|July 2002 Vol. 1 No.7||<<<Home|
The Pancreas – Under Attack by Cow-Milk
Most likely you will never know you have a pancreas, yet without it you would become very sick, and likely die. So this little organ is working 24/7 for you, most of the time without a single complaint. Anatomically, the pancreas is about six inches long and two inches wide, weighs about 3 ounces, and is situated in the posterior, upper left part of your abdomen. In the butcher shop this organ is sold as sweetbread (from a cow). Based on its functions, the pancreas would best be thought of as two separate organs: the organ that makes digestive juices (the exocrine pancreas) and the one that makes hormones for the whole body (endocrine pancreas).
The “exocrine pancreas” produces enzymes (delivered through a duct to the first part of the small intestine) that digest proteins, fats and carbohydrates, so they can be absorbed through the intestine. The “endocrine pancreas” produces hormones, like insulin, which regulate the use and storage of the body's main energy sources, glucose (sugar) and fats. These hormones (delivered through the blood stream) are produced in very specific clumps of cells (islets). The insulin-producing cells are called beta cells.
Type 1 (Childhood) Diabetes – The Milk-Drinkers Disease
Type 1 diabetes is often referred to as childhood type diabetes, because this has historically been the most common kind of diabetes in children, and also as insulin dependent diabetes mellitus (IDDM), because patients must take daily injections of insulin for the rest of their lives. However, this relatively common disease is not restricted to children and many times appears for the first time in adulthood. Over 1.6 million Americans have type 1 diabetes. A more common form of diabetes is called type 2 (adult onset and non-insulin dependent). This type 2 form is due to the high-fat Western diet and resulting obesity, and occurs at least nine times more frequently than type 1.
The evidence incriminating cow-milk consumption in the cause of type 1 diabetes is sufficient to cause the American Academy of Pediatrics to issue this warning, "Early exposure of infants to cow's milk protein may be an important factor in the initiation of the beta cell destructive process in some individuals." and "The avoidance of cow's milk protein for the first several months of life may reduce the later development of IDDM or delay its onset in susceptible people." (The American Academy of Pediatrics Work Group on Cow’s Milk Protein and Diabetes Mellitus – 1994).
The Milk-Invader and Molecular Mimicry
The problems all begin because of the natural condition of the intestine of a very young infant. Proteins produced by mother, and found in human mother’s breast milk, serve to promote an infant’s health and immunity from disease. During the first few months of life the intestinal wall of an infant is quite permeable in order to allow the passage of these intact proteins into the infant’s body. Unfortunately, serious health problems can develop when foreign proteins are allowed into the infant’s permeable intestinal tract. Cow-milk proteins are unique in that they are usually the first foreign proteins entering an infant’s gut and body, because most baby formulas are usually cow-milk based.
Once the cow-milk proteins are absorbed into the bloodstream, our immune system recognizes them as invaders, which as far as our bodies are concerned, could be the foreign protein of a virus’s coat or a bacteria cell wall. The immune system responds with an appropriate defense – antibodies are made against the foreign protein, and immune cells, called T-cells, are directed to find and destroy these trespassers.
Unfortunately, in an effort to do the right thing, some people’s immune systems become slightly confused and attack not only the foreign cow-milk proteins, but also the insulin-producing beta cells of the pancreas. The reason this happens in only some people, and not everyone, is unknown. One explanation has to do with the difference in the permeability of intestinal walls. Some intestines allow proteins into the body more easily, because of injuries caused by viruses, environmental chemicals, medications (NSAID, like Motrin and Advil), and the unhealthy, high-fat, high cholesterol diet. This condition is sometimes called a “leaky gut.” A very “leaky gut” will indiscriminately allow the influx of foreign proteins into the body.
