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«Tactics of Diabetes Control Turkish immigrant experiences with chronic illness in Berlin, Germany. Cornelia Guell PhD by Research The University of ...»

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Diabetes can be described as an endocrinological illness, regarding the hormone insulin, or a metabolic illness as it affects our metabolism. A healthy pancreas secretes the hormone insulin. Insulin is vital to transport glucose (that is sugar we consume with carbohydrates) to our cells. Without this key – either because it is insufficiently or not at all produced, and/or there is resistance to insulin’s action in the cells – our cells (mainly liver, muscle and fat cells) lack this vital energy source to work properly. The glucose building up in the blood stream harms organs, the vascular and nervous system. This explains both the immediate symptoms of diabetes, excessive urinating and thirst, as the body tries to wash out too much glucose in the blood, as well as effects on vision, general constitution etc., and the long-term effects of organ damage. The long name is diabetes mellitus (Latin for honey). Many languages know diabetes as sugar sickness (German: Zuckerkrankheit or Zucker, Turkish: şeker hastalığı or şeker, Arabic: sokkor).

While the scientific community can agree on above definition of diabetes as an illness of elevated blood sugar, there is much discord over definition and classification of diabetes. Diabetes can have many different causes and require different treatment. Diabetes is therefore classified in several types. The World Health Organisation (WHO) changed its diabetes classification several times, and still the only real agreement within the international medical scientific community seems to be that diabetes is not one disease but encompasses several forms. Difficult to pin diabetes down to one easy definition, WHO (1999) finally summarised: “The term diabetes mellitus describes a metabolic disorder of multiple aetiology [causation] characterized by chronic hyperglycaemia [high blood glucose levels] with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both.” As the causation of diabetes varies, WHO (1999) classifies different types. Type 1 diabetes mellitus refers to the situation in which diabetes is due to the destruction of the cells (specifically the beta cells of the Islets of Langerhans) that produce insulin. This type of diabetes usually develops in childhood or teenage years but can also develop in adults. Previous terms, later deemed imprecise, were juvenile diabetes and insulin dependent diabetes (WHO 1999).

This thesis is concerned with type 2 diabetes mellitus. Type 2 diabetes mellitus refers to the situation in which the pancreas still produces insulin but is unable to produce enough to keep blood glucose at normal levels. Most people with type 2 diabetes are insulin resistant, which means that the cells where insulin acts, such as those of the muscle and liver, respond poorly to insulin (DeFronzo et al.

1997). Consequently, higher levels of insulin are required to keep blood glucose normal and diabetes develops when the pancreas is no longer able to produce enough insulin to overcome the insulin resistance. Insulin resistance is particularly associated with obesity and physical inactivity. Previous but somewhat confusing terms for type 2 diabetes include adult onset diabetes (but with increasing levels of childhood obesity type 2 diabetes is increasingly seen in children) and non-insulin dependent diabetes (however, some people with type 2 diabetes require insulin to properly control their blood glucose levels). There are further types such as gestational diabetes which occurs during pregnancy, and current research in Africa and elsewhere tries to unravel the mystery of a type of diabetes that appears in later age but resembles much more type 1 diabetes in its causation.

The above classification is less than ten years old, and much classificatory confusion proceeded. In 1965, WHO published a first classification of juvenile diabetes and adult onset diabetes in accordance to the age of the first recognised onset of diabetes (Zimmet et al. 2004). 1980 followed the distinction of type 1 insulin-dependent diabetes mellitus and type 2 non-insulin dependent diabetes mellitus, and 1985 type 1 and 2 were omitted to retain the clinical description insulin-dependent (IDDM) and non-insulin dependent (NIDDM) diabetes. It also included other types such as malnutrition-related diabetes mellitus (MRDM), gestational diabetes mellitus (GDM) and impaired glucose tolerance (IGT). Today, WHO’s finally revised classification (WHO 1999) is internationally largely accepted, yet still considered somewhat incomplete and not always clear cut (Unwin and Zimmet 2009). It tried to capture the different causation of diabetes in accordance to current research knowledge but the rapid innovations in research render such an exercise challenging. Rock (2005: 117) suggests that recent research, particular in genetics, only adds further complexity to such classifications, for example emerging “types of type 2 diabetes” such as MODY (maturity onset diabetes of the young).

