Do the former colonizing powers, like their former colonies, have “postcolonial medicine,” and if so, where does it take place, who practices it, and upon whom? How has British medicine in particular responded to the huge cultural shifts represented by the rise of the New Commonwealth and associated postcolonial immigration? I address these questions through a case study of the medical and political responses to vitamin D deficiency among Britain’s South Asian communities since the 1960s. My research suggests that in these contexts, diet frequently became a proxy or shorthand for culture , while disease justified pressure to assimilate. As historians have demonstrated over the last two decades, the practice of medicine and medical research across a diversity of colonial and imperial contexts shared a particular relationship with power, whether that power be examined at the institutional, the political, or the social level.      Historians have recently begun to examine postwar medicine in the new nations that replaced Europe’s imperial colonies under the rubric “postcolonial medicine.” Research approaches (and thus outcomes) in the history of medicine have followed two major paths: some scholars have used the term “postcolonial” largely empirically, to designate the      Here, I certainly use the term “postcolonial” to indicate the period from the end of World War II until the present; my investigations will not delve extensively into colonial matters. However, I also incorporate the connotation that the social and cultural effects of colonialism do not simply disappear with its political and governmental apparatus, and that therefore researchers should interrogate emergent practices and institutions in the light of their colonial predecessors and antecedents. If, as much current scholarship in the history of medicine suggests, “colonial medicine” was transformative of medical practice and medical knowledge in colonizing, as well as colonized, societies, then its impact should persist and shape medicine, broadly construed, in the former as well as the latter locales, even after the end of formal empire. Thus I ask, did a distinctively “postcolonial” form of medicine emerge in the former imperial centers, as it did in the former colonies? If a metropolitan “postcolonial medicine” does exist, what does it look like, who practices it, and upon whom? Using the case of rickets and osteomalacia in Britain’s diverse South Asian communities since the 1950s, I will argue that the bodies of immigrants and ethnic minorities became the metropolitan sites of imperial medicine’s “postcolonial” development.          Britain struggled with terrible labor shortages in the years during and immediately following World War II. It addressed this problem in part through a very active program of labor recruitment in its dominions, colonies, and former colonies, building on the long-held imperial tradition that all British subjects were entitled to unrestricted entry to the United Kingdom: it was, after all, “home.” As other historians have noted, this      As the postwar economy and reconstruction work slowed in the 1960s, Britain’s appetite for foreign  labor diminished. A sense of a shrinking labor marketplace, as well as anxieties about racial and cultural mixing, fueled demands for controls on immigration and the dispersal of immigrant and ethnic communities. Outbreaks of violence in highly diverse communities further exacerbated indigenous fears and, some scholars argue, politicized immigrant and ethnic populations as well.      This, then, was the context in which British medical practitioners and policymakers found themselves again facing an “old” illness. Rickets in the postwar era has been widely regarded by doctors and scholars alike as a “historical” disease—a disappearing symptom of Victorian industrialization and urbanization. Reconsidering it through a postcolonial lens encourages us to drag our gaze away from this nineteenth-century disease experience (and the expectations with which that weight of history has imbued rickets) and to refocus on the condition as potentially “foreign,”      At the same time, the case studies of elite research units working with rickets in Manchester and London also illustrate certain continuities between colonial and postcolonial medicine, not least in the ways in which the newly available postcolonial bodies  were co-opted by existing research programs and interpreted through the lens of ongoing debates within communities of clinicians and medical researchers.zenanas (enclosed women’s quarters) and rendering available for study the bodies of women and girls. Thus Western female researchers, like the pioneering women doctors before them, were encouraged to go to India “where they were needed,” while Indian women were admitted, if not actively recruited, into the growing indigenous scientific workforce.	In 1929 Walter Fletcher, secretary of the British Medical Research Council (MRC), returned a set of research reports to George Newman, chief medical officer to Britain’s Ministry of Health (MoH).	