Diabetes & Holistic Medicine


How to Treat the Root Cause of Diabetes

Image Credit: Sally Plank

After about age 20, we may have all the insulin-producing beta cells we’re ever going to get. So, if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It’s not just any fat; it’s saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a resultof free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren’t just based on test tube studies. When researchers have infused fat directly into people’s bloodstreams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by “defects in both insulin secretion and insulin action,” and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics; so, their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, “insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat].” This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. “[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action,” contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn’t just toxic to the pancreas. The fats found predominantly in meat and dairy—chicken and cheese are the two main sources in the American diet—are considered nearly “universally toxic.” In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So, either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It’s not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, “may contribute to the development of insulin resistance and its clinical consequences.” After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So, what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn’t develop lung cancer, everyone who eats a lot of saturated fat doesn’t develop diabetes—there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.

The reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance may be because saturated fats appear to impair blood sugar control the most.

The association between fat and insulin resistance is now widely accepted. Insulin resistance is due to so-called ectopic fat accumulation, the buildup of fat in places it’s not supposed to be, like within our muscle cells. But not all fats affect the muscles the same. The type of fat, saturated vs. unsaturated, is critical. Saturated fats like palmitate, found mostly in meat, dairy, and eggs, cause insulin resistance. But oleate, found mostly in nuts, olives, and avocados, may actually improve insulin sensitivity.

What makes saturated fat bad? Saturated fat causes more toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals, and inflammation, establishing a vicious cycle of events in which saturated fat induces free radicals, causes dysfunction in the little power plants within our muscle cells (mitochondria)—which then causes an increase in free radical production, and an impairment of insulin signaling. I explain this in my video Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation from saturated fat has been demonstrated to raise insulin resistance through free radical production. Saturated fat also has been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacylglycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance, the cause of type 2 diabetes.

While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create toxic breakdown products like ceramide that causes lipotoxicity. Lipo– meaning fat, as in liposuction. This fat toxicity in our muscles is a well-known concept in the explanation of triggers for insulin resistance.

I’ve talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer, and heart disease. But, they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources, while trans fats originate in meat and milk, in addition to partially hydrogenated and refined vegetable oils.

That’s why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. In a study done by Swedish researchers, insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.

We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst. But, they don’t just lead to inhibition of insulin signaling, the activation of inflammatory pathways, and the increase in free radicals; they also cause an alteration in gene expression. This can lead to a suppression of key mitochondrial enzymes, like carnitine palmitoyltransferase, which finally solves the mystery of why those eating vegetarian have a 60% higher expression of that fat-burning enzyme. They’re eating less saturated fat.

So, do those eating plant-based diets have less fat clogging their muscles, and less insulin resistance too? There haven’t been any data available regarding the insulin sensitivity, or inside-the-muscle-cell fat of those eating vegan or vegetarian—until now. Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Those eating plant-based diets have the unfair advantage of being much slimmer; so, they found omnivores who were as skinny as vegans, to see if plant-based diets had a direct benefit—as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.

They found significantly less fat trapped in the muscle cells of vegans compared to omnivores at the same body weight, better insulin sensitivity, better blood sugar levels, better insulin levels, and, excitingly, significantly improved beta cell function (the cells in the pancreas that make the insulin). They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that plant-based diets are beta cell-protective as well, helping also to prevent our seventh leading cause of death, diabetes.

This is the third of a three-part series, starting with What Causes Insulin Resistance? and The Spillover Effect Links Obesity to Diabetes.

Even if saturated fat weren’t associated with heart disease, its effects on pancreatic function and insulin resistance in the muscles would be enough to warrant avoiding it. Despite popular press accounts, saturated fat intake remains the primary modifiable determinant of LDL cholesterol, a leading risk factor for our leading killer–heart disease. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

How low should we shoot for in terms of saturated fat intake? As low as possible, according to the U.S. National Academies of Science Institute of Medicine: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

How Exactly Does Type 2 Diabetes Develop?