This seems to correspond with the current distinction into type 1 and type 2 diabetes.

Also, the American Diabetes Association (ADA) produced a series of recommendations throughout these decades of changing WHO reports that largely concurs with WHO’s typology and is also used outside the USA. Less agreement, however, can be reported on diagnostic criteria. It is generally accepted that the cut point for diagnosing diabetes should be when levels of blood sugar levels start posing a risk to the body; what this cut point is remains controversial (Unwin and Zimmet 2009).

A differentiated classification appeared as early as 1889, when Etienne Lancereaux (1829-1910) divided diabetes into diabète maigre (“lean diabetes”), which resisted any therapeutic attempts and was deemed incurable, while diabète gras (“fat diabetes”) showed a promising response to dietary changes (Schadewaldt 1989: 53ff). The (written) history of diabetes goes back to antiquity. This following history may mainly concern type 1 diabetes as its quite dramatic presentation and short life expectancy received much attention in historic medical texts. That is not to say that some ancient texts do not also contain complaints that would today be associated with type 2 diabetes, afflicting the wealthy – and quite likely obese – elites and rulers. The first physician documented to have used the expression “diabetes” was the 3rd century B.C. Alexandrian Demetrious of Apamea (Schadewaldt 1989: 46). The word “diabetes” referred to the ancient Greek word diabeinein, literally translated “to go to excess” but was commonly used for a wine siphon (Engelhard 1989: 3). In Greco-Roman physicians oversaw the sweetness of the urine – as many other (Western) physicians did for a long time. The adjunct mellitus in diabetes mellitus was added much later by Thomas Willis (1621-1675) who first reported the sweetness of diabetic urine. He did not, however, attribute the honey-like taste to sugar in the urine but to salt and sulphur in the blood that

decomposed in excessively inflowing liquefied body substance (Schadewaldt 1989:

52). This (today) somewhat peculiar theory combined ancient notions of impurities of the blood with his contemporaries’ views on the importance of chemicals in the understanding and treatment of disease (ibid. 52). Historians today know of much earlier records of “honey urine” (Sanskrit: madu mehé) in ancient Indian medical

texts (probably written between 300 B.C. and 600 A.D.) in which taste (Sanskrit:

rasa) – technically meaning “fluid” – played an important role7 (Müller 1989: 164).

These ancient Indian textbooks of the Susruta, Charaka and Vagbhata mentioned diabetic symptoms quite comprehensively and leave as much historic controversies as to why this knowledge had not been passed on to Greek medicine, and whether it was known that diabetic urine actually contained sugar (Schadewald 1989: 48).

Moreover, historic records have emerged that point towards the knowledge of the sweetness of diabetic urine in Arab medical texts, specifically of the Islamic physician Avicenna (980-103) (ibid. 50). It is also possible that Paracelsus (1493recognised the urine’s sweetness (he spoke of dulcedo) earlier than Willis (ibid. 52). It was not until 1776 though, when Matthew Dobson (1745-1784) first isolated the white cane-sugar-like residue in the urine, and not until 1838 that glucose was first chemically identified in diabetic urine (independently) by Apollinaire Bouchardat (1806-1886) and Eugène Melchior Peligot (1811-1890) (Engelhardt 1989: 4ff).

Paracelsus also changed the focus of diabetes research towards the metabolic system in general (Schadewaldt 1989: 52). In 1869 the young pathology research student Paul Langerhans (1847-1888) submitted a short doctorate thesis on the microscopic anatomy of the little explored organ pancreas, identifying nine different pancreatic cells (ibid. 60). The beta cells of, what by 1893 Edouard Laguesse had coined, the Islets of Langerhans were to become the focus of pancreatic diabetes research. Although the function of these cells remained unknown for many years, some researchers became increasingly enthusiastic about diabetes as a pancreatic illness, as diabetes patients showed changes in their pancreatic islet cells (ibid. 63).