And yet studies of nutrition and diet, wherever they were performed, could not adopt wholesale or exclusively the laboratory-driven model of “objective” biomedical research, however attractive from an imperial point of view. The researchers depended heavily on data about daily life readily available only to its objects—in this case, the Indian girls and women themselves—and were necessarily interested in customs, practices, and identities. In this discipline, even metropolitan studies of nutrition and public health were forced to adopt colonial medicine’s nearly anthropological methods. And as the case of rickets and osteomalacia in postwar Britain will demonstrate, when those metropolitan studies were also addressing non-white bodies, they often echoed the focus on “racial habits”but will help us by suggesting new problems for more primary work by investigators here.”	Fletcher’s response to Wilson and Surie’s studies, and to nutritional-deficit diseases in India generally, also typifies the colonial mode and moment. His reply to Newman enthused: “there is a great field for work in India by trained investigators and especially with regard to nutrition as related to osteomalacia and rickets. . . . Any progress they make will not only help India enormously, sic] deficiencies.”	In such discussions of medical research in India, Fletcher and his colleagues were treading a very familiar path. It was characteristic for empirical work in the colonies to be regarded—at least by researchers within elite Western institutions—as providing raw material for analytical work in the metropole. Similarly, colonially based medical research commonly pathologized social practices of which the colonial power and colonizing culture disapproved.	Wilson and Surie’s observations—as was often the case for colonial research work—reached a relatively small, if powerful, audience.	Rickets and, in adolescents and adults, osteomalacia are conditions caused by vitamin D deficiency: without vitamin D , the body cannot absorb calcium or phosphorus, and therefore cannot properly build bones. In the Lancet, for example, editorialized in 1940 that      	With improved air quality, housing, and diet, as well as new understandings of supplementation, florid nutritional rickets had virtually disappeared from British cities by the 1930s, somewhat to the disgruntlement of clinicians involved in medical education, particularly in pediatrics.	  it must be galling to the research workers, laboratory and clinical, who have given the whole story of rickets a reasonably simple explanation in terms of vitamin-D deficiency to find [that] “mild cases are still seen too frequently even 	Vitamin D deficiency was, of course, a medical concern during World War II, as the Medical Research Council actively campaigned for the enrichment of basic foodstuffs. It is far from coincidental that the secretary of the MRC in this period was Edward Mellanby, who first defined rickets as a nutritional-deficiency disease  and one that could be prevented by dietary supplementation.	After the war, small- or large-dose supplementation continued to be the routine clinical response to nutritional rickets, although “careless” or “preoccupied” mothers were increasingly blamed for their children’s now-rare condition.	Simultaneously, studies and criticisms of mass supplementation through the fortification of basic foodstuffs increased, particularly as the era of rationing drew to a close. From 1951 to 1964, successive Conservative governments—and more determinedly, the Treasury bureaucracy—sought to free themselves (and food manufacturers) from the obligation of managing the British diet through the provision of welfare foods and mandatory fortification.	By 1955, the Ministry of Health requested the British Paediatric Association “to enquire into the incidence of infantile hypercalcaemia and to consider whether the disease had any relationship to the intake of vitamin D.”	  more cases [of hypercalcaemia] have been reported in Great Britain and Northern Ireland than in other parts of the world. There is evidence that the fortification of foods has materially increased in Great Britain. . . . The disease does, however, appear to be rare in the United States where fortification is less extensive, although the practice of supplementation is probably more common.	In fact, subsequent studies revealed that in the period 1953–55 approximately a dozen cases in total were reported in the United States, while the United Kingdom averaged almost a hundred per year.	Partly as a result of reductions in fortification, partly as a result of increasingly biochemical understandings of the D deficiency diseases, and, as we will see, partly because of the emergence of a new “at-risk” population, rickets again became the focus of considerable clinical and media attention. It reentered the policy arena in the late 1950s and 1960s. The decline of overt rickets, and the intense biochemical investigation of blood chemistry in the 1950s and early 1960s, had brought with them yet another contested category of rickets: “biochemical rickets.” Initially diagnosed by blood tests for abnormally low levels of serum calcium and raised levels of serum alkaline-phosphatase, “biochemical rickets” could be discovered in children and adults showing neither clinical nor radiological signs of disease. Obviously, such a definition of rickets/osteomalacia greatly increased its rate of incidence (particularly among the majority community), and therefore the public health significance of the condition—at least for those who accepted the category. Not everyone did: policymakers and the ministries resisted the idea of asymptomatic rickets well into the 1970s. In response to a 1973 parliamentary question from Baroness Summerskill, for example, Lord Aberdare told the House of Lords rather dismissively: “Recent reports of . . . alleged ‘biochemical rickets’ that is, without clinical signs, in the indigenous population of one city are being considered by an expert panel of the Committee on the Medical Aspects of Food Policy and it is too early to say what, if any, action is needed.”	