A number of nutritional factors may influence the development of type 1 diabetes or type 1-related autoimmunity. One study has found, for example, that eating vegetables daily during pregnancy reduced the risk of a child's eveloping type 1-associated autoimmunity (Brekke and Ludvigsson 2010). However, other studies have not found associations between diet and type 1 diabetes development. For example, Virtanen et al. (2011) found only a weak protective effect of a few foods eaten during pregnancy and the development of type 1 related autoimmunity in the offspring (those foods were butter, low-fat margarine, berries, and coffee; most foods showed no association). Some additional dietary factors are either discussed below, or on other pages, such as breastfeeding or vitamin D.
Note that diet is linked to environmental chemical exposure: many chemicals enter our bodies via foods, such as pesticides (on or in the food), food packaging materials that leach out of packages into the food, or persistent chemicals that accumulate in the food chain. Numerous diets are associated with lower chemical exposure levels, such as: organic (Oates et al. 2014; Lu et al. 2006), fresh foods (limiting packaging) (Rudel et al. 2011), vegetarian (Ji et al. 2010), vegan (Arguin et al. 2010 Schecter et al. 2001), and the WHO recommended diet (Ax et al. 2014). Your nutrition can also impact the toxicity of environmental chemicals in your body (Hoffman et al. 2017).
Note also that the effects of diet can vary, depending on the person. A large study that measured glucose responses to consistent meals found highly variable responses by person (Zeevi et al. 2015). In other words, your diabetes may vary!
Norris 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 U.S. 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. In a subsequent study, the authors found that genetic factors may be one factor affecting this process (Norris et al. 2014).
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 her children (Fronczak et al. 2003). Another study from Norway also found that the mother's blood levels of fatty acids was not associated with the risk of type 1 diabetes in her children (Sørensen et al. 2012). And, a study from Finland also found no link between the mother's dietary intake of fatty acids during pregnancy and later type 1 diabetes development in her children (Niinistö et al. 2014).
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). Cod liver oil taken during the first year of life is also protective against type 1 diabetes (Stene et al. 2003).
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.
In U.S. children who already had developed both antibodies and type 1 diabetes, omega-3 intake was associated with higher residual insulin production (C-peptide levels). This implies that omega-3s may help preserve the functioning of the insulin-producing pancreatic beta cells over time, even in people who already have type 1 diabetes (Mayer-Davis et al. 2013).
In a case study, a 14 year old boy with new-onset type 1 diabetes was treated with high-doses of omega 3s and vitamin D. These seem to have helped preserve what was left of his beta cell function (Baidal et al. 2016).
A Swedish study found that higher fatty fish consumption was associated with a reduced risk of Latent Autoimmune Diabetes in Adults (LADA, i.e., type 1 diabetes in adults), but did not affect the risk of type 2 diabetes. Similar results were found with omega-3 intake and fish oil supplementation (Löfvenborg et al. 2014).
A group of people with metabolic syndrome (a group of conditions common in people with 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).
A prospective, randomized, double-blind, placebo-controlled clinical trial from Iran found that women with gestational diabetes who took omega-3s had better outcomes than those who did not, including better glucose levels, triglycerides, LDL-cholesterol, and HDL-cholesterol concentrations (Jamilian et al. 2015; Taghizadeh et al. 2016). A review of studies on fish oil supplements and gestational diabetes (which, for some reason, only included 2 studies...) found that DHA-enriched fish oil had no effect on gestational diabetes prevention, but did reduce insulin resistance in women with gestational diabetes. Not surprisingly, they conclude there is not enough evidence to support or refute the use of fish oil supplements during pregnancy (Ostadrahimi et al. 2016).
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). However, a very large study from around the world found that high fish intake during pregnancy (more than 3x per week) was associated with an increased risk of childhood obesity (Stratatkis et al. 2016). Whether this could be due to the chemicals in fish, I don't know...
Omega 3 fatty acids may also be protective against type 2 diabetes, according to a long-term study of Finnish men, even when mercury levels were taken into account (Virtanen et al. 2014). A randomized, controlled trial is now investigating whether omega 3s or curcumin (found in the spice turmeric) can prevent type 2 diabetes (Thota et al. 2016).
In laboratory animals, flax oil during pregnancy protects the offspring from the negative effects of maternal diabetes and high blood sugar in the womb (Correia-Santos et al. 2015; Correia-Santos et al. 2014). A proper fatty acid ratio during pregnancy and lactation can prevent diabetes in the offspring of NOD mice, an animal model of type 1 diabetes (Kagohashi and Otani 2015). Omega-3s also protect beta cells from the effects of a high-fat diet or chemicals that cause beta cell dysfunction and death (Wang et al. 2015). In rats, animals who received both vitamin D and omega 3 fatty acids had lower blood sugar levels than untreated rats after islet transplantation (Gurol et al. 2016).