Once the cow-milk protein is in the blood then a phenomenon, known as “molecular mimicry,” occurs. Foreign proteins, like cow-milk, stimulate the production of antibodies directed against small segments of their proteins – specific sequences of amino acids. Unfortunately, these same sequences of amino acids are also found on the body’s own tissues (a copy or mimic of the foreign protein segment). In the case of type 1 diabetes, a segment of 17 amino acids has been identified on the cow-milk protein that is identical to a segment on the surface of the insulin-producing beta cells of the pancreas.1 Antibodies appropriately produced to attack and destroy the cow-milk protein find the beta cells first -- they attach to the cell surfaces, activating T-cells, which then attack and destroy these insulin-producing cells. Once these cells are destroyed, the pancreas can no longer produce sufficient amounts of insulin for the body’s needs.
The Handicap of Diabetes
Even though the process of beta cell destruction may take three to five years on the average, the onset of the disease usually appears to be sudden and is often catastrophic. The apparently well child (or adult) becomes very ill with symptoms of excessive thirst, urination, and fatigue – many times followed by coma, and sometimes death. The lifesaving treatment is very specific: replacement of insulin by daily injections.
Once the beta cells are destroyed they will not grow back, therefore the disease is permanent and the patient will always require insulin (unless some future technology changes this). Insulin replacement therapy is far from perfect and does not correct all of the underlying metabolic problems. A patient living with a damaged pancreas has an increased risk for premature development of serious complications, such as kidney failure, blindness, heart attacks, osteoporosis, and cancer. As you will recall, these are also the problems faced by people without diabetes who are on the Western diet. But the threats to a diabetic’s health are much greater.
Diabetics are metabolically handicapped people, hampered in their ability to defend and repair themselves from outside injuries, like an infection or an unhealthy diet (the high-fat, high-cholesterol Western diet). Therefore, to help counteract this disadvantage, people with this disease must be cared for with vigilance – and that means very careful control of their blood sugars with insulin injections, a wholesome lifestyle, and most-importantly, a health-supporting diet. This is a diet of starches with vegetables and fruits – the less meat, dairy, processed foods and vegetable oil the better. By this effort, the type 1 diabetic has the best chance to avoid premature death and serious complications. In fact, the only people I have met with long-standing diabetes who still have all their parts working after 40 years of disease, have been those following a low-fat nearly vegetarian diet – the best example are those few fortunate people following the Kempner Rice Diet from Duke University – sometimes for 50 years.
Inherited by an Education
There is some inherited tendency to develop type 1 diabetes, but it is only a tendency, and actually most people (90%) who develop this disease do not have close relatives with it. In about 30% of identical twins, both get diabetes. To bring out this genetic tendency requires an environmental toxin. Infectious agents, like viruses, have been suspected to cause type 1 diabetes. More likely, when an infection like a virus is involved, it acts as a nonspecific stress, late in the process of disease development, that increases the body’s needs for insulin and precipitates a rise in blood sugar earlier than would have occurred otherwise. Rather than through genetic inheritance or a transmitted virus, the past 20 years of accumulated evidence has shown the tendency to run in families is largely fostered by mother and father teaching sons and daughters to consume dairy products. Since the cow-protein is the culprit activating the immune reaction, low-fat dairy products would cause at least as much harm as the full-fat versions.
Evidence Incriminating Cow-Milk:
1) Population Studies (Epidemiology):
When populations of people who are genetically similar have a different incidence of disease then something in the environment must be suspected as the cause. The strongest contact we have with our environment is our food. This environmental relationship is further confirmed when people migrate from an area of low incidence to high incidence, and increase their risk of developing disease. This migration phenomena has been seen, for example, when Samoan children move to New Zealand and when Asians move to England.2
There is a strong correlation between total cow-milk consumption and type 1 diabetes, worldwide.3 For example, Finland, a high milk-consuming population, has 36 times more type 1 diabetes than does a country of low consumption, like Japan.4 A similar relationship has been found within a single country, for example, between 9 regions of Italy – regions consuming the most milk have the most diabetes.5
Type 1 diabetes is one of the fastest growing diseases in the world. There has been a rapid increase (greater than 10-fold) in type 1 diabetes in European countries in the past few decades, especially in children under five years.6 This rise clearly points to an environmental, rather than a genetic cause. This rise has been paralleled by an increase in fluid milk intake.
