MILK – THE PROMOTER OF CHRONIC WESTERN DISEASES
Bodo C. Melnik * Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Sedanstrasse 115, D-49090 Osnabrück, Germany
Medical Hypotheses 6 January 2009 journal homepage: www.elsevier.com/locate/mehy
Ronald Peters, MD – Comments
The purpose of cow’s milk is to get a wobbly newborn calf up and running with the herd before it gets eaten by a predator. This explains the elevated insulin and IGF (growth hormone) levels which increase weight gain and growth that greatly benefits the young calf. However, these effects are not designed for young, or old, humans. According to this author, long-term milk consumption is a contributor to chronic diseases, including acne, atherosclerosis, diabetes mellitus, obesity, cancer, and neurodegenerative diseases. The dairy industry has convinced us that milk is essential for calcium and strong bones, which is not true. Green vegetables, beans and tofu have more calcium than milk and it is more bioavailable for the body to absorb and utilize. Think about it – a cow eats grass and makes six or seven gallons of milk a day (for her calf). Many people are addicted to their daily dairy intake, but I have seen again and again, if they eliminate it for a month, they feel better.
s u m m a r y
Common chronic diseases of Western societies, such as coronary heart disease, diabetes mellitus, cancer, hypertension, obesity, dementia, and allergic diseases are significantly influenced by dietary habits. Cow’s milk and dairy products are nutritional staples in most Western societies. Milk and dairy product consumption is recommended by most nutritional societies because of their beneficial effects for calcium uptake and bone mineralization and as a source of valuable protein. However, the adverse long-term effects of milk and milk protein consumption on human health have been neglected. A hypothesis is presented, showing for the first time that milk protein consumption is an essential adverse environmental factor promoting most chronic diseases of Western societies. Milk protein consumption induces postprandial hyperinsulinaemia and shifts the growth hormone/insulin-like growth factor-1 (IGF-1) axis to permanently increased IGF-1 serum levels. Insulin/IGF-1 signalling is involved in the regulation of fetal growth, T-cell maturation in the thymus, linear growth, pathogenesis of acne, atherosclerosis, diabetes mellitus, obesity, cancer and neurodegenerative diseases, thus affecting most chronic diseases of Western societies. Of special concern is the possibility that milk intake during pregnancy adversely affects the early fetal programming of the IGF-1 axis which will influence health risks later in life. An accumulated body of evidence for the adverse effects of cow’s milk consumption from fetal life to childhood, adolescence, adulthood and senescence will be provided which strengthens the presented hypothesis.
Insulin and the insulin-like growth factor system
The insulin-like growth factor (IGF) system is essential for normal embryonic and postnatal growth and plays an important role in the function of a healthy immune system, lymphopoiesis, myogenesis and bone growth among other physiological functions. Growth hormone (GH) and IGFs play an important role in growth and tissue homeostasis. GH secreted by the anterior pituitary binds to GH receptor, expressed on most peripheral cells of the body. In peripheral tissues and predominantly in the liver, GH induces the synthesis and secretion of the 7.65 kDa polypeptide hormone IGF-1, the mediator of the growth stimulating activity of GH. More than 90% of circulating IGFs are bound to IGF-binding protein-3 (IGFBP-3), the rest to IGFBP-1, -2, -4, -5, and -6, and less than 1% of IGFs circulate as free IGFs in the plasma. IGF-1 signal transduction is mediated primarily by the IGF-1-receptor (IGF1R), a tyrosine kinase receptor, which is able to form heterodimers with insulin receptor (IR). IGF-2 binds to IGF-2-receptor (IGF2R), a scavenger receptor down-regulating IGF-2. IGF-2 is also able to bind to IGF1R. Insulin primarily binds to IR-A and IR-B, but also binds with lower affinity to IGF1R. IGF-1 and IGF-2 bind to IR with lower affinity (Fig. 1). IGF1R signal transduction is mediated primarily by the activation of the Ras-Raf-MAP kinase pathway and the phosphoinositide 3-kinase (PI3 K)/Akt pathway. IGF-1 acts a strong mitogen inducing cell growth and proliferation but inhibits apoptosis [1]. The IR-B isoform is the form best known for the classic metabolic responses induced upon insulin binding and this isoform has low affinity for IGFs [1]. The IR-A isoform arises from alternative splicing of exon 11 encoded by the IR gene. Activation of the IR-A by insulin or IGF-2 leads to mitogenic responses similar to those described for IGF1R. Increased signalling via IR-A has been associated with the development of cancer [2]. In this regard, insulin and IGF-2 signal transduction via IR-A and IGF-1 signalling via IGF1R induce and amplify mitogenic responses (Fig. 1). and adult animals, especially when IGF-1 was administered together with the protease inhibitor casein, the primary protein in milk. High milk consumption in humans is associated with a 10–20% increase in circulating IGF-1 levels among adults and a 20–30% increase among children [7–14]. Girls with a milk intake below 55 ml/day had significantly lower IGF-1 serum concentration compared to girls consuming more than 260 ml/day [15]. In 2109 European women, IGF-1 serum levels positively correlated with the intake of milk [16]. It is important to notice that dairy products increase IGF-1 levels more than any other dietary sources of protein like meat [9–16]. Moreover, milk consumption raises the ratio of IGF-1/IGFBP-3 indicating an increasedVbioavailability of IGF-1 [8–10,12].
The insulinotropic effect of milk and milk products
Fermented and non-fermented milk products give rise to insulinaemic responses far exceeding what could be expected from their low glycaemic indexes (GI). Despite low GIs of 15–30, milk products produce three to sixfold higher insulinaemic indexes (II) of 90–98 [17]. A large and similar dissociation of the GI and II exists for both whole milk (GI: 42 ± 5; II: 148 ± 14) and skim milk (GI:37 ± 9; II: 140 ± 13) [18]. It has been suggested that some factor within the protein fraction of milk is responsible for milk’s insulinotropic effect [18]. Skim milk has been identified as a potent insulin secretagogue in type 2 diabetic patients [19]. Except for cheese with an insulin score of 45, milk and all dairy products including yoghurt, ice cream, cottage cheese, and fermented milk products have potent insulinotropic properties [20]. In a one-week intervention study of 24 pre-pubertal eight-yearold boys the effect of daily intake of 53 g of either lean meat or skim milk (1.5 l per day) was studied with regard to insulin and IGF-1 responses. In the skim milk group insulin significantly increased by 105% (from 22 to 45 pmol/l) and IGF-1 significantly increased by 19% (from 209 to 249 ng/ml) [12]. There was no significant increase in either insulin or IGF-1 in the meat group. This study clearly showed that milk protein consumption induces hyperinsulinaemia and increased IGF-1 serum levels. The addition of an ordinary amount of 200 ml milk to a meal with a low GI increased the insulin response by 300% to a level typically seen from a meal with a very high GI like white bread [21]. The comparison of 43 breast-fed and 43 cow’s milk formula-fed one-week-old term infants showed higher insulin levels in the cow’s milk formulafed group at 90 and 150 min postprandial [22].