The 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 an animal 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). In rats, fish oil contaminated with POPs-- despite overall beneficial effects-- led to lower antioxidant capacity and more oxidative stress as compared to uncontaminated oil (Hong et al. 2015). Whether the overall effects are positive or negative, it does appear that POPs reduce the healthy effects of fish oil.
DHA, one of the omega-3 fatty acids found in fish, appear to protect the immune system (in animals) from low-level mercury exposure, and may reduce the risk of autoimmune diseases associated with that exposure (Gill et al. 2014). A pilot study found that DHA supplementation is safe in infants with genetic risk of type 1 diabetes (Chase et al. 2015).
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. The FDA now recommends that pregnant and breastfeeding women eat fish that are low in chemicals such as mercury (Wenstrom et al. 2014).
Perfluorinated chemicals (PFCs, e.g., found in Scotchguard and teflon) are associated with lower essential fatty acids in pregnant women, vital to fetal growth (the female babies also weighed less) (Kishi et al. 2015). Whether this association is causal is not known, but would be alarming if so. In fact, animal studies are attempting to figure out mechanisms by which PFCs affect fatty acids in the fetus (e.g., Lee et al. 2015).
There is confusion over the links between saturated fats and health. While the general opinion is that saturated fats are "bad" for your health, the research is not so clear. Using heart disease as an example, recent studies have found no link between dietary saturated fats and heart disease. However, higher levels of saturated fat in your blood are related to an increased risk of heart disease, as well as type 2 diabetes. We might assume that the saturated fat in our diet would influence the saturated fat in our blood, but it appears that dietary carbohydrates may be even more important than dietary fats in determining blood fat levels. People with metabolic syndrome who consumed various diets, high or low carb and high or low saturated fat, showed no relation between fat consumption and blood fat levels, but did have a relation between a high carb diet and high fat in their blood (Volk et al. 2014).
All saturated fatty acids do not necessarily increase the risk of type 2 diabetes. Some types are associated with an increased risk, but others with a decreased risk (Forouhi et al. 2014). Rodents fed cream from pasture-raised cows had better metabolic outcomes than those fed regular cream, for example (Benoit et al. 2014). An interesting Swedish study found that high-fat dairy products (but not low-fat) actually were associated with a decreased risk of type 2 diabetes. Both high and low fat meat products were associated with an increased risk (Ericson et al. 2015). (Meat has been linked to type 2 diabetes in other studies as well; what exactly in the meat is problematic is still being worked out (Kim et al. 2015). Organic meat appears to be higher in beneficial fatty acids than commercial meat (Średnicka-Tober et al. 2016).
A higher consumption of omega 6 fatty acids has been linked to a lower risk of type 2 diabetes, in a study from Finland (Yary et al. 2016).
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).
In rodents, feeding them a high-fat diet is an easy way to make them obese. Saturated fats can cause inflammation, which in turn causes insulin resistance. Meanwhile, unsaturated fats do not (Wen et al. 2011).
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).
Different researchers have also found similar results-- that a high-fat diet in pregnant mice resulted in two generations of their offspring having a higher body size and increased insulin resistance. In the third generation, however, only the females developed the high body size, and only via their fathers (not mothers). Again, the changes were found to be associated with gene expression (Dunn and Bale, 2011).
Is sugar consumption linked to type 1 diabetes development? Most people think it is not, but some recent research may start to question that assumption. Babies introduced to sugar-sweetened beverages (including fruit juice) during the first year of life developed type 1 diabetes 5 months faster than children who started drinking these beverages at an older age (Crume et al. 2014). A long-term study from Colorado found that among those who had already developed autoimmunity or were of high genetic risk, sugar intake increased the risk of developing type 1 diabetes. Sugar intake was not associated with the original development of autoimmunity however, implying that sugar may exacerbate the later stage development of type 1 (Lamb et al. 2015). Also, daily intake of more than 2 sweetened beverages per day is associated with the development of LADA, Latent Autoimmune Diabetes in Adults (essentially type 1 but in adults), as well as type 2 diabetes (Löfvenborg et al. 2016).
The 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, gestational diabetes, 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). U.S. adolescents with higher added sugar intake had a higher risk of metabolic syndrome, no matter their BMI, total calorie intake, or physical activity level (Rodríguez et al. 2016). The consumption of sugar-sweetened soft drinks (but not diet soft drinks) prior to pregnancy is associated with an increased risk of gestational diabetes (Donazar-Ezcurra et al. 2017).