Insulin resistance is the cause of both prediabetes and type 2 diabetes. Ok, so what is the cause of insulin resistance? Insulin resistance is now accepted to be closely associated with the accumulation of fat within our muscle cells. This fat toxicity inside of our muscles is a major factor in the cause of insulin resistance and type 2 diabetes, as it interferes with the action of insulin. I’ve explored how fat makes our muscles insulin resistant (see What Causes Insulin Resistance?), how that fat can come from the fat we eat or the fat we wear (see The Spillover Effect Links Obesity to Diabetes), and how not all fats are the same (see Lipotoxicity: How Saturated Fat Raises Blood Sugar). It’s the type of fat found predominantly in animal fats, relative to plant fats, that appears to be especially deleterious with respect to fat-induced insulin insensitivity. But this insulin resistance in our muscles starts years before diabetes is diagnosed.

In my video, Diabetes as a Disease of Fat Toxicity, you can see that insulin resistance starts over a decade before diabetes is actually diagnosed, as blood sugar levels slowly start creeping up. And then, all of the sudden, the pancreas conks out, and blood sugars skyrocket. What could underlie this relatively rapid failure of insulin secretion?

At first, the pancreas pumps out more and more insulin, trying to overcome the fat-induced insulin resistance in the muscles, and high insulin levels can lead to the accumulation of fat in the liver, called fatty liver disease. Before diagnosis of type 2 diabetes, there is a long silent scream from the liver. As fat builds up in our liver, it also becomes resistant to insulin.

Normally, the liver is constantly producing blood sugar to keep our brain alive between meals. As soon as we eat breakfast, though, the insulin released to deal with the meal normally turns off liver glucose production, which makes sense since we don’t need it anymore. But when our liver is filled with fat, it becomes insulin resistant like our muscles, and doesn’t respond to the breakfast signal; it keeps pumping out blood sugar all day long on top of whatever we eat. Then, the pancreas pumps out even more insulin to deal with the high sugars, and our liver gets fatter and fatter. That’s one of the twin vicious cycles of diabetes. Fatty muscles, in the context of too many calories, leads to a fatty liver, which leads to an even fattier liver. This is all still before we have diabetes.

Fatty liver can be deadly. The liver starts trying to offload the fat by dumping it back into the bloodstream in the form of something called VLDL, and that starts building up in the cells in the pancreas that produce the insulin in the first place. Now, we know how diabetes develops: fatty muscles lead to a fatty liver, which leads to a fatty pancreas. It is now clear that type 2 diabetes is a condition of excess fat inside our organs, whether we’re obese or not.

The only thing that was keeping us from diabetes – unchecked skyrocketing blood sugars – is that the pancreas was working overtime pumping out extra insulin to overcome insulin resistance. But as the so-called islet or Beta cells in the pancreas are killed off by the fatty buildup, insulin production starts to fail, and we’re left with the worst of both worlds: insulin resistance combined with a failing pancreas. Unable to then overcome the resistance, blood sugar levels go up and up, and boom: type 2 diabetes.

This has implications for cancer as well. Obesity leads to insulin resistance and our blood sugars start to go up, so our pancreas starts pumping out more insulin to try to force more sugar into our muscles, and eventually the fat spills over into the pancreas, killing off the insulin-producing cells. Then, we develop diabetes, in which case we may have to start injecting insulin at high levels to overcome the insulin resistance, and these high insulin levels promote cancer. That’s one of the reasons we think obese women get more breast cancer. It all traces back to fat getting into our muscle cells, causing insulin resistance: fat from our stomach (obesity) or fat going into our stomach (saturated fats in our diet).

Now, it should make sense why the American Diabetes Association recommends reduced intake of dietary fat as a strategy for reducing the risk for developing diabetes.




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 breastfeedingor 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); certain dietary components, such as omega 3 fatty acids, can counteract pollution-induced inflammation, for example (Hennig et al. 2018).
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!

