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 (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). 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 some 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. Over 80 per cent of people with type 2 diabetes are overweight (NHS Direct, 2005). Type 2 diabetes occurs mostly in people over the age of 40, but is now increasingly affecting people at a much younger age. Symptoms include tiredness, irritability, nausea, hunger, weight loss, recurrent skin infections, blurred vision, tingling sensations in the hands and feet and dry, itchy skin. 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 2 diabetes accounts for over 80 per cent of all cases of diabetes seen. While rising obesity levels have contributed to the increase in the incidence of type 2 diabetes, the increase in obesity does not explain the threefold increase in the number of cases of type 1 diabetes seen over the last 30 years. This 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.
A third type of diabetes, gestational diabetes, develops in some women during pregnancy but usually disappears after giving birth.
Diabetes affects over one million people in the UK but there may be as many as a million others who have the disease but do not know it yet. The WHO describes the global rise in diabetes as epidemic (WHO, 2006a). 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. It is predicted that at least 366 million people will have diabetes by 2030 (WHO, 2006a). 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. Large, population-based studies in China, Canada, USA and several European countries suggest that even moderate reduction in weight and half an hour of walking each day reduces the risk of diabetes considerably (WHO, 2006a).
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).
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 temporary nature, indeed they were sustained over time in a group of 14 diabetic men continuing on the high-carbohydrate, 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). 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 fat they consume.
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.
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. 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 breast fed 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 breast feed 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).
Taken together, the evidence suggests that avoiding milk and milk products may offer protection from diabetes (types 1 and 2).
Obesity is epidemic in Western societies and constitutes a major public health concern. A recent study published in the British Journal of Medicine reports that being obese during middle-age can increase the risk of developing dementia later in life (Whitmer et al., 2005). The research is based on data collected from detailed health checks made on 10,276 men and women between 1964 and 1973 (when they were aged 40 to 45). Dementia was diagnosed in seven per cent of participants between 1994 and 2003. Results showed that being obese increased the risk of dementia by 74 per cent while being overweight increased it by 35 per cent. The link between obesity and dementia in women was stronger than that in men. This is in agreement with a Swedish study which found that the higher a woman’s body mass index (BMI), the greater the risk of dementia (Gustafson et al., 2003). In this study the relationship between BMI and dementia risk was investigated in 392 Swedish adults who were assessed between the ages of 70 and 88. During the 18-year study, 93 participants were diagnosed as having dementia. Women who developed dementia had a higher average BMI compared to women without dementia. For every one unit increase in BMI at age 70 years, the risk of dementia increased by 36 per cent. This raises concerns that the current obesity epidemic could lead to a steep rise in the numbers of people suffering from dementia in the future. The evidence suggests that leading a healthy lifestyle could help to reduce the risk of dementia (See Overweight and obesity).
The most common type of ear infection (otitis media) affects the middle ear, the space between the eardrum and the inner ear. The middle ear is usually filled with air but it can fill up with fluid (during a cold for example) and ear infections happen when bacteria, viruses or fungi infect the fluid and cause swelling in the ear. Ear infections are common in childhood and can be extremely painful, causing a considerable amount of distress. Chronic otitis media is when ear infections keep recurring, for example Glue ear is a type of chronic otitis media. Ear infection is the most common health problem doctors see in young children with around one in 10 children having an ear infection by the time they are three months old (NHS Direct, 2005). It can be a serious problem; otitis media is the most common cause of hearing loss in children today (Bernstein, 1993).
Ear infections are often linked to colds or other problems of the respiratory system. However, recent reports link ear infections to food allergies (Hurst, 1998; Aydogan et al., 2004; Doner et al., 2004). Researchers from Georgetown University in the US examined the role of food allergy in ear infection in 104 children with recurrent ear problems (Nsouli et al., 1994). The children were tested for food allergies and those who tested positive excluded that particular food for 16 weeks, then reintroduced it. Results showed that 78 per cent of the children with ear problems also had food allergies, the most common allergenic foods were cow’s milk (38 per cent), wheat (33 per cent), egg white (25 per cent), peanut (20 per cent) and soya (17 per cent). 86 per cent of these children responded well to eliminating the offending food, and of these, 94 per cent suffered a recurrence of ear problems on reintroducing the offending food.
A different approach was taken in a Finnish study of 56 children with cow’s milk allergy and 204 children without cow’s milk allergy. These researchers examined the occurrence of ear infection in children known to have cow’s milk allergy. Results showed that 27 per cent of those with the allergy suffered from recurrent ear infections compared to just 12 per cent of those who did not have the allergy (Juntti et al., 1999). It was concluded that children with cow’s milk allergy experience significantly more ear infections.