There are notable exceptions to this strong positive correlation between cow-milk consumption and type 1 diabetes – but there is also a scientific explanation for the discrepancies.7,8 Examples of this apparent inconsistency are seen in Iceland, New Zealand, and the Maasai people of Tanzania, Africa. In these populations there is high milk consumption and low diabetes. The explanation is: cow-milks from different herds have important differences in their proteins. The cow-milk found in populations with a low incidence of type 1 diabetes has a much lower fraction of A1 and B betacaseins (instead they have the A2 variant). The A1 and B forms of betacaseins are believed to be the proteins that cause the body to respond by destroying the insulin-producing cells of the pancreas. When these variants of cow-milk are taken into consideration then the correlation of cow-milk consumption and type 1 diabetes becomes evident. It is estimated that 80% of dairy cows have this A1 and or B variant. One reason this may be so frequently found is because cows have been selectively bred this way to increase the protein content of the cow-milk (a quality desired by dairy producers).9
2) Case Studies:
Studies comparing populations of people with type 1 diabetes with healthy individuals indicate the risk of developing type 1 diabetes is 5.4 times greater in high milk consumers (3 or more glasses a day) compared to those who drink less milk (less than 3 glasses a day).10
3) Milk-induced Changes in the Immune System:
Children newly diagnosed with type 1 diabetes have been found to have increased levels of antibodies directed to several different cow-milk proteins.11-13
Antibodies against cow-milk protein (specifically bovine serum albumin and an ABBOS peptide of 17 amino acids) were found to react with a similar-looking sequence of amino acids on the beta cells of the pancreas in 100% of children newly diagnosed with type 1 diabetes.1
Antibodies to insulin often appear in children who develop type 1 diabetes. This is caused by exposure of an infant (before the age of three months) to cow’s insulin (bovine insulin) found in the milk the child drinks.14 These antibodies to cow-milk also attack human insulin and may be the trigger for the autoimmune response that causes diabetes.
Immune cells, known as T-cells, have been found to proliferate in response to cow-milk proteins in newly diagnosed type 1 diabetic children.9 These T-cells, once activated by cow-milk, then attack the beta cells of the pancreas and destroy them. Molecular mimicry appears to be involved.
Avoidance of cow-milk through exclusive breast feeding prevents the development of antibodies to cow-milk protein (beta casein).15 Only bottle-fed infants show reactions to cow-milk proteins. Increased levels of antibodies to these cow-milk proteins are found in children with type 1 diabetes.
Please note: A nursing mother consuming cow-milk can pass the proteins to her infant through her breast milk.16 Whether this kind of cow-milk protein consumption is a cause of type 1 diabetes is not known, but it would be prudent for a nursing mother to avoid cow-milk in her diet.17
4) Animal studies:
Experimental animals (mice and rats) fed cow-milk have been found to develop diabetes.18-20 It is important to note that soy protein and wheat protein have also caused experimental animals to develop diabetes.21 This is another reason breast feeding exclusively is the right choice and why soy-based infant formulas are not an acceptable substitute for cow-milk based formulas (see next month’s newsletter for even more compelling reasons to use soy with caution). For maximum benefit for the young child, feed mother’s breast milk exclusively for six months and then as a decreasing part of the diet until the child is two years of age. (For a comprehensive discussion of the importance of breast feeding read The McDougall Program for Women).
