Diabetes mellitus is a chronic disease caused by too much sugar (glucose) in the blood. Blood sugar levels rise when there is not enough insulin in the blood, or the insulin that is in the blood does not work properly. Insulin is an important hormone secreted by the beta cells of the islets of Langerhans in the pancreas. It regulates blood sugar levels by, for example, promoting the uptake of glucose into the cells. When things go wrong, high levels of glucose in the blood can cause damage to the nerves and blood vessels. Without treatment diabetes can lead to long-term health problems including kidney failure, gangrene, sensory loss, ulceration, blindness, cardiovascular disease and stroke.
There are two main types of diabetes; type 1 and type 2. A third type of diabetes, gestational diabetes, develops in some women during pregnancy but usually disappears after giving birth. Type 1 (insulin-dependent diabetes) occurs when the body produces little or no insulin. People who have type 1 diabetes must check the levels of glucose in their blood regularly and will need treatment for the rest of their lives. Type 1 diabetes is sometimes called juvenile-onset diabetes because it tends to develop before the age of 40, often in the teenage years. The peak age for diagnosis in the UK is between 10 and 14 years but is becoming younger with a steep rise in the under-fives (Williams and Pickup, 2004). Over the past 60 years, the worldwide incidence of type 1 diabetes has been increasing by 3-5 per cent per year, doubling approximately every 20 years with a rapid increase in the number of very young children affected (TEDDY Study Group, 2008). Symptoms include a frequent urge to urinate, extreme thirst and hunger, weight loss, fatigue, irritability and nausea. The cause of type 1 diabetes is poorly understood, but evidence suggests it involves a combination of genetic factors and environmental triggers. Type 1 diabetes is usually treated with regular injections of insulin to regulate blood sugar levels.
Type 2 diabetes occurs either when the body does not produce enough insulin or when it cannot use the insulin produced. This type of diabetes is linked with obesity. If you are overweight or obese (you have a body mass index of 30 or more), you are at greater risk of developing type 2 diabetes. In particular, fat around your abdomen (tummy) puts you at increased risk because it releases chemicals that can upset the body’s cardiovascular and metabolic systems (NHS Choices, 2012m). Type 2 diabetes occurs mostly in people over the age of 40, but is now increasingly affecting people at a much younger age.
The main symptoms are common to both types of diabetes: feeling very thirsty, urinating frequently, particularly at night, feeling very tired and weight loss with loss of muscle bulk. Other symptoms of type 2 diabetes include: itchiness around the vagina or penis, or regular bouts of thrush (a yeast infection), blurred vision that is caused by the lens of your eye becoming very dry, cramps, constipation and skin infections. Not all symptoms occur and those that do might be subtle and may go unnoticed for years. Blood sugar levels in type 2 diabetes can be controlled by lifestyle changes including regular exercise coupled to diet control and weight loss.
Type 1 diabetes is an autoimmune disease where the immune system’s ‘soldiers’, known as T-cells, destroy the body’s own insulin-producing beta cells in the pancreas. This type of response is thought to involve a genetic predisposition (diabetes in the family) coupled to an environmental trigger.
In the UK, about 90 per cent of all adults with diabetes have type 2 diabetes. While rising obesity levels have contributed to the increase in the incidence of type 2 diabetes, the increase in obesity does not explain the huge increase in the number of cases of type 1 diabetes seen over the last few decades. The number of under-fives with Type 1 diabetes has increased fivefold over 20 years (Gillespie et al., 2004). Furthermore, new research shows that the UK now ranks fifth out of 88 countries in the incidence of type 1 diabetes in children. A league table compiled by the charity Diabetes UK from data from the International Diabetes Federation shows that Finland tops the international league table with a rate of 57.6 per 100,000 children in 2011. Sweden is next with a rate of 43.1, then Saudi Arabia 31.4, and Norway 27.9 and then the UK with 24.5 children in every 100,000 diagnosed (Iacobucci, 2013). Type 1 diabetes is the most common form of the disease in children; over 90 per cent of children under the age of 16 with diabetes have type 1. However, type 2 diabetes (normally affecting adults in the post 40 age group) now seems to be emerging in young adults too at the level of a global epidemic driven by the increasing burden of obesity (Wilmot et al., 2010; Song, 2012). This raises the possibility of a serious public health challenge in the next few decades.
Between 1996 and 2011, the number of people diagnosed with diabetes rose from 1.4 to 2.9 million in the UK. An estimated 850,000 people are thought to have the disease but not yet know it. If current trends continue by 2025 it is estimated that five million people in the UK will have diabetes (Diabetes UK, 2012). A report published in the journal Diabetic Medicine projects that the NHS’s annual spending on diabetes will increase from £9.8 billion to £16.9 billion over the next 25 years, this rise means that in 2035, the NHS could be spending 17 per cent of its entire budget on treating diabetes (Hex et al., 2012).
The global rise in diabetes is epidemic. In 1985 an estimated 30 million people worldwide had diabetes; a decade later this figure had increased to 135 million and by 2000 an estimated 171 million people had diabetes. In 2011, 347 million people worldwide were affected and the WHO projects that diabetes will be the seventh leading cause of death in 2030 (WHO, 2013b). The increase in diabetes is attributed to a range of factors including population growth, ageing, unhealthy diets that are high in saturated fat and cholesterol, obesity and lack of physical exercise.
Diabetes has become one of the major causes of premature illness and death in many, but not all, countries. Indeed, diabetes occurs much more in some parts of the world, principally in developed countries. Diabetes tends to occur more in cultures consuming diets high in animal fats and less in cultures consuming diets high in complex carbohydrates. As carbohydrate intake increases and saturated animal fat intake decreases from country to country, the number of deaths from type 2 diabetes plummets from 20.4 to 2.9 people per 100,000 (Campbell and Campbell, 2005).
In England and Wales, the rates of diabetes fell markedly between 1940 and 1950. This is because during the Second World War, and in the period following it, people tended to eat less fat and sugar and more plant foods, and therefore more fibre, antioxidants, complex carbohydrates, vitamins and minerals (Trowell, 1974). All available land was used; many people grew their own vegetables and vegetable patches were cultivated all over the country. Gardens, flowerbeds and parks were dug up and planted with vegetables; even the moat around the Tower of London (drained in 1843) was used for growing vegetables. Then as rationing came to an end and people moved away from whole grains towards a more processed diet, rates of diabetes increased again (Trowell, 1974). The conclusion must be that a high-carbohydrate, low-fat plant-based diet offers some protection against type 2 diabetes.
The risk factors for type 2 diabetes (obesity, poor diet and lack of exercise) are well-documented and there are many steps people can take to limit their chances of developing type 2 diabetes. One obvious step is to reduce the amount of saturated fat in the diet, this means cutting down on meat and dairy and increasing the intake of fruit, vegetables, whole grains, pulses, nuts and seeds. Simple lifestyle measures have been shown to be effective in preventing or delaying the onset of type 2 diabetes.
To help prevent type 2 diabetes and its complications, the WHO recommends the following:
- Achieve and maintain healthy body weight
- Be physically active – at least 30 minutes of regular, moderate-intensity activity on most days (more activity is required for weight control)
- Eat a healthy diet of between three and five servings of fruit and vegetables a day and reduce sugar and saturated fats intake
- Avoid tobacco use – smoking increases the risk of cardiovascular diseases
Prevention of diabetes is crucial to lowering disease incidence and minimising the public health burden. There is a large body of evidence showing that plant-based diets can lower the risk of diabetes. A study of the relationship between diet and chronic disease in a cohort of 34,192 California Seventh-day Adventists revealed that the vegetarian Adventists were much healthier than their meat-eating counterparts: the meat-eaters were twice as likely as the vegetarians to suffer from diabetes (Fraser, 1999). This study also revealed that obesity increased as meat consumption increased; the difference between vegetarian and non-vegetarian men and women was 6.4kg and 5.5kg respectively (Fraser, 1999). More recently, a meta-analysis of studies examining the role of diet and lifestyle in diabetes prevention found that diets rich in whole-grain, high-fibre cereal products and non-oil-seed pulses (chick peas, beans, peas and lentils) are beneficial, whereas, frequent meat consumption was found to increase the risk (Psaltopoulou et al., 2010). They also found that four cups per day of filtered coffee or tea reduced diabetes risk but that alcoholic beverages should not exceed 1-3 drinks per day. They concluded that obesity is the most important factor accounting for more than half of new diabetes cases; even modest weight loss has a favourable effect in preventing diabetes and physical exercise, with or without diet, contributes to a healthier lifestyle and lowers the risk.
Vegetarian and vegan diets offer significant benefits for diabetes management. One study compared the effects of a low-fat vegan diet with that of a conventional diabetes diet on glycaemia, weight and plasma lipids in a clinical trial (Barnard et al., 2009). Type 2 diabetics were randomly assigned either a low-fat vegan diet or a diet following American Diabetes Association guidelines. Their weight and plasma lipids were measured at the start, middle and end of the 74-week trial. Both groups lost weight but those on the conventional diet had restricted calorie intake whilst the vegan group did not. Both diets were associated with a sustained drop in plasma lipid concentrations. The reduction in triglycerides (fats in blood) in the vegan group was substantial as was the decrease in cholesterol levels (the total cholesterol level fell by 0.53mmol/L and 0.18mmol/L in the vegan and conventional diet groups respectively). Around six in 10 adults in England have cholesterol levels of 5mmol/l or above, you should aim to have a cholesterol level under 4mmol/l (BHF, 2013). So a reduction of 0.5mmol/L could be significant in reducing the risk of heart disease. In an analysis controlling for medication changes, the low-fat vegan diet was found to improve glycaemia and plasma lipids more than the conventional diabetes diet. In other words, the vegan diet offered significantly more benefits.
A further review of the literature revealed how observational studies show that vegetarians are about half as likely to develop diabetes compared with non-vegetarians. They also describe how in clinical trials in individuals with type 2 diabetes, low-fat vegan diets improve glycaemic control to a greater extent than conventional diabetes diets. This beneficial effect is largely due to weight loss but may also be partly attributable to the reduced intake of saturated fats and high-glycaemic-index foods coupled to the increased intake of dietary fibre and vegetable protein. Vegetarian and vegan diets also improve plasma lipid concentrations and have been shown to reverse atherosclerosis progression, thus lowering the risk of heart disease (Barnard et al., 2009a).
Further studies confirm the beneficial role of plant-based diets in the prevention and treatment of diabetes. A review of both observational studies and intervention trials concluded that a low-fat, plantbased diet can improve control of weight, glycaemia and cardiovascular risk. The authors of this review concluded that vegetarian and vegan diets present potential advantages in managing type 2 diabetes that merit the attention of individuals with diabetes and their caregivers (Trapp and Barnard, 2010). In summary, the current literature indicates that vegetarian and vegan diets present huge potential advantages for the management of type 2 diabetes.
The importance of high-fibre diets in diabetes has been studied extensively since the 1970s by James Anderson, Professor of Medicine at the University of Kentucky. Anderson used a high-fibre, high-carbohydrate low-fat diet to treat 25 type 1 and 25 type 2 diabetics (Anderson, 1986). The experimental diet consisted mostly of whole plant foods (although it did contain a small amount of meat). After three weeks, Anderson measured blood sugar levels,weight and cholesterol levels and calculated their medication requirements. The results were astounding. Remember in type 1 diabetes no insulin is produced so it seems unlikely that a change in diet would help. However, Anderson’s patients required 40 per cent less insulin medication than they had needed before the trial. In addition to this, their cholesterol levels dropped by an average of 30 per cent too. This is just as important in lowering the risk factors for secondary outcomes of diabetes such as heart disease and stroke. Type 2 diabetes is generally more treatable and the results among the type 2 patients were even more impressive: 24 out of the 25 participants consuming the high-fibre, low-fat diet were able to stop taking their insulin medication completely! These benefits were not of a temporarynature, indeed they were sustained over time in a group of 14 diabetic men continuing on the highcarbohydrate, high-fibre diet for four years (Story et al., 1985).
The evidence is overwhelming: a high-carbohydrate, high-fibre diet provides effective, positive and safe treatment for diabetes and lowers the associated risk for coronary artery disease (Anderson et al., 1990). More recent studies have shown increasing dietary fibre in the diet of patients with type 2 diabetes is beneficial and should be encouraged as a disease management strategy (Anderson et al., 2004; Barnard et al., 2009; Post et al., 2012). Of course it should be noted that this is not a special diet for diabetics; most people would benefit from increasing their fibre intake while reducing the amount of dietary fat they consume.
As stated, it is thought that type 1 diabetes involves a genetic susceptibility coupled to an environmental trigger. It has been suggested that an increased environmental pressure may reduce the need for a strong genetic susceptibility in order for type 1 diabetes to develop (Vehik et al., 2008). Modern molecular genetics has enabled scientists to identify genes linked to type 1 diabetes and develop a hierarchy of susceptibility based on the number of these genes that a person carries. People carrying a high proportion of the high risk genes are referred to as having a ‘high-risk HLA genotype’. Researchers from the Diabetes and Metabolism Division of Medicine at the University of Bristol looked at the frequency of these high risk genes in a group of 194 patients who were diagnosed with type 1 diabetes as children over 50 years ago (between 1922 and 1946). They compared them to a group of 582 age-matched and sex-matched individuals diagnosed between 1985 and 2002. Results showed that the frequency of the high-risk genotype was 12 per cent lower in the individuals diagnosed recently compared with the older group (Gillespie et al., 2004). Other studies from Finland and the US have found a similar disparity (Hermann et al., 2003; Vehik et al., 2008).
