Part of my issue is that, while milk is a source of calcium, it does not prevent fractures in elderly women. In combination with vitamin D it does alter the way the bones look, but that doesn’t translate to protection. Have a look at the seventy-five thousand person lifetime study: “The 3-year risk of any fracture combined or separately was not associated with intake of calcium or vitamin D.”
Milk is also promoted for all populations, and is very commonly advertised by African-American or Asian athletes. But reasonable estimates of African Americans show “approximately three fourths of African-Americans have the potential for symptoms of lactose intolerance.” A new slogan: “Milk: It Gives a Body Gas” did not make the Dairy Board cut. The intolerance of most ethnic groups to large quantities of milk has been known since the 1960′s.
I’ve also been known to cite the data on the correlation between cow’s milk intake and the risk of autoimmune diabetes in genetically susceptible populations. But I was unprepared by a new researcher’s thoughts on the possibility that milk might be promoting beta cell increased division and leaving us open to insulin resistant diabetes.
Here’s the abstract. It’s worth thinking about, and maybe even a dietary change would be in order for prediabetics.
Milk signalling in the pathogenesis of type 2 diabetes.
Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany. email@example.com
The presented hypothesis identifies milk consumption as an environmental risk factor of Western diet promoting type 2 diabetes (T2D). Milk, commonly regarded as a valuable nutrient, exerts important endocrine functions as an insulinotropic, anabolic and mitogenic signalling system supporting neonatal growth and development. The presented hypothesis substantiates milk’s physiological role as a signalling system for pancreatic β-cell proliferation by milk’s ability to increase prolactin-, growth hormone and incretin-signalling. The proposed mechanism of milk-induced postnatal β-cell mass expansion mimics the adaptive prolactin-dependent proliferative changes observed in pregnancy. Milk signalling down-regulates the key transcription factor FoxO1 leading to up-regulation of insulin promoter factor-1 which stimulates β-cell proliferation, insulin secretion as well as coexpression of islet amyloid polypeptide (IAPP). The recent finding that adult rodent β-cells only proliferate by self-duplication is of crucial importance, because permanent milk consumption beyond the weaning period may continuously over-stimulate β-cell replication thereby accelerating the onset of replicative β-cell senescence. The long-term use of milk may thus increase endoplasmic reticulum (ER) stress and toxic IAPP oligomer formation by overloading the ER with cytotoxic IAPPs thereby promoting β-cell apoptosis. Both increased β-cell proliferation and β-cell apoptosis are hallmarks of T2D. This hypothesis gets support from clinical states of hyperprolactinaemia and progeria syndromes with early onset of cell senescence which are both associated with an increased incidence of T2D and share common features of milk signalling. Furthermore, the presented milk hypothesis of T2D is compatible with the concept of high ER stress in T2D and the toxic oligomer hypothesis of T2D and may explain the high association of T2D and Alzheimer disease.
Copyright © 2010 Elsevier Ltd. All rights reserved.
- PMID: 21251764
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