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). Goran et al. (2013) review the evidence that high fructose exposure during development (in the womb and during infancy) can "act as an obesogen by affecting lifelong neuroendocrine function, appetite control, feeding behaviour, adipogenesis, fat distribution and metabolic systems. These changes ultimately favour the long-term development of obesity and associated metabolic risk." In lab animals, fructose causes high blood sugar, glucose intolerance, decreased insulin secretion, and increased glucagon secretion (showing it affects both beta cells and alpha cells in the pancreas) (Asghar et al. 2016).
A pretty convincing intervention study found that replacing fructose/sugars with other starchy carbohydrates (like bread) improved metabolism in children in just 10 days, including lower blood pressure, weight, triglycerides, and LDL cholesterol. Glucose tolerance improved, as did insulin levels. Sugar levels were reduced from 28% of calories (!) to 10%, so not even eliminated, just reduced. The children in this study were obese or had metabolic syndrome (Lustig et al. 2015).
Chemical artificial sweeteners can increase glucose intolerance by changing the gut microbiota in mice-- and humans as well (Suez et al. 2014).
A systematic review of human and animal studies found that overall, using low-energy sweeteners in place of sugar tens to lead to lower caloric intake and lower body weight in both children and adults (Rogers et al. 2015).
Dietary intake of fiber in early life is not associated with the development of autoimmunity or type 1 diabetes, according to a large international longitudinal study (the TEDDY study) (Beyerlein et al. 2015).
However, in mice, a high fiber diet produced fatty-acids that were protective against type 1 diabetes development (Mariño et al. 2017).
Fiber is also linked to a reduced risk of type 2 diabetes (InterAct Consortium 2015).
Numerous studies have found that higher coffee consumption is associated with a lower risk of type 2 diabetes-- animal studies also show a protective effect, involving multiple mechanisms (Akash et al. 2014; Muley et al. 2012). Decaf coffee and caffeinated tea have also been associated with a decreased risk (Huxley et al. 2009), although another study found that only green tea -- not black tea -- was associated with a decreased risk (Iso et al. 2006).
However, coffee consumption may be associated with an increased risk of autoimmunity and type 1 diabetes in adults (latent autoimmune diabetes in adults, LADA) (Löfvenborg et al. 2014). And, maternal intake of caffeine during pregnancy is associated with an increased risk of obesity in the offspring (Li et al. 2014).
Chocolate, meanwhile, protects pancreatic beta cells and reduces insulin resistance and high blood sugar, delaying diabetes -- at least in rats (Fernández-Millán et al. 2015). In a large, long-term study of physicians, the more chocolate eaten (well, up to 2 servings per week), the lower the risk of type 2 diabetes-- although only in younger and normal body-weight men (Matsumoto et al. 2015). And even better-- children with type 1 diabetes who ate dark chocolate (25 grams, 2-5 times/week) had better blood sugar control than those who ate milk chocolate or no chocolate (Scaramuzza and Zuccotti, 2015).
Moderate alcohol consumption is associated with a reduced risk of type 2 diabetes (Knott et al. 2015). As for adult-onset type 1, it's more complicated. Moderate alcohol consumption is associated with a reduced risk of insulin resistance, but a higher risk of autoimmunity. Overall, the risk of adult-onset type 1 was lower with more alcohol consumption, but that only held true in people with low antibody levels (Rasouli et al. 2014). Note that chronic alcohol consumption increases the risk of type 2 diabetes (Kim et al. 2015).
While many metals can be toxic at high levels, they can be necessary for life in very low levels (e.g., calcium, iron, etc.). (See the heavy metals page for a discussion of metal exposures at higher levels; the levels discussed here are all at very low levels, in the trace level range).
A few studies have found that higher zinc levels in drinking water (again, not TOO high-- still in the trace level range), 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 (Samuelsson et al. 2011). And a study form Canada found that zinc and calcium intakes during the year before diagnosis were marginally protective against type 1 diabetes risk in youth (Benson et al. 2010). In Sardinia, Italy, trace elements like zinc, copper, chromium, manganese in stream sediments were associated with a lower risk of type 1 diabetes (Valera et al. 2015).
While not all studies have found a link between type 1 and zinc (e.g., Estakhri et al. 2011), an overall review of the evidence linking zinc to both type 1 and type 2 diabetes-- a link that has been suggested for almost 70 years-- suggests that zinc may be a potential therapy for both diabetes prevention and blood glucose control (Chimienti 2013).
