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Male Bacteria Oppose Diabetes

Tuesday, 26 February 2013 by

Reading Time: 2 minutes

This editorial piece has largely been provided by Olive Leavy – editor of Nature Reviews Immunology.[1] Although numerous gene polymorphisms associated with autoimmune disease risk have been identified, additional factors — including environmental factors and sexual dimorphism (with a higher incidence of autoimmunity in females) — are also thought to have important roles in driving

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The fact we are not ill more often is due to the remarkable capacity our bodies have to revert to a state of ‘homeostasis’ – a somewhat dull word provided by Walter Cannon in the early 20th century to summarise the work of the physiologist Claude Bernard who was based in Paris in the 1850s. It has dominated biology, physiology and medicine ever since. Homeostasis is regularly used to describe the exquisite intrinsic ability we possess to respond to, counteract and adapt to external and internal sources of damage and disturbance to maintain health/function in us and other living organisms.

A more contemporary – albeit controversial term to describe this is: ‘Homeodynamics’.[1] This is the concept that we are not static but constantly adapting. Homeodynamics, accounts for the fact that the internal milieu of complex biological systems is not permanently fixed, is not at equilibrium, and is subject to dynamic regulation and interaction among various levels of organisation. Aging, senescence and death are the final manifestations of unsuccessful homeodynamics and in utero exposure represents the first opportunity and experience  for remodelling and constant adaptation.

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Comment: It’s common knowledge that a protective navy of bacteria normally floats in our intestinal tracts. Antibiotics at least temporarily disturb the normal balance. But it’s unclear which antibiotics are the most disruptive, and if the full array of “good bacteria” return promptly or remain altered for some time. In studies in mice, University of Michigan scientists have shown for the first time that two different types of antibiotics can cause moderate to wide-ranging changes in the ranks of these helpful guardians in the gut. In the case of one of the antibiotics, the armada of “good bacteria” did not recover its former diversity even many weeks after a course of antibiotics was over.

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