Sensible Action: Cow-milk Avoidance:
The dairy industry makes attempts to argue against their products causing type 1 diabetes. (You can view their very selective use of the scientific literature to defend the safety of their products here: http://www.nationaldairycouncil.org/lvl04/nutrilib/relresearch/diabetes_6.html)
These arguments don’t fool the American Academy of Pediatrics and hundreds of top scientists worldwide, and they don’t fool me. I would suggest you take the less risky road for your family. Since cow-milk is ideal for baby cows and was never intended for human children, act naturally and avoid a potential tragedy. With the same action you will be reducing the risk of constipation, arthritis, ear infections, asthma, bed-wetting, eczema, lactose intolerance, and obesity, as well as future cancers, strokes and heart disease. There is no human nutritional requirement for cow-milk. It is deficient in dietary fiber, essential fats, niacin, vitamin C, and iron, and overloaded with calories, saturated fat, environmental chemicals, and disease pathogens (bacteria and viruses).
The dairy industry’s main selling point is calcium; however a thorough review by researchers at the Department of Nutritional Sciences, University of Alabama, of 57 studies on cow-milk and bone health came to this conclusion: “In fact, of the studies providing strong evidence, only 29% showed favorable effects and 14% showed unfavorable effects on bone status. These values suggest that there is little risk of harm to the skeletal system if recommendations to the general population to consume dairy foods are heeded. However, these values do not provide a solid body of evidence to support this recommendation.”22 By the way, most of the studies reviewed here were paid for by the dairy industry – and they still failed to show their products met the manufacturer’s multimillion dollar advertising claims. No one has ever become ill or died from a lack of cow-milk. Without a doubt, the opposite is true for billions of people.
Pancreatic cancer is the fifth leading cause of cancer death in the United States. Because of the deep location of the pancreas inside the abdomen, diagnosis of the disease is difficult, and as a result it is nearly always fatal in a matter of months – 90% have died within 12 months of diagnosis. Even with the best that modern medicine has to offer, approximately 25,000 people die from this disease yearly. Therefore, if you want to effectively win the war on cancer of the pancreas you must do so by prevention.
The only well-established causative factor is cigarette smoking. However, diet, I believe, is the most likely cause of most cases. This is disease of developed countries – where the rich Western diet is consumed. There are data that show a diet high in fruits and vegetables is associated with a lower risk of pancreatic cancer.23,24 Obesity, alcohol, coffee, saturated fat, animal protein, high-fat dairy products, and low physical activity increase the risk. There is also an association with chronic pancreatitis and diabetes – both are diseases of the Western diet (discussed above and below).
Prevention is the key to dealing with pancreatic cancer. But what can be done for those less fortunate patients already with pancreatic cancer? A case control study demonstrated that patients with metastatic pancreatic cancer who ate a diet of fruits and vegetables (a macrobiotic diet) lived longer (17 months versus six months) and enjoyed an improved quality of life.25 This study from researchers at Tulane University showed half of those on the macrobiotic diet were alive after one year, compared to only 10% on the regular diet. The researchers concluded that the macrobiotic approach may be an effective treatment, writing "This exploratory analysis suggests that a strict macrobiotic diet is more likely to be effective in the long-term management of cancer than are diets that provide a variety of other foods."
Pancreatitis is an inflammatory condition of the pancreas that is very painful and at times deadly. The mortality rate of acute pancreatitis is about 10%. Chronic forms of pancreatitis can devastate a person’s life over many years. Patients suffer abdominal pain and malnutrition, and have a higher risk of pancreatic cancer. Chronic alcohol abuse and an unhealthy diet are known to cause acute and chronic pancreatitis.26 A high protein ketogenic diet has been reported to cause pancreatitis that killed a child.27 (The Atkins diet is a high protein, ketogenic diet). Diets high in sugar and fat will cause the level of blood fats, known as triglycerides, to rise in some people. The elevated triglycerides seem to interfere with the circulation of the pancreas and cause severe inflammation, known as pancreatitis. A low-fat, complex carbohydrate diet and alcohol avoidance is the foundation to preventing further attacks.
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2. Verge C. Environmental factors in childhood IDDM. A population-based, case-control study. Diabetes Care. 1994 Dec;17(12):1381-9.