Among people who already have type 1 diabetes, lower zinc levels and higher copper levels were correlated with higher blood glucose levels (a higher HbA1c). In addition, people with type 1 had lower zinc and higher copper levels than those without diabetes (Lin et al. 2014). A different study, this one of Greek children and adolescents with type 1 diabetes, found that those with lower magnesium levels had a higher HbA1c (Galli-Tsinopoulou et al. 2014). An Egyptian study also found that children with type 1 diabetes have low magnesium levels as well as a higher HbA1c and cholesterol levels (Shahbah et al. 2016).
A study compared trace metal levels in people with type 1 diabetes, type 2 diabetes, and without diabetes. They found that those with type 1 diabetes had lower levels of chromium, manganese, nickel, lead, and zinc, and those with type 2 diabetes had lower levels of chromium, manganese, and nickel, as compared to people without diabetes (Forte et al. 2013). Additional studies have also found associations between various trace element levels in people with type 2 diabetes vs those without diabetes (Hansen et al. 2017; Simić et al. 2017; Zhang et al. 2017). Low magnesium levels have been linked to pre-diabetes in Dutch adults, for example (Kieboom et al. 2017), and low chromium levels linked to type 2 diabetes and pre-diabetes in Chinese adults (Chen et al. 2017).
In laboratory animals, the gasoline additive MTBE interferes with zinc and glucose levels in rats (Saeedi et al. 2016).
A study from Denmark found that zinc levels at the time of birth were not associated with the later development of type 1 diabetes (Kyvsgaard et al. 2016).
A study found that higher iron intake (via infant formula or supplements) in the first four months of life was associated with a higher risk of developing type 1 diabetes (Ashraf et al. 2010).
Higher iron levels during pregnancy are linked to glucose intolerance in the mother (Zein et al. 2014) and gestational diabetes (Bowers et al. 2016; Fernández-Cao et al. 2016; Khambalia et al. 2015; McElduff 2017; Rawal et al. 2017).
Meanwhile higher calcium intake is associated with a lower risk of gestational diabetes (Osorio-Yáñez et al. 2016).
Nicotinamide 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. Pregnant women with type 1 diabetes have a higher risk of complications if they are deficient in vitamin C (Juhl et al. 2017). And, vitamin supplements during pregnancy do not appear to be associated with the offspring's risk of developing celiac disease (an autoimmune condition common in people with type 1 diabetes) (Yang et al. 2017).
Czernichow et al. (2009) found that anti-oxidant supplements were not protective against metabolic syndrome. 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.
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.
For type 2 diabetes and obesity, a review finds "marginal" benefits for supplementing with antioxidants including zinc, lipoic acid, carnitine, cinnamon, green tea, and possibly vitamin C plus E. The evidence is weaker for supplementing with omega-3s, coenzyme Q10, green coffee, resveratrol, and lycopene (Abdali et al. 2015).
Folic acid (folate), a B vitamin, when given to pregnant and lactating rats in high doses, caused insulin resistance in their offspring (Keating et al. 2015). In humans, folic acid supplements in early pregnancy may increase the risk of gestational diabetes (Zhu et al. 2016). (Since folic acid also decreases the risk of certain birth defects, it may be important to have the right amount. Ask your doctor please).Advanced Glycation End products (AGEs) are found in heat processed foods such as grilled meat, 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). Another study has found that AGEs may also increase the risk of metabolic syndrome in mice as well as humans (Cai et al. 2014).
I do not have time to review all the food additives linked to diabetes or obesity. I will mention that MSG is a potential obesogen (Shannon et al. 2016). DOSS, another food additive (and a laxative, and an oil dispersant), is also a potential obesogen (Bowers et al. 2016).
Some authors argue that food additives (including glucose, salt, emulsifiers, organic solvents, gluten, microbial transglutaminase, and nanoparticles) increase intestinal permeability, activate autoimmunity, and are responsible for the increasing incidence of autoimmune disease (Lerner and Matthias 2015).
Dangerous Fruit: Mystery of Deadly Outbreaks in India Is Solved (by Ellen Barry, 2017, New York Times), describes how kids were dying -- with very low blood sugar-- and it turns out it was caused by eating lychee (litchi) fruit on an empty stomach. Apparently lychee fruit contain chemicals (hypoglycin) that inhibit the body's ability to synthesize glucose, causing low blood sugar, and in some cases leading to death (Shrivastava et al. 2017).
van Abeelen et al. 2012). If mothers experienced the famine while pregnant, their offspring show impaired insulin secretion and lower glucose tolerance in their 50s (de Rooj et al. 2006a; de Rooij et al. 2006b; Ravelli et al. 1998). The offspring also seem to prefer fatty foods in adulthood, although their total caloric intake was not different (Lussana et al. 2008). Their female offspring also had a higher risk of increased weight and more fat deposition later in life (Stein et al. 2007), as well as higher cholesterol levels and triglycerides (Lumey et al. 2009). For some health effects, the risk varied depending on the time during pregnancy that the famine occurred (e.g., 1st vs 3rd trimester). But for type 2 diabetes, the risk was increased during any period of gestation (Roseboom et al. 2011).
