Vegetarians International Voice for Animals

Why do people become diabetic?

Why do people become diabetic?

Genetics

Our genetic make-up plays an important role in this disease and a certain set of genes can make us more or less susceptible to developing diabetes. However, even those with a greater susceptibility do not necessarily go on to develop the disease.

Type 1 diabetes

This is a brief overview of the heredity factors which influence type 1 diabetes (Diabetes UK, 2010b):

  • If a mother has type 1 diabetes, the risk for her child of developing it is about two per cent.
  • If a father has it, the risk for his child is about eight per cent.
  • If both parents have this condition, the risk is up to 30 per cent.
  • If a child develops it, the risk is around 10 per cent for other siblings. If a twin develops it, the risk for a non-identical sibling is around 15 per cent. If it is an identical twin, the risk rises to 40 per cent.

Several gene variants have been identified as contributing to type 1 diabetes susceptibility but only a small proportion of genetically susceptible individuals – less than 10 per cent – go on to develop the disease (Knip et al., 2005). This implies that environmental factors are necessary to trigger the autoimmune reaction which destroys insulin producing cells.

Type 2 diabetes

This is a brief overview of the impact of heredity on type 2 diabetes (Diabetes UK, 2010b):

  • If one of the parents has the condition, the risk for their child of developing it is 15 per cent.
  • If both parents have the condition, the risk is around 75 per cent.
  • If a non-identical twin develops this type of diabetes, the risk is ten per cent for the other twin. If an identical twin has the condition, the risk for the other twin is 90 per cent.

As shown in the next chapter, lifestyle and environmental factors play an enormous role in type 2 diabetes. Therefore, even individuals with susceptible genes, or people who have already developed type 2 diabetes, don’t necessarily have to live with the condition for the rest of their lives.

Lifestyle and environmental factors

Lifestyle plays an enormous role in either increasing or decreasing the risk of developing the disease. Even if both parents have diabetes, it doesn’t necessarily follow that the child will develop it, too.

Type 1 diabetes

It has been known for many years that type 1 diabetes is triggered by some external stimulus. The widely accepted theory is that a viral or another infection might be the culprit, making the body attack its insulin producing cells by mistake. However, the hypothesis that cow’s milk is the main trigger was put forward in the 1990’s (Karjalainen et al., 1992; Gerstein, 1994; Åkerblom and Knip, 1998) and has been progressively more accepted ever since.

 

If an individual has a certain combination of genes making them more susceptible to type 1 diabetes, the environmental trigger is the key which opens the door to the disease but if the trigger is avoided, diabetes may never develop. The theory is as follows (Campbell and Campbell, 2004; Knip et al., 2005):

A baby with a susceptible genetic make-up is exposed to cows’ milk early in life, perhaps through an infant formula. The baby’s immune system might be further compromised by a virus infection, increasing the risk for type 1 diabetes. When the milk proteins reach the
small intestine they are not fully digested – i.e. broken down into individual amino acids – but are instead broken down into amino acid chains. These fragments may be absorbed through the gut wall into the blood where the immune system recognises them as foreign intruders and begins attacking them through an immune response. Coincidentally, the structure of
some of these fragments is identical to the surface structure of insulin producing cells (ß-cells) in the pancreas (Karjalainen et al., 1992; Martin et al., 1991) and the body cannot distinguish between the two. Pancreas ß-cells are therefore attacked and destroyed by the immune system as well as the milk protein fragments and the infant becomes diabetic. Type 1
diabetes is irreversible as the cells cannot regenerate.

The process of ß-cell destruction can be fast and aggressive, leading to disease manifestation within a few months, or it can be slow and last for years, in some cases even more than 10 years with ß-cells being gradually destroyed over this period (Knip et al.,
2005). However, the fast progression of the disease is rare (Knip, 2002).

Research has established which milk proteins are responsible for this dramatic autoimmune reaction. Karjalainen et al. (1992) suggest that the main one is bovine serum albumin (BSA), which is different in structure to human albumin (milk protein). They tested the blood of type 1 diabetic and non-diabetic children for the presence of antibodies against incompletely digested BSA. The results were astonishing – all diabetic children had antibody levels
as much as seven times higher than the healthy children and there was no overlap in the antibody levels between the diabetic and healthy children – i.e. all diabetic children had high levels but none of the non-diabetic children did.

After that, a number of studies ensued and all but one found markedly elevated levels of BSA antibodies in the blood of diabetic children (Hammond-McKibben and Dosch, 1997).

Another protein abundant in cow’s milk is ß-casein, which also generates a specific immune response (Cavallo et al., 1996). The structure of human ß-casein is similar in many respects to bovine ß-casein (from cow’s milk) but 30 per cent of the molecule is different in structure. This difference is assumed to be the reason why the immune system reacts to it. Again there are structural similarities between bovine casein and the surface molecules of ß-cells in the pancreas, just as there is with BSA, provoking an immunological cross-reactivity – the
immune system attacks ß-casein molecules as well as the ß-cells (Cavallo et al., 1996; Becker et al, 1995).

A Chilean study conducted around the same time focused on the combination of susceptible genes and cow’s milk (Perez-Bravo et al., 1996). The findings revealed that genetically susceptible children weaned too early onto cow’s milk-based formula had 13.1 times greater risk of developing type 1 diabetes than children breast-fed for at least three months and who
did not have susceptible genes.

In 2000, an extensive study of children from 40 different countries confirmed a link between diet and type 1 diabetes (Muntoni et al., 2000). The study set out to examine the relationship between dietary energy from major food groups and type 1 diabetes. Energy intake per se was not associated with type 1 diabetes but energy from animal sources (meat and dairy foods) showed a significant association whereas energy from plant sources was inversely associated with diabetes. In other words, the more meat and milk in the diet, the higher the incidence of diabetes and the more plant-based foods in the diet, the lower the incidence.

In the meantime, it was discovered that there are five autoantibodies – antibodies which will attack their own host body – and the presence of these autoantibodies can predict the development of type 1 diabetes (Knip, 2002). In addition to the two which attack ß-cells, together with two supporting antibodies, there is one which will attack insulin itself. It was suggested that cow’s insulin present in formula milk increases the formation of these
antibodies (Vaarala et al., 1999). A Finnish study of children at increased risk of type 1 diabetes (having at least one close relative with the disease) showed that the immune system of infants given cow’s milk formula as early as three-months old, reacted strongly to cow’s insulin by forming these specific antibodies (Paronen et al., 2000).

Results of another study following infants from birth (Åkerblom et al., 2002) showed that exclusively breastfeeding for only a short period followed by the introduction of cow’s milk, predisposed these children to ß-cell-destroying autoimmune reactions by inducing formation of four culprit autoantibodies. Other population studies have shown that if three or four of these antibodies are present in blood, the risk of developing type 1 diabetes in the next five to 10 years is 60–100 per cent (Knip et al., 2005).

Type 2 diabetes

Type 2 diabetes often accompanies obesity. In fact, obesity is the main risk factor, particularly abdominal obesity, and over 80 per cent of people with diabetes are overweight or obese (U.S. Department of Health and Human Services, 2007). It has recently been shown that the association between type 2 diabetes and abdominal obesity is equally significant for both

sexes (Paek and Chun, 2010).

 

According to latest statistics (NHS, 2011), almost a quarter of adults in England (22 per cent of men and 24 per cent of women) were classified as obese. In addition, 44 per cent of men and 33 per cent of women in England were classified as overweight. The numbers of obese children – 16 per cent of boys and 15 per cent of girls (aged two to 15) – are also alarming. With these rising numbers of overweight people, the risk of diabetes is ever-increasing.

Percentage of overweight and obese people in England in 2009 (NHS, 2011):


Age group

sex

Overweight (%)

Obese (%)

Overweight or obese (%)

Over 16

Women

33

24

57

Men

44

22

66

Two to 15

Girls

13

15

28

Boys

15

16

31

 

Comparing diets and diabetes rates in different countries reveals that as carbohydrate intake goes down and fat intake goes up, the number of diabetics rapidly increases (Campbell, 2004; Barnard, 2007). The difference cannot be ascribed to genetics as when people move to countries where the ‘Western’ style diet predominates and they adopt these eating habits, their rates of type 2 diabetes increase above the national average (Tsunehara et al., 1990).

An extensive, 21-year study involving over 25,000 adults in the USA found that diabetes is less frequent among vegetarians and vegans. Those on meat-free diets had a 45 per cent reduced risk of developing diabetes compared to the population as a whole. Meat
consumption was positively associated with selfreported diabetes in both males and females
(Snowdon and Phillips, 1985).