3. Dahl-Jorgensen K. Relationship between cows' milk consumption and incidence of IDDM in childhood. Diabetes Care. 1991 Nov;14(11):1081-3.
4. LaPorte R. Geographic differences in the risk of insulin-dependent diabetes mellitus: the importance of registries. Diabetes Care. 1985 Sep-Oct;8 Suppl 1:101-7.
5. Fava D. Relationship between dairy product consumption and incidence of IDDM in childhood in Italy. Diabetes Care. 1994 Dec;17(12):1488-90.
6. Patterson C. Is childhood-onset type I diabetes a wealth-related disease? An ecological analysis of European incidence rates. Diabetologia. 2001 Oct;44 Suppl 3:B9-16.
7. Elliott R. Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999 Mar;42(3):292-6.
8. Thorsdottir I. Different beta-casein fractions in Icelandic versus Scandinavian cow’s milk may influence diabetogenicity of cow's milk in infancy and explain low incidence of insulin-dependent diabetes mellitus in Iceland. Pediatrics. 2000 Oct;106(4):719-24.
9. Cavallo M. Cell-mediated immune response to beta casein in recent-onset insulin-dependent diabetes: implications for disease pathogenesis. Lancet. 1996 Oct 5;348(9032):926-8.
10. Virtanen S. Cow's milk consumption, HLA-DQB1 genotype, and type 1 diabetes: a nested case-control study of siblings of children with diabetes. Childhood diabetes in Finland study group. Diabetes. 2000 Jun;49(6):912-7.
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13. Saukkonen T. IgA bovine serum albumin antibodies are increased in newly diagnosed patients with insulin-dependent diabetes mellitus, but the increase is not an independent risk factor for diabetes. Acta Paediatr. 1995 Nov;84(11):1258-61.
14. Vaarala O. Cow's milk formula feeding induces primary immunization to insulin in infants at genetic risk for type 1 diabetes. Diabetes. 1999 Jul;48(7):1389-94.
15. Monetini L. Bovine beta-casein antibodies in breast- and bottle-fed infants: their relevance in Type 1 diabetes. Diabetes Metab Res Rev. 2001 Jan-Feb;17(1):51-4.
16. Jakobsson I. Dietary bovine beta-lactoglobulin is transferred to human milk. Acta Paediatr Scand. 1985 May;74(3):342-5.
17. Murch S. Diabetes and cows' milk. Lancet. 1996 Dec 14;348(9042):1656.
18. Elliott R. Dietary prevention of diabetes in the non-obese diabetic mouse. Diabetologia. 1988 Jan;31(1):62-4.
19. Karges W. Immunological aspects of nutritional diabetes prevention in NOD mice: a pilot study for the cow's milk-based IDDM prevention trial. Diabetes. 1997 Apr;46(4):557-64.
20. Scott F. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats: dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells. Diabetes. 1997 Apr;46(4):589-98.
21. Akerblom H. Putative environmental factors in Type 1 diabetes. Diabetes Metab Rev. 1998 Mar;14(1):31-67.
22. Weinsier R. Dairy foods and bone health: examination of the evidence. Am J Clin Nutr. 2000 Sep;72(3):681-9.
23. Stolzenberg-Solomon R. Prospective study of diet and pancreatic cancer in male smokers. Am J Epidemiol. 2002 May 1;155(9):783-92.
24. Potter D. Pancreas cancer--we know about smoking, but do we know anything else? Am J Epidemiol. 2002 May 1;155(9):793-5.
25. Carter J. Hypothesis: dietary management may improve survival from nutritionally linked cancers based on analysis of representative cases. J Am Coll Nutr. 1993 Jun;12(3):209-26.
26. Athyros V. Long-term follow-up of patients with acute hypertriglyceridemia-induced pancreatitis. J Clin Gastroenterol. 2002 Apr;34(4):472-5.
27. Stewart W. Acute pancreatitis causing death in a child on the ketogenic diet. J Child Neurol. 2001 Sep;16(9):682.
John McDougall All Rights Reserved