In a study of the Ukraine famine, the more severe the famine during pregnancy, the higher the risk of type 2 diabetes in the offspring. Early gestation seems to be the most susceptible time (Lumey et al. 2015). In a study of the Chinese famine of 1959-62, those exposed to famine during fetal life or childhood had a higher risk of diabetes and higher average blood sugar levels (HbA1c) in adulthood than those unexposed. Those exposed during adolescence or adulthood did not have a higher risk after adjusting for other factors (Wang et al. 2017). In Bangladesh, young adults exposed to famine prenatally were underweight but still had higher blood glucose levels after a meal. Those exposed to famine after birth were more likely to be overweight, and had higher fasting blood glucose levels (Finer et al. 2016).
Researchers are now looking into whether these effects continue to the 2nd generation, that is, the grandchildren of women who were pregnant during the famine. They have found that the children of fathers (who were exposed in the womb) were heavier and more obese than those unexposed (Veenendaal et al. 2013). A study from China found that prenatal exposure to famine was associated with high blood glucose and type 2 diabetes in the first generation, and high blood glucose in the second generation of offspring as adults-- especially if both parents were exposed in the womb (Li et al. 2016).
One more interesting finding is that excess food during a boy's "slow growth period" (before puberty) is associated with an increased death rate from diabetes in his grandchildren (but only his son's children, not his daughter's). This evidence is from studies done in the Överkalix region in Sweden, using data collected since the 1890s. Some sort of nutrition-linked mechanism passed through the male line is likely the cause, but we don't know what it is (Kaati et al. 2002). This 2014 article in the science journal Nature describes this and other studies, and explains a possible link with epigenetic mechanisms: Epigenetics: The sins of the father (Hughes 2014).
In animals, we can also see the effects of famine, or at least lower food consumption. Primates whose mothers ate less food during pregnancy, but then a normal diet after birth, had higher fasting glucose, fasting insulin, and insulin resistance-- in all, metabolic changes that could predispose them to type 2 diabetes (Choi et al. 2011). The authors note that these results are similar to those found in rodents and sheep as well. In sheep in fact, the grand-piglets of sheep who experienced too much or too little food during pregnancy had metabolic effects such as excess weight and lipid disturbances. In other words, these effects may be able to be passed down to multiple generations (Gonzalez-Bulnes et al. 2014).
To mimic malnutrition in rodents, researchers can use a protein-deficient diet. When researchers fed mother rats such a diet, they 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). Interestingly, the offspring of mother mice fed a low protein diet have both lower body weight/fat mass and higher food intake throughout life than controls. The researchers found that these changes were associated with gene expression (Jousse et al. 2011).
Animals experiments also show that the risk of obesity and diabetes can be affected by the nutrition of prior generations. Both obesity and malnutrition can increase the risk of diabetes in grandchildren of lab rats. Malnutrition through the maternal line had a stronger effect than obesity through the paternal line (Hanafi et al. 2015).
If prior generations have experienced under-nutrition for multiple generations (50, in this case), undernourished rats have low birth weight, insulin resistance, and higher visceral fat, higher insulin levels, and higher susceptibility to chemical-induced diabetes. These abnormalities are not reversed after 2 generations of normal nutrient feeding. Again, epigenetic mechanisms may be behind this pattern (Hardikar et al. et al. 2015).
On the other hand, another animal experiment shows that if mothers experience a change of diet that promotes obesity, their children will be fatter, not surprisingly. However the grandchildren and great-grandchildren seem to recover from the obesity, no matter what their diet. That implies there is some possibility of reversing these trends (Tait et al. 2015). Similarly, if mothers have an obesity-promoting diet while pregnant, their offspring have worse outcomes, but when they receive a normal diet after birth, they partially recover (Li et al. 2015).
In mice, a 4-day fast-mimicking diet helped to regenerate beta cells, in mouse models of both type 1 and type 2 diabetes, as well as in human islet cells from people with type 1 diabetes (Cheng et al. 2017).
Omega-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.
To download or see all the references on this and other diet-related pages, including breastfeeding, cow's milk, gluten, and more, see the collection Diet, nutrition, gut, microbiome and diabetes/obesity in Pubmed.