New research also suggests that eating just one serving of meat per week significantly increases the risk of diabetes (Vang et al., 2008). It looked at the link between meat intake and the occurrence of diabetes in 8,000 adult Seventh Day Adventists Adventists (a Christian branch following a similar lifestyle but different diets), all of whom were nondiabetic
at the start of the study. Those who followed a ‘low-meat’ diet over the 17 years of this long-term study had a staggering 74 per cent increase in their risk of developing type 2 diabetes compared to participants who followed a meat-free diet for the same period. Part of this difference was attributable to obesity and/or weight gain but even after allowances were made for this, meat intake remained an important risk factor.

So what is it that makes animal products so detrimental to health? The main enemy is fat.

A study published in 2004 produced an outstanding discovery (Petersen et al., 2004) and confirmed the findings of previous studies (Phillips et al., 1996; Krssak et al., 1999). The researchers tested healthy young adults whose parents or grandparents had had type 2
diabetes for insulin resistance. Some were insulin resistant to one degree or another and further tests uncovered the reason why. Inside their muscle cells were microscopic drops of fat and this fat interfered with the cells’ ability to correctly react to insulin. Even though their bodies produced sufficient insulin, fat inside their cells inhibited the appropriate reactions.

Muscle cells normally store small quantities of fat as energy reserve but in the insulin-resistant people, fat had built up to levels which were 80 per cent higher than in other young (healthy) people. Even though the affected people were slim, fat had nevertheless accumulated in their cells. The fat particles were intramyocellular lipids and the study showed (as did previous studies – Phillips et al., 1996; Krssak et al., 1999) that these lipids start accumulating many years before type 2 diabetes manifests.

It was later confirmed by other studies that insulin resistance in muscles and liver is strongly linked to fat storage in these tissues (Delarue and Magnan, 2007; Morino et al., 2006).
Under normal conditions, fat is metabolised by the cells’ own powerhouses – mitochondria – but it appears that people with type 2 diabetes have fewer mitochondria in their cells than they need to successfully burn all the supplied fat. As a consequence, the fat accumulates inside the cells (Barnard, 2007).

In order to understand the extent to which diet influences intracellular fat metabolism, another study was conducted (Sparks et al., 2005). Healthy young men (average age 23 years) were put on a special, high-fat diet that drew some 50 per cent of its calories from fat – a diet not too different from that which many people in Western countries consume. After just three days, intracellular lipids had increased considerably, showing that accumulation of fat inside cells is extremely rapid.

Further tests produced some surprising results – that fatty foods had a profound effect on those genes necessary for the existence and proper functioning of mitochondria. In fact, fatty foods turned off those genes that normally help mitochondria to burn fat. A high-fat diet therefore caused the body to accumulate more fat in muscle cells while at the same time
slowing down the body’s ability to burn this fat. This dual process then inhibited the ability of the cells to respond to insulin.

Humankind’s evolutionary history may provide some answers as to why this happens. When food was predominantly scarce, our ancestors’ bodies developed particular mechanisms to store fat on the occasions when they had access to energy-rich food – it was vital for their survival (Barnard, 2007). We live in a very different world now where for most of us
food is rarely, if ever, scarce yet our bodies are still programmed to store fat when it is available.

To establish how insulin sensitivity changes when fat intake increases or decreases, and to determine the importance that genetic make-up has on diet, a study of healthy African-American and Caucasian women was conducted (Lovejoy et al., 1998). The women were
put on either a high-fat diet (50 per cent fat, 35 per cent carbohydrate, 15 per cent protein) or a low-fat diet (20 per cent fat, 55 per cent carbohydrate, 15 per cent protein) for three weeks. The results showed that insulin sensitivity of all women on the high-fat diet decreased by six per cent, whilst in African-American women on the low-fat diet it increased by six per cent and by 20 per cent in the Caucasian women. The study not only revealed the greater
propensity of people on high fat diets to develop diabetes but revealed sharp ethnic differences.

A recent study looked at cell metabolism in relation to insulin resistance more closely (Hoeks et al., 2010) and the conclusions were in line with the above – elevated fat levels in blood and/or intramuscular fat accumulation can cause reduction in mitochondrial function.

The predominant diet in many countries, including the UK, is high in fat, animal products and sugary foods and low in complex carbohydrates. Not only is this diet largely responsible for ever increasing numbers of overweight or obese people but it also increases the risk of diabetes and cardiovascular disease.