So, what does this all mean? The important point here is that increasing environmental exposure is now able to trigger type 1 diabetes in people who are less genetically susceptible than the generation above them. In other words, the rapid rise of type 1 diabetes must be due to a major environmental factor rather than genes.
But what is this elusive environmental trigger? A growing body of evidence suggests it may be a component of the diet. In 2000 an extensive study of children from 40 different countries confirmed a link between diet and incidence of type 1 diabetes (Muntoni et al., 2000). The study set out to examine the relationship between dietary energy from major food groups and incidence of type 1 diabetes. The total energy intake was not associated with type 1 diabetes incidence. However, energy from animal sources (meat and dairy foods) was associated and energy from plant sources was inversely associated with diabetes. This means that the more meat and milk in the diet, the higher the incidence of diabetes and the more plant-based food in the diet, the lower the incidence.
As stated, type 1 diabetes is thought to involve both a genetic predisposition and an environmental trigger. The trigger may be a virus or some component of food. In the early 1990s a Canadian research group suggested that cow’s milk proteins might be an important environmental trigger providing specific peptides that share antigenic epitopes with host cell proteins (Martin et al., 1991). This means that the proteins in cow’s milk look the same as proteins in our own bodies; these similarities can confuse our immune system and initiate an inappropriate (autoimmune) response that can lead to diabetes.
The milk protein casein is similar in shape to the insulin-producing cells in the pancreas. Because the body may perceive casein as a foreign invader and attack it, it may also start to attack the pancreas cells having confused them for casein, again leading to diabetes (Cavallo et al., 1996). Some studies have suggested that bovine serum albumin (BSA) is the milk protein responsible. In a study of 142 children with type 1 diabetes, all the diabetic patients had higher serum concentrations of anti-BSA antibodies compared to 79 healthy children (Karjalainen et al., 1992). These antibodies may react with proteins on the surface of the beta cells of the pancreas and so interfere with insulin production.
Other studies suggest it is the cow’s insulin present in formula milk that increases the risk of type 1 diabetes in infants (Vaarala et al., 1999). Research shows that some infants may be more vulnerable to type 1 diabetes later in life if exposed to cow’s milk formula while very young. A Finnish study of children (with at least one close relative with type 1 diabetes) examined whether early exposure to insulin in cow’s milk formula increased the risk of type 1 diabetes. Results showed that infants given cow’s milk formula at three-months-old had immune systems which reacted far more strongly to cow’s insulin (Paronen et al., 2000). This raises concerns that exposure to cow’s insulin plays a role in the autoimmune process leading to type 1 diabetes.
A review of the clinical evidence suggests that the incidence of type 1 diabetes is related to the early consumption of cow’s milk; children with type 1 diabetes are more likely to have been breastfed for less than three months and to have been exposed to cow’s milk protein before four months of age (Gerstein et al., 1994). The avoidance of cow’s milk during the first few months of life may reduce the risk of type 1 diabetes. Infants who cannot breastfeed from their mothers may benefit more from taking a plant-based formula such as soya-based formula rather than one based on cow’s milk. Other studies support the finding that both early and adolescent exposure to cow’s milk may be a trigger for type 1 diabetes (Kimpimaki et al., 2001; Thorsdottir and Ramel, 2003).
Further evidence suggesting that the early exposure to cow’s milk in infancy (including cow’s milk infant formula) may be a trigger for type 1 diabetes in some children was provided in a substantial review of 27 case-control studies and one prospective cohort study looking at the associations of breastfeeding and/or the early introduction of cow’s milk and formula with the development of type 1 diabetes. Eight of the studies showed that breastfeeding can protect against type 1 diabetes while seven additional studies emphasised that a short period or absence of breastfeeding could be a risk factor for type 1 diabetes. The authors concluded that a short duration and/or a lack of breastfeeding may constitute a risk factor for the development of type 1 diabetes later in life (Patelarou et al., 2012).
The hunt for the elusive environmental trigger responsible for the global rise in the incidence of type 1 diabetes continues. Theories include: the hygiene hypothesis (a lack of early childhood exposure to infectious agents and parasites weakens immunity and increases susceptibility to allergic and autoimmune diseases), a viral agent, vitamin D deficiency and the breast milk versus cow’s milk argument. It may be that no single factor is responsible for the increase in the incidence of diabetes all over the world, a multi-factorial process might be involved and there may be some overlap between the various hypotheses (Ergo, 2013). However, taken together, the evidence suggests that avoiding milk and milk products may offer protection from diabetes (types 1 and 2).
For more information see Viva!Health’s fully-referenced scientific report The Big-D: Defeating Diabetes through Diet and easy-to-read guide The Big-D: defeating diabetes with the D-Diet at www.vegetarian.org.uk/campaigns/diabetes