Dr John James of the Colorado Allergy and Asthma Centres in the US suggests that food allergies can cause inflammation in the nasal passages and lead to the build up of fluid in the middle ear, but he acknowledges that the link between food allergy and ear infection may be hard to prove (James, 2004). The possibility of cow’s milk allergy should be considered in all cases of ear infection, particularly in children.
Food poisoning is a common, often mild, but sometimes deadly illness (NHS, 2006). It is caused by the consumption of food or drink that is contaminated with bacteria, parasites or viruses. Most cases result from bacterial contamination. Food poisoning happens in one of two ways: either in the food (for example in undercooked meat or unpasteurised milk), or on the food (if it is prepared by someone who has not washed their hands). The length of the incubation period (the time between swallowing the bacteria and symptoms appearing) varies from hours to days, depending on the type of bacteria and how many were swallowed. The most common symptoms of food poisoning are sickness, vomiting, abdominal pain and diarrhoea. According to the Food Standards Agency, it is estimated that over five million people in the UK are affected by food poisoning each year (NHS Direct, 2006). It usually lasts for less than three days, but can continue for up to a week. The greatest danger lies in the loss of fluids and salts from prolonged diarrhoea. The results can be deadly in infants and over 60s. Also, in these patients, the bacteria may enter the bloodstream infecting other parts of the body and may cause death unless the person is treated promptly with antibiotics.
Most cases of food poisoning are related to the consumption of animal products (meat, poultry, eggs, fish and dairy) as plants tend not to harbour the types of bacteria capable of causing food poisoning in humans. Intensive animal husbandry technologies, introduced to minimise production costs, have led to the emergence of new zoonotic diseases – animal diseases that can be transmitted to humans (WHO, 2006b).Escherichia coli (E. coli) O157 was identified for the first time in 1979 and has since caused illness and deaths (especially among children) owing to its presence (in several countries) in minced beef, unpasteurised cider, cow’s milk, manure-contaminated lettuce and alfalfa and manure-contaminated drinking-water (WHO, 2006b). In a joint report between the FSA Scotland and the Scottish Executive it was noted that the main source of E. coli O157 is from cattle and sheep, but that more cases of E. coli O157 are now associated with environmental contamination, including contact with animal faeces or contamination by faeces of water supplies, than with food (FSA/SE, 2001). If plants do cause food poisoning it is generally because they have been contaminated with animal excreta, human sewerage or handled with dirty hands during preparation. Safe disposal of manure from large-scale animal and poultry production facilities is a growing food safety problem in much of the world (WHO, 2006b).
The most common cause of food poisoning in the UK is the bacterium Campylobacter, which has been found in poultry, unpasteurised milk, red meat and untreated water. The next most common cause isSalmonella, which has been found in unpasteurised milk, eggs, meat and poultry (NHS Direct, 2005).Salmonella causes the greatest number of deaths: 119 deaths England and Wales in 2000 (POST, 2003). In a small number of cases, people infected with Salmonella will go on to develop pains in their joints, irritation of the eyes and painful urination; this is called Reiter’s syndrome and can last for months or years and may lead to chronic arthritis (Centers for Disease Control and Prevention, 2006). Listeria, sometimes found in soft cheeses and pates, can cause severe illness (listeriosis) in vulnerable groups such as pregnant women, babies, the elderly and people with reduced immunity. The Government advises pregnant women to avoid soft mould-ripened cheese, such as Camembert and Brie, blue cheese and all types of meat pâté. Other bacteria that can cause food poisoning include species of Staphylococcus and Clostridium. Certain strains of otherwise normal intestinal bacteria can cause food poisoning. For example, E. coli is usually harmless but the strain E. coli O157 can cause kidney failure and death.
The majority of food poisoning cases in the UK are caused by consuming contaminated meat or dairy products. For example, of the Staphylococcal food poisonings reported in the UK between 1969 and 1990, 53 per cent were due to meat products (especially ham), 22 per cent were due to poultry, eight per cent were due to milk products, seven per cent to fish and shellfish and 3.5 per cent to eggs (Wieneke et al., 1993).
While most cases of food poisoning are associated with meat and poultry, the link between milk products and food poisoning should not be discounted: 20 separate outbreaks of food poisoning in England and Wales associated with the consumption of milk and dairy products were reported to the Public Health Laboratory Service Communicable Disease Surveillance Centre between 1992 and 1996 (Djuretic et al., 1997). 600 people were affected and over 45 were admitted to hospital. Salmonella species were responsible for 11 of the outbreaks, Campylobacter species for five, E. coli O157 for three andCryptosporidium parvum for one. Outbreaks were associated with hotels, a psychogeriatric hospital, schools, a Royal Air Force base, a farm visit, an outdoor festival and milk supplied directly from farms. Milk was implicated in 16 of the outbreaks, 10 of which were associated with unpasteurised milk. Two outbreaks were associated with eating contaminated ice-cream and two with eating contaminated cheese.