Omega-3 Fatty Acids

Type 1 Diabetes

A trial of pregnant women with type 1 diabetes found that those given supplements of omega-3 fatty acids showed an increase in beta cell function over the course of the pregnancy (as measured by fasting c-peptide levels), as compared to those who did not take supplements (Horvaticek et al. 2017)! Meanwhile, the fatty acid levels of infants were associated with the later development of type 1 diabetes-related autoimmunity. Specifically, fatty acids derived from fish may be protective, as are those consumed via breastmilk as well. Higher omega-6 to omega-3 ratios were associated with an increased risk (Niinistö et al. 2017).
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). A meta-analysis found that omega-3 or omega-6 fatty acid supplementation in children did not affect the overall risk of preclinical or clinical type 1 diabetes, although omega-3 fatty acid intake in early life might reduce the risk of preclinical type 1 (Liu et al. 2018).
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.
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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). In another case study, An 8 year old child took high-dose vitamin D and omega-3 fatty acids, and shows near-normal blood sugar levels 1.5 years after diagnosis, only taking 1.5-2 units of insulin per day (Cadario et al. 2017). The same authors found success with at least one other person as well (Cadario et al. 2018).
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).
Fish oil may also be helpful for treatment of diabetic neuropathy (Lewis et al. 2017Mirhashemi et al. 2016; Yorek 2017).

Metabolic Syndrome, Type 2 Diabetes, Gestational Diabetes, and Obesity

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). Another trial, of people with type 2 diabetes, found that omega 3s improved lipid levels and inflammation (Mazaherioun et al. 2017).
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. 2017Jamilian et al. 2015Taghizadeh 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… Another study from Mexico found that higher levels of omega-3s and omega-6s during pregnancy were associated with lower height (but not other metabolic measures, e.g., not glucose levels etc.) in offspring around the time of puberty (Al-Hinai et al. 2018). Again, I don’t know what would explain this finding.
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).

Diabetes Complications

Omega-3 fatty acid supplementation for 12 weeks in people with diabetic nephropathy had favorable effects on insulin levels, triglycerides and cholesterol (Soleimani et al. 2017).

Laboratory Studies

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. 2015Correia-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). Another study of NOD mice also shows that omega 3s drastically reduce the development of diabetes, blocked autoimmunity, and normalized glucose levels (Bi et al. 2017). 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).

Chemicals and Omega-3s

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).
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.

Other Fats

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). Actually, an analysis of the data from 20 prospective studies on omega 6s found that linoleic acid (found in nuts and vegetable oils) has long-term benefits for the prevention of type 2 diabetes (Wu et al. 2017).
Higher levels of certain trans fats are associated with a higher risk of diabetes in U.S. adults, as well as higher glucose and insulin levels, higher insulin resistance, and higher HbA1c (a measure of long-term blood glucose control) (Liu et al. 2018). 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).

Laboratory Studies

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).
Another fatty acid found in many foods, butyric acid, can cause detrimental effects on liver cells and pancreatic beta cells (alone, and in conjunction with arsenic). The diabetes medication metformin may be protective against these effects (Ahangarpour et al. 2017).

Sweeteners and The Glycemic Index

Type 1 Diabetes

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

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).

Type 2 Diabetes, Obesity, and Metabolic Syndrome

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). Another meta-analysis found that sugar-sweetened beverages are associated with higher fasting glucose and insulin levels (McKeown et al. 2017). The intake of these beverages is also associated with coronary heart disease (Malik 2017). 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).

What about sugar?

For the latest science on the effects of sugar, fructose, HFCS, sugar-sweetened beverages on health– including diabetes and obesity, see:


a website developed and maintained by scientific researchers in the field.
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). Additional studies by the same authors found that the children had improved markers of cardiovascular risk (Gugliucci et al. 2017), and developed less liver fat, less visceral fat, and better insulin function (Schwarz et al. 2017).
Some researchers suggest that reducing added sugar by 20% in the U.S. would yield $10 billion in lower medical costs by 2035, and significantly lower the incidence of type 2 diabetes, heart disease, liver disease, and obesity (Vreman et al. 2017).