As Aberdare’s response suggests, nutritional rickets and osteomalacia, whether biochemical, radiological, or clinical, were still marked out as diseases of impoverished city-dwellers. As in the prewar period, such populations contained a significant proportion of immigrants—but this time, the affected immigrants were almost exclusively from the “New Commonwealth,” especially India, Bangladesh, and Pakistan. Whether recruited to ease Britain’s postwar labor crunch, driven out by poverty or the xenophobic regimes of new East African nations, or simply drawn by historic ties and the rhetoric of Commonwealth, “these people” became a highly visible—and not always welcome—new presence in industrial towns and cities across the United Kingdom.      	It is in relation to this new population that both the continuities and the disjunctures of “postcolonial” medicine become clearer. Compare “tropical medicine”—arguably the archetypal discipline of colonial medicine—with the spectrum of medical responses to postcolonial immigration and the emergence of nonwhite ethnic communities in postwar Britain. 	Like tropical medicine, medical approaches to the postcolonial immigrants often—both institutionally and intellectually—served state and industrial interests, and engaged actively with social and policy debates. But unlike the “tropical diseases” of colonial medicine, the diseases of (or at least the diseases commonly identified with) the emergent postcolonial communities in Britain—for instance, rickets, tuberculosis, leprosy, sickle-cell anemia, and thalassemia—were not organized into a single medical specialty with its own institutions, programmatic aims, or distinctive and consistent methodologies. Rather, the ailments of immigrant and ethnic populations became selectively visible to medical researchers when those conditions justified or facilitated ongoing research programs. Lancet, the British Medical Journal, Proceedings of the Nutrition Society, and other prominent journals used the term “Asian Rickets” throughout the period covered by this paper, and well into the 1980s, to the apparent satisfaction of their wide professional readership, and even in articles actively disputing theories of unusual Asian susceptibility.	As local campaigners and health workers have noted, rickets and osteomalacia were far from the biggest or most pressing medical problems faced by Asian immigrants and their British-born descendants; in the years 1955–80, clinical rickets and osteomalacia were diagnosed in only a few score Asian children, adolescents, and elderly per year, and all were easily and successfully treated.	Given its relatively minor epidemiological impact, and its tractability to simple, cheap, and effective medical treatment, why did rickets draw so much medical and policy attention to an otherwise underserved population? In part, this was because its reappearance in the United Kingdom was an affront to public expectations and eroded political and medical achievements. In 1967, W. T. C. Berry, then secretary of the Committee on Medical Aspects of Food Policy , testily declared to the Nutrition Society’s annual meeting: “Rickets excited great emotion, largely because it is thought that it is reappearing and this is a sign of social regression.”	“Asian rickets,” however, was not just an embarrassing public health problem: for some medical research communities, it was also a solution of sorts. Consider the case of metabolic medicine, and particularly the elite (and expensive) area of metabolic biochemistry. In 1963, the prestigious Manchester Royal Infirmary took the major step of opening a new Metabolic Unit, built with a £30,000 grant from the Wellcome Fund. S. W. Stanbury headed the Unit, and when the University made the additional significant commitment of endowing it as a professorial one in 1965, he was appointed as a second full-time professor of medicine. This joint institutional investment reflected the view that such disorders were part of “the new frontier”  in medicine, and illustrates the status accorded to metabolic research.	Studies of vitamin D metabolism and related aspects of lipid metabolism in both chronically ill and acutely ill patients were among the Metabolic Unit’s early topics of research, and thus at the heart of its institutional development and identity. But remember that the vitamin D deficiency diseases were in steep decline across the United Kingdom in this period. A 1960–61 survey performed by the British Paediatric Association , and intended to explore the impact of reductions in vitamin D fortification on the incidence of both rickets and hypercalcemia, showed extremely low rates of both conditions in the native population: “In 1960–61, the total of rickets (in non-immigrants) reported to the British Paediatric Association . . . by all paediatricians in Britain was 1.5 per month, and in 1961–62, 1.0 per month.”sic] from backward countries.”	