Food poisoning may result from milk and milk products if they have not been properly heated (pasteurised) or if they have become contaminated following pasteurisation. A report published in the New England Journal of Medicine reported how 142 cases of listeriosis in Los Angeles in 1985 led to 48 deaths (Linnan, 1988). An extensive investigation traced the source to a cheese factory where it was found that a Mexican-style soft cheese had been contaminated with unpasteurised milk.
Bacteria are too small to see and they do not taste or smell of anything so it is difficult to detect their presence. The risk of food poisoning can be minimised by following some basic hygiene rules. This means washing hands before handling food, washing salads thoroughly (to remove contaminating bacteria from manure for example), making sure all food is covered and chilled. If meat is to be consumed it must be thawed and cooked properly to kill harmful bacteria. It is important to keep raw meat (and its juices) away from other foods. Avoiding unpasteurised milk, raw eggs and undercooked meat further reduces the risk of food poisoning. Of course the safest option is to follow a plant-based diet free of red meat, poultry, fish, milk and eggs. Excluding animal foods from the diet will dramatically decrease the risk of food poisoning.
Gallstones are solid pieces of stone-like material that form in the gall bladder, which is a small organ on the right hand side of the body, below the liver. It stores a green liquid called bile, which is produced by the liver to help the body digest fats. As we eat, bile is released from the gall bladder into the intestines through a thin tube called the bile duct.
Gallstones are formed when some of the chemicals stored in the gall bladder harden into a solid mass. They may be as small as a grain of sand or as large as a golf ball. Some people may have one large stone while others may have many small ones. About one in 10 people over 50 in the UK have gallstones.
Gallstones are made up from a mixture of water, cholesterol and other fats, bile salts and the pigment bilirubin. They occur when the composition of the bile is abnormal, the outlet from the gall bladder is blocked (perhaps by infection), or if there is a family history of gallstones. Gallstones can cause inflammation of the gall bladder (cholecystitis), which may then block the bile duct leading to obstructive jaundice. The passage of a gallstone along the bile duct to the duodenum can be extremely painful.
Obesity is a major risk factor for gallstones, especially in women, who are twice as likely as men to develop gallstones. Risk increases with age; people over 60 are at a higher risk. Diet is also a causal factor. A study published in the British Medical Journal in 1985 reported that meat-eaters are twice as likely to develop gallstones as vegetarians (Pixley et al., 1985). Since then the low incidence of gallstones in vegetarians compared to meat-eaters has been well documented (Key et al., 1999). Indeed vegetarian diets have been shown to be beneficial for both the prevention and treatment of gallstones (Leitzmann, 2005). The main risk factors appear to be low fibre intake, high saturated fat and cholesterol intake and obesity. A recent Australian study reported an inverse association between dietary fibre and gallstones (Segasothy and Phillips, 2000). In other words, the more fibre in the diet, the lower the risk of gallstones. Polish researchers examined the diets of patients suffering from gallstones and found that they were characterised by their low fibre diet (Ostrowska et al., 2005). Patients with gallstones ate less wholemeal products, fruit and vegetables and pulses. Furthermore, obese women with gallstones ate significantly more milk, yogurt, meat and meat products.
It is important is to eat as healthily as possible. If you are overweight, losing some weight may help. A well-balanced diet, which includes vegetables, fruit, and whole wheat cereals including bread and is low in animal fat, is considered the best for most people (British Liver Trust, 2005).
Insulin-like growth factor 1 (IGF-1) is a hormone produced in the liver and body tissues of mammals. One important role for IGF-1 is to promote cell growth and division, this is important for normal growth and development. IGF-1 from cows is identical to human IGF-1 in that the amino acid sequence of both molecules is the same (Honegger and Humbel, 1986). Amino acids are the building blocks of proteins and there are 20 different amino acids. All proteins consist of amino acids joined together like beads on a string and the nature of the protein (how it behaves) is determined by the order in which the amino acids occur along the string. In both human and bovine IGF-1 the same 70 amino acids occur in exactly the same order, which would suggest that bovine IGF-1 behaves the same way in humans as it does in cows. As previously stated, the use of recombinant bovine somatotrophin (rBST) in cows increases levels of IGF-1 in their milk, however, it should be noted that cow’s milk from cows that are not treated with rBST also contains IGF-1.
It has been suggested that IGF-1 is not destroyed during pasteurisation. Furthermore it has also been suggested that it is not completely broken down in the gut and that it may cross the intestinal wall in the same way that another hormone, epidermal growth factor (EGF), has been shown to do. EGF is protected from being broken down when food proteins (such as the milk protein casein) block the active sites of the digestive enzymes (Playford et al., 1993). This allows the molecule to stay intact and cross the intestinal wall and enter the blood. This raises concerns that IGF-1 from cow’s milk could increase normal blood IGF-1 levels and so increase the risk of certain cancers linked to IGF-1.
As stated, IGF-1 regulates cell growth, development and division; it can stimulate growth in both normal and cancerous cells. Even small increases in serum levels of IGF-1 in humans are associated with increased risk for several common cancers including cancers of the breast, prostate, lung and colon (Wu et al., 2002). The link between IGF-1 and cancer is becoming increasingly apparent in the scientific literature.
In the first prospective study to investigate the relationship between the risk of breast cancer and circulating IGF-1 levels, researchers at Harvard Medical School analysed blood samples originally collected from 32,826 women aged between 43 and 69 years during 1989 and 1990. From this group, 397 women were later diagnosed with breast cancer. Analysis of IGF-1 levels in samples collected from these women compared to samples from 620 controls (without breast cancer) revealed a positive relationship between circulating IGF-1 levels and the risk of breast cancer among premenopausal (but not postmenopausal) women. It was concluded that plasma IGF-1 concentrations may be useful in the identification of women at high risk of breast cancer (Hankinson et al., 1998a).
To investigate the link between prostate cancer risk and plasma IGF-1 levels, a study was conducted on 152 men with prostate cancer and 152 men without the disease. Analysis revealed a strong positive association between IGF-1 levels and prostate cancer risk (Chan et al., 1998). In agreement, a Swedish study compared IGF-1 levels in 210 prostate cancer patients with those in 224 men without the disease and found that there was a strong positive correlation between the risk of prostate cancer and raised serum levels of IGF-1. It was concluded that high levels of IGF-1 may be an important predictor for risk of prostate cancer (Wolk et al., 1998).
In a study into the link between the risk of lung cancer and IGF-1, serum IGF-1 levels were measured in 204 lung cancer patients registered at the University of Texas M.D. Anderson Cancer Centre and compared to those in 218 people without lung cancer. Results showed that high levels of IGF-1 were associated with an increased risk of lung cancer (Yu et al., 1999).
In order to assess colorectal cancer risk in relation to IGF-1, a research group at Harvard Medical School analysed blood plasma samples originally collected from a pool of 14,916 men. In a 14-year follow-up of these men, 193 had been diagnosed with colorectal cancer. Analysis of IGF-1 levels in samples taken from these men and 318 controls revealed an increased risk for colorectal cancer among the men who had the highest levels of circulating IGF-1 and it was concluded that circulating IGF-1 is related to future risk of colorectal cancer (Ma et al., 1999).
In summary, the literature strongly supports a link between high circulating IGF-1 levels and cancer, but what has this to do with the consumption of cow’s milk and dairy products? The answer is a lot: circulating IGF-1 levels are higher in people who consume milk and dairy products. Researchers at Bristol University investigating the association of diet with IGF-1 in 344 disease-free men found that raised levels of IGF-1 were associated with higher intakes of milk, dairy products and calcium while lower levels of IGF-1 were associated with high vegetable consumption, particularly tomatoes. In their study, published in the British Journal of Cancer, it was concluded that IGF-1 may mediate some diet-cancer associations (Gunnell et al., 2003).
US researchers from Harvard Medical School and Bringham and Women’s Hospital in Boston also investigated the link between IGF-1 levels and diet. They examined circulating IGF-1 levels in 1,037 healthy women. The most consistent finding was a positive association between circulating IGF-1 and protein intake; this was largely attributable to cow’s milk intake (Holmes et al., 2002). In another study, researchers at the Fred Hutchinson Cancer Research Centre in Washington investigated the link between plasma levels of IGF-1 and lifestyle factors in 333 people thought to be representative of the general population. They too found that milk consumption was linked to IGF-1 levels (Morimoto et al., 2005). One study actually quantified the effect of cow’s milk on circulating IGF-1 levels in 54 Danish boys aged 2.5 years. In this study an increase in cow’s milk intake from 200 to 600ml per day corresponded to a massive 30 per cent increase in circulating IGF-1. It was concluded that milk contains certain compounds that stimulate IGF-1 concentrations (Hoppe et al., 2004). Cow’s milk contains many other bioactive compounds such as hormones and cytokines, growth factors, and many bioactive peptides (Playford et al, 2000), which may also affect IGF-1 levels.
In conclusion, the research shows that nutrition has an important role in determining serum IGF-1 levels (Yaker et al., 2005). Whether the increase in IGF-1 caused by cow’s milk occurs directly (by IGF-1 crossing the gut wall), or indirectly (as a result of the action of other factors), the research is clear. The consumption of cow’s milk and milk products is linked to increased levels of IGF-1, which in turn are linked to various cancers.