Artificial Sweeteners

A systematic review of human and animal studies found that overall, using low-energy sweeteners in place of sugar tends to lead to lower caloric intake and lower body weight in both children and adults (Rogers et al. 2015). However, there may be other health effects. For example, chemical artificial sweeteners can increase glucose intolerance by changing the gut microbiota in mice– and humans as well (Suez et al. 2014). Also in mice, artificial sweeteners can cause body weight gain (Bian et al. 2017). In humans, maternal consumption of artificially sweetened beverages during pregnancy is associated with a higher risk of offspring obesity/overweight at age 7 (Zhu et al. 2017).

Fruit, Vegetables, and Fiber

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).
Fresh fruit consumption, meanwhile, has been linked to a lower risk of diabetes in Chinese adults, as well as a lower risk of death or complications in those with diabetes (Du et al. 2017).
Children who ate a diet high in vegetables and grains, and low in refined cereals and sweet beverages during early childhood had a reduced risk of celiac disease (which is common in people with type 1 diabetes) (Barroso et al. 2018).

Low Blood Sugar from Lychee Fruit– Huh?

This isn’t diabetes but it is pretty interesting. The article, 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).

The Good News: Coffee, Chocolate, and Alcohol!

Numerous studies have found that higher coffee consumption is associated with a lower risk of type 2 diabetes, and animal studies also show a similarly protective effect (Akash et al. 2014Carlström and Larsson 2018Muley 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)– at least in people with higher genetic risk of type 1 (Rasouli et al. 2018). Interestingly, coffee has different associations with different autoimmune diseases, in that it is associated with a decreased risk of some and increased risk of others (Sharif et al. 2017). Coffee is also associated with a higher risk of metabolic syndrome in people with type 1 diabetes (Stutz et al. 2018). And, maternal intake of caffeine during pregnancy is associated with an increased risk of obesity in their children (Li et al. 2014). In rats, maternal intake of caffeine during pregnancy reduces beta cell mass, but increased glucose tolerance in adult offspring, especially female offspring (Kou et al. 2017).
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; Martin et al. 2016). 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). A review of the use of dark chocolate in people with diabetes finds that it may slowing the progression to type 2 diabetes, lessen insulin resistance, and help prevent cardiovascular complications in people with diabetes (Shah et al. 2017).
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).
Resveratrol, the stuff found in red wine, has been found to help ameliorate the progression of autoimmune diseases in some cases (Oliveira et al. 2017).

Zinc and Other Trace Elements

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 metalspage 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), overall reviews 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; Maret 2017).
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). Another Egyptian study found that children with type 1 diabetes have low levels of various trace elements, including selenium, zinc, magnesium, and copper (Alghobashy et al. 2018).
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. 2017Simić et al. 2017; Zhang et al. 2017). In people with type 2 diabetes, trace element levels are linked to lipid levels (Wolide 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). These minerals may interact with other dietary factors to influence risk. For example, higher magnesium intake is linked to a lower risk of type 2 diabetes, especially in people with a poorer quality diet (low fiber, higher glycemic index) (Hruby et al. 2017).
In laboratory animals, the gasoline additive MTBE interferes with zinc and glucose levels in rats (Saeedi et al. 2016). Also in rodents, zinc helps prevent diabetes-induced kidney damage (Yang et al. 2017).
High iron levels or iron metabolism markers are associated with type 2 diabetes (Huth et al. 2015; Orban et al. 2014), diabetes complications (Mojiminiyi et al. 2008), as well as with insulin resistance in people without diabetes (Krisai et al. 2016).

Exposure During Development

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). Another found higher iron levels in blood around the time of birth was associated with a higher risk of developing type 1 by age 16 (Kyvsgaard et al. 2017). A review found that dietary iron was associated with an increased risk of type 1 diabetes, but not iron in drinking water (Søgaard et al. 2017).

Gestational Diabetes

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 and Other Vitamins and Antioxidants

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).
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). However dietary intake of antioxidants is associated with a reduced risk of type 2 diabetes, although once people reached a certain level, there was a plateau where more wasn’t better (Mancini 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.
For people with diabetes and kidney disease, high doses of vitamin E had beneficial effects on markers of kidney injury, inflammation, and oxidative stress, but did not affect fasting blood glucose or insulin resistance (Khatami et al. 2016).