Though it was not until 1889, that Mering (1845-1908) and Minkowski (1858-1931) discovered by chance that the dogs whose pancreas they had removed were developing severe diabetes and that it therefore must be the pancreas itself that was the source of diabetes (ibid. 61ff). What followed was years of scientific investigation of pancreatic function, subsequent findings of its secretion and ultimately attempts to isolate pancreatic extract for the therapy of diabetes. Research The six rasas: sweet (madhura), sour, salty, sharp, bitter, astringent.

proved difficult, leading towards many wrong conclusions and much frustration in

the scientific community that almost brought the endeavour to a halt (Bliss 1996:


The dedication of medical scientists to finding a cure for diabetes might be comparable to today’s efforts in the field of cancer and HIV/AIDS. For much of its history, (type 1) diabetes was an acute, quickly deadly disease. Willis mentioned

diabetics’ weight-loss and growing weakness in the 17th century (Schadewaldt 1989:

52) and Indian Sanskrit texts already contained accounts of diabetic coma (ibid. 48).

Many of these ancient accounts of diabetes highlighted the rarity of the illness – the genetic component of diabetes, as we know today, would have been precluded by the sometimes quite rapid premature deaths. Throughout history, the main therapeutic advice for diabetes had mainly been diet. Celsus (25 B.C. - 50 A.D.) already recommended diet (and even physical exercise), and so did Galen, Aretaeus and many of their “humoral” contemporaries (ibid. 49). Some of these therapies proved entirely unhelpful if not dangerous, as the residue of sugar in urine was interpreted as a sugar deficiency, or as many physicians concentrated on their patients’ wasting and hunger and prescribed a high-caloric diet. Nutritional advice during the last couple of centuries included the “meat diet”, “milk cure”, “cereal diet”, “fat diet” and “potato diet” (Schadewaldt 1989: 84ff).

The possibly most effective diet was Frederick Madison Allen’s (1879-1964) early 20th century “starvation therapy” (Bliss 1996: 33ff). Contrary to many of his predecessors and colleagues, the American diabetologist Allen did not believe that it was the diabetics’ undernourishment that needed attention. Exploring how a certain diet could not worsen laboratory dogs’ diabetes, he developed a low caloric diet that reduced all food intake. Often to the horror of family and even hospital staff, already very skinny patients who had lost much initial weight through their diabetes were put on a radical diet. His therapy proved quite effective – if it were not for his patients’ lack of discipline that often undermined his strict dietary constraints. Some of his famous patients (prominent in medical text books for their extreme skeletal figures) who kept to their diets showed marked improvement and prolonged life expectancy.

Others, however, died of undernourishment. Allen’s “ruthlessness” caused much controversy in a country “where being well-fed was still a sign of good health” (Bliss 1996: 35). Pictures emerging after WWII of KZ survivors reminded doctors of this era in diabetes therapy (ibid. 39).

But medical history should change with the discovery of insulin. In summer 1921 Frederick Banting (1891-1941) and his student assistant Charles Best (1899discovered insulin at Toronto University, and in 1922 patients were successfully treated with insulin which was subsequently commercially produced. In 1923 this milestone in medical history was recognised with the Noble Prize, although many controversies over authorship preceded and succeeded Banting’s discovery (Bliss 1996). In his engaging account, the Canadian medical historian Bliss (1996) traced this outstanding narrative, exploring the complexities that shape and negotiate medical sciences, their contributors and findings. The young, inexperienced provincial doctor Banting more or less stumbled across insulin in a series of amateurish and haphazard laboratory tests. His supervisor Macleod tried to provide some training and subsequent staff assistance to turn the discovered pancreatic extract into therapeutic insulin. The extract was called “insulin” (Latin insula for island), although nobody could actually prove the islets of Langerhans as the source (nor was anyone in Toronto aware that this name had already been proposed by Schafer in 1916 who did not know of de Meyer’s same idea in 1909) (ibid. 126ff).

Ultimately, some historians argue that insulin had been “discovered” earlier – as both the Romanian Nicolae Paulesco (1896-1931) and the German Georg Zülzer (1870probably had insulin in their hands (Bliss 1996: 125ff; Drügemöller and Norpoth 1989: 431). However, while these experienced researchers were concerned by the side effects and inconsistencies in the effects of insulin, the novices Banting and Best ignored or overlooked such problems. Finally, it was their collaboration with the small American drug-company Eli Lilly whose intensive clinical work started producing insulin commercially for a large market and transformed the company into an industry giant (ibid. 154ff).

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