In London, Charles Dent, professor and principal investigator at the University College Hospital (UCH) Metabolic Ward, which he had opened in 1951, was also becoming aware of a shift. In 1960, he had responded eagerly when consulted on a suspected case of nutritional  rickets in an immigrant child: “The family being Turkish Cypriots makes me think very strongly that we may have an instance here of classical rickets due to oral dietary deficiency, undoubtedly the rarest cause of rickets nowadays in British people”; Dent mused: “curiously enough we see it much more often in visiting imigrants  were fortified here we would have the problem of persuading the Asians to use it in the same way that we have difficulty in persuading them to take supplements and get into what sunshine there is!”	The ethnic communities themselves were not voiceless, and they actively deployed the data and medical attention produced by and about their bodies. In 1976, the Community Relations Committee requested a meeting with the DHSS to address the question of dietary deficiency among the Ugandan Asians. The CRC representatives to the meeting  did accept that “rickets and deficiency states in Ugandan Asian immigrants . . . were primarily due to cultural factors”; nonetheless, they called for the provision of religiously acceptable school meals, and especially “suitable fortification of food.”	Perhaps these ethnic populations could even be said to have colonized their researchers in turn; certainly O’Riordan became a strong advocate of fortification and other active interventions from the DHSS, and opposed its education-alone policy. Writing in 1978 to E. M. Widdowson, head of the Dunn Nutritional Laboratory and then chairing COMA, he complained:      	  I am rather concerned that so little practical progress seems to have been made in achieving some form of vitamin D fortification to prevent vitamin deficiency in Asian immigrants. I wonder if you could let me know what the current situation is and what the hold up seems to be. It is a long time since we showed that the addition of vitamin D to chaphatti flour, corrected vitamin D deficiency in Asians.	Doctors approaching the problem of “Asian rickets” from a public health or clinical perspective were even more critical. Dr. Sam Tucker, a London pediatrician, argued that while 20 percent of Asians in his district of South-all suffered from rickets, “not one European child” had the condition: “If that’s not a condemnation of our methods, I don’t know what is.”New Statesman entered the fray, accusing COMA of being dilatory, and of failing to address “a rickets epidemic” in Asian children, to the great annoyance of the Department.Guardian newspaper was equally scalding in its criticism, and focused on questions of ethnic prejudice:      	By 1979, the left-wing 	  Health education workers and minority groups have complained that the DHSS has never publicly acknowledged the seriousness of the rickets problem. . . . Despite frequent representations to the Government, the DHSS has not taken up the suggestion that certain foods eaten by the Asian community, such as chapatti flour, should be fortified with vitamin D. Now Dr. Carlos Ferreyra, chairman of the Community Health Group for Ethnic Minorities, has written to the Prime Minister comparing the present Government’s reaction to rickets to the attitude in the 1940s.		  At that time, he said, when rickets was affecting the white population, food was fortified and an extensive programme of nutrition education was undertaken. . . . However, COMA, the DHSS committee looking at aspects of food policy has advised against food fortification and suggested instead only ad-hoc nutritional advice.	Internal memos offer perhaps the best picture of the state of affairs within the DHSS during this crisis. In response to one harshly critical article, Darke wrote to a colleague:      is pathetic. The one action which would not solve the problem, and might well land us in NO FORT therefore PUBLICITY. HOW DO WE DO IT? TV is the answer.”	  This sort of “article pressure” is always worrying. I think at night of all the Asian children with rickets who could be cured or their illness prevented so easily. Is it my fault? To some extent we have failed. In 1972, our hunch was education but the massive Departmental machine etc etc and our own problems means that [we] cannot easily launch a campaign. What is needed is TV and radio time in short bursts at intervals to repeat and repeat the message. We have not access to radio and TV!! Our pathetic attempt at education via leaflets 	Darke was not to get her television ads: the idea was comprehensively dismissed as “a very expensive way of reaching a very small target.”is new, and suggestive of a distinctively “postcolonial medicine” in Britain. The Manchester example hinted at a novel (if still empire-building) integration of clinical, epidemiological, and laboratory research, drