoantibodies in children at genetic risk of type 1 diabetes. Omega-3s can reduce inflammation, and the lack of omega-3s in Western diets may predispose people to inflammation. Yet the same authors later found that omega-3 levels were not associated with later development of type 1 in these children (Miller et al. 2011). So, it is possible that omega-3s may be protective against type 1 autoantibody development, but be less significant later in the disease process. An earlier study of the same children found that the mother's dietary intake of omega-3 fatty acids during pregnancy did not affect the risk of autoimmunity in children (Fronczak et al. 2003). Cod liver oil, however, taken during pregnancy, has been associated with a reduced risk of type 1 diabetes in offspring. Both omega-3 fatty acids and vitamin D are present in this oil, and either or both may play a role (Stene et al. 2000). Virtanen et al. (2010) found that the fatty acids associated with milk and ruminant meat fat consumption were associated with an increased risk of type 1 related autoimmunity. Linoleic acid, however, was associated with lower levels of autoimmunity, in children genetically at risk of type 1 diabetes.
A group of people with metabolic syndrome (a group of conditions common in people with type 1 or 2 diabetes) were given omega-3 fatty acid supplements or a placebo for six months. Those taking the supplements were found to have lower markers of autoimmunity and inflammation, as well as more weight loss, compared to people who did not take the supplements (Ebrahimi et al. 2009). Adequate intake of omega-3s during pregnancy may also decrease the risk of obesity in the offspring. Higher levels of omega-6 fatty acids in relation to omega-3s in umbilical cord blood has been associated with higher obesity in children at age 3 (Donahue et al. 2011). Chemicals and omega-3sThe presence of environmental contaminants in food may also play a role in the effects of nutritional factors. Some contaminants may interfere with the beneficial effects of foods. For example, in a study linking insulin resistance to persistent organic pollutants, the researchers concluded that beneficial aspects of omega-3 fatty acids in salmon oil could not counteract the harmful effects caused by the persistent organic pollutants in that oil (Ruzzin et al. 2010). Fish is one source of omega-3 fatty acids, but according to an editorial in the American Journal of Clinical Nutrition (AJCN), it may be better to rely on plant-based sources instead (Feskens 2011). Studies on fish consumption and type 2 diabetes are inconsistent: some show that higher dietary intake of omega 3s decreases the risk of type 2, some show no connection, and some even show that higher fish consumption increases the risk of type 2 diabetes (Djousse et al. 2011; Villegas et al. 2011). It may be that the chemicals in fish can explain these inconsistencies. A study shows that plant-based omega 3s have different effects than marine-based omega 3s in relation to type 2 diabetes (Brostow et al. 2011), possibly due to the contaminants present in fish. Other fatsA high fat diet, especially one high in saturated fats, has been linked to type 2 diabetes and insulin resistance. It appears that saturated fatty acids (but not unsaturated fats) activate immune cells, which produce an inflammatory protein, which in turn then makes cells more insulin resistant (Wen et al. 2011). Mothers who consumed higher levels of trans fats had an increased risk of excess body fat, and so did their breastfed infants (Anderson et al. 2010). Can the effects of a high fat diet be passed down to subsequent generations? In animal studies, a high-fat diet that causes obesity in mothers can affect the metabolism and weight of her offspring. But what about a high fat diet in fathers? In one study, the female offspring of heavier father rats (fed a high-fat diet) had defects in their insulin and glucose levels, like their fathers. Unlike their fathers, they were not heavier than the controls (Ng et al. 2010). Other researchers fed mice a high fat diet with fat composition similar to a standard Western diet, and then bred them and fed them the same diet for multiple generations. Over four generations, the offspring became gradually heavier, and developed higher insulin levels, despite not eating more calories. The diet was associated with changes in gene expression (Massiera et al. 2010). Glycemic index and sweetenersThe glycemic index is a measurement of how high a certain food raises blood glucose levels after it is eaten. Foods that have a high glycemic index will cause blood glucose to rise more, triggering insulin production (in people who still produce insulin), then leading to falling blood glucose levels. One prospective study has found that a higher glycemic index diet leads to a faster progression to type 1 diabetes. The group of people on this diet, however, did not have higher levels of autoantibodies, showing that the diet may affect disease progression but not disease initiation. The mechanisms involved may include oxidative stress, caused by high blood glucose levels after meals, or perhaps insulin resistance. Whatever the mechanism, a high glycemic index diet may place additional stresses on beta cells that are already under an autoimmune attack (Lamb et al. 2008). The consumption of sugar-sweetened beverages has been associated with type 2 diabetes, obesity, and metabolic syndrome. A meta-analysis of a 11 prospective studies (of over 300,000 people) found that those who consumed 1-2 sweetened beverages per day had a 26% greater risk of developing type 2 diabetes than those who consumed fewer than one serving per month. The risk was 20% higher for developing metabolic syndrome. Sugar-sweetened beverages include soft drinks, fruit drinks, iced tea, and energy/vitamin water drinks (Malik et al. 2010). High-fructose corn syrup is another sweetener linked to obesity. Rats given access to high-fructose corn syrup gained more weight than those given access to sucrose, despite eating the same number of calories (Bocarsly et al. 2010).