Other Vitamins

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). Another study also found high folate and low vitamin B12 levels during pregnancy were associated with gestational diabetes (Lai et al. 2017). (Since folic acid also decreases the risk of certain birth defects, it may be important to have the right amount. Ask your doctor please).
A deficiency in vitamin A causes high blood sugar and loss of pancreatic beta cells in adult mice (Trasino et al. 2015).

Food Processing: AGEs and Food Additives

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). In animals, a diet with lower levels of AGEs during development protects the pancreas islet cells as compared to a diet with higher AGE levels (Borg et al. 2017). Another study found that AGEs may also increase the risk of metabolic syndrome in mice as well as humans (Cai et al. 2014).

Heating food can also produce acrylamide, a toxic chemical used in industry, found in cigarette smoke, and also sometimes found in food such as potato chips and french fries. It is associated with lower insulin levels in US adults (Lin et al. 2009). Industrial workers exposed to higher levels of acrylamide have higher rates of death from diabetes (Swaen et al. 2007). Exposing young rats to acrylamide decreased beta cell mass and increased alpha cell mass (Stošić et al. 2018).
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). A review of food additives finds that many of them have effects on the immune system that could contribute to metabolic disease like diabetes, obesity, or metabolic syndrome (Paula Neto et al. 2017).
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).

Feast, Famine, or Fast

Most of us are not worried about famine anymore (crossing fingers), but there are some interesting studies that show that experiencing a famine in early life can increase the risk of type 2 diabetes later in life. The Dutch famine during 1944-45 provided an opportunity to study this phenomenon. People who were children during this famine have an increased risk of type 2 diabetes later in life (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).

Transgenerational Effects

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).

Laboratory Studies

In animals, we can also see the effects of famine, or at least lower food consumption. In rodents, prenatal food restriction followed by a high-fat diet after weaning led to numerous changes in metabolism, including insulin levels, changes in islet cells, and glucose intolerance (Xiao et al. 2017). 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).

Feast AND Famine

In some developing countries, mothers may be both undernourished (in micronutrients) and overnourished (with gestational diabetes), exposing the offspring to increased disease risk through multiple pathways. These factors may play a role in the diabetes epidemic in India, for example (Krishnaveni and Yajnik 2017).

The Bottom Line

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.
Diabetes Care. 2012 Apr;35(4):930-8. doi: 10.2337/dc11-1869.

Fish Consumption and Incidence of Diabetes: meta-analysis of data from 438,000 individuals in 12 independent prospective cohorts with an average 11-year follow-up.



Ecological data suggest an inverse correlation between fish consumption and diabetes prevalence. However, epidemiological data on fish intake and diabetes incidence are controversial and inconclusive. Therefore, we aimed to assess the literature and determine the association between fish consumption and diabetes risk quantitatively.


Prospective cohort studies published through August 2011 in peer-reviewed journals indexed in PubMed were selected. Additional information was retrieved through Google or a hand search of the references from relevant articles. The weighted relative risk (RR) and corresponding 95% CI for incident diabetes was estimated using random-effects models.


A database was derived from nine eligible studies (12 independent cohorts), including 438,214 individuals with an average 11.4-year follow-up. Compared with those who never consumed fish or ate fish less than once per month, the pooled RR of incident diabetes was 0.99 (95% CI 0.85-1.16) for individuals who ate fish five or more times per week (P(trend) = 0.80). Similar results were found for long-chain n-3 polyunsaturated fatty acid intake. Study location was an effect modifier. An inverse association between fish intake and diabetes incidence was found by combining studies conducted in Eastern but not Western countries.


Accumulated evidence generated from this meta-analysis does not support an overall inverse association of fish or fish oil intake with incidence of diabetes. The null association was modified by study location (Eastern vs. Western countries), which may reflect the possible difference between Eastern and Western dietary patterns. Further studies are warranted.



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