ZincA few studies have found that higher zinc levels in drinking water may be protective against type 1 diabetes. For example, Zhao et al. (2001) found that higher levels of zinc and magnesium were associated with lower rates of type 1 diabetes in southwest England. In Norway, a study found that higher zinc levels in water was associated with a lower risk of type 1 diabetes, but the association was not statistically significant (Stene et al. 2002). In Finland, a study found that low zinc levels in drinking water was associated with a higher incidence of type 1 diabetes (Ulf et al. 2010).
Nicotinamide and other antioxidantsNicotinamide is a component of vitamin B3 that has been shown to protect against diabetes in animals, and prevent beta cell damage in the laboratory (Gale et al. 2004). Even better, one study found that it prevented the development of type 1 diabetes in children with type 1-associated autoantibodies (Elliott et al. 1996). On the basis of these and other studies, a large, double-blind, placebo-controlled trial was conducted in Europe, the U.S. and Canada, called the European Nicotinamide Diabetes Intervention Trial (ENDIT). This trial gave nicotinamide to first degree relatives of people with type 1 diabetes who already had developed type 1-associated autoantibodies. Unfortunately, it found no difference in the development of diabetes between the two groups during the 5 year follow-up period. The study gave high doses of the vitamin, up to 3 g/day (30-50 times higher than the RDA) (Gale et al. 2004). Read this study and you can almost feel the disappointment-- we can identify who is at risk of developing type 1 but we can’t do a thing about it.
Another double-blind, placebo controlled study in Sweden gave high doses of anti-oxidants (including nicotinamide, vitamin C, vitamin E, Beta-carotene, and selenium) to people after they were already diagnosed with type 1 diabetes and also found that they had no effect in protecting the beta cells against the damage of free radicals (Ludvigsson et al. 2001). There is no evidence linking the anti-oxidants alpha- or beta-carotene levels and the development of type 1 related autoimmunity in another study as well (Prasad et al. 2011).
Uusitalo et al. (2008) also found that if pregnant women took anti-oxidants and trace minerals (including retinol, beta-carotene, vitamin C, vitamin E, selenium, zinc, or manganese) during pregnancy, there was no effect on the risk of the child's developing type 1-related autoimmunity. Czernichow et al. (2009) found that anti-oxidant supplements were not protective against metabolic syndrome, a group of conditions common in people with type 1 or 2 diabetes. Yet they also found that the people who had the highest levels of some anti-oxidants (beta-carotene, vitamin C, and vitamin E) in the beginning of the study, presumably due to a diet rich in plant foods, did have a lower risk of developing metabolic syndrome (see the types of diabetes page for information on the relationship between type 2 and type 1). While these studies did not find promising results concerning anti-oxidant supplements, they also did not find that these supplements did any harm. But wait, the story might be more complicated... Free radicals may play a role in the inflammatory process that destroys the beta cells in type 1 diabetes (Ludvigsson et al. 2001) (see the oxidative stress page for more information about its potential role in type 1 diabetes). Therefore, anti-oxidants have been thought to protect the body from oxidative stress due to the production of free radicals. But, there is some animal evidence that anti-oxidant supplements may also increase insulin resistance, showing that the relationship may not be so simple. When the researchers gave certain mice an anti-oxidant, they were more likely to become insulin resistant (Loh et al. 2009). Perhaps this finding could help explain why anti-oxidant supplements have not been found to be protective against type 1 diabetes (see the insulin resistance page for information on the role of increased insulin resistance in type 1 diabetes). Food processing: AGEsAdvanced Glycation End products (AGEs) are found in heat processed foods and have been linked to type 1 and type 2 diabetes in animal studies. They appear to predispose people to oxidative stress and inflammation, and may affect the fetus if the mother consumes them during pregnancy. A study has found that the level of AGEs that a mother eats are correlated with insulin levels in the baby. It found that if mothers have high AGE levels, and infant food is high in AGEs, it may raise the risk of diabetes in the offspring (Mericq et al. 2010).ProteinResearchers fed mother rats a diet that was deficient in protein, and found higher rates of diabetes in the offspring. They also found that one of the offspring's genes was "silenced"-- a gene associated with type 2 diabetes development. Nutrition, then, may have effects on gene expression that are linked to type 2 diabetes development (Sandovici et al. 2011). The bottom lineOmega-3 fatty acids may be protective against type 1 diabetes, but more studies would be necessary to confirm this finding. Eating high glycemic-index foods may accelerate the progression of type 1 diabetes, but this association should also be confirmed. Taking anti-oxidant supplements does not appear to reduce the risk of type 1 diabetes, but it is possible that a diet high in anti-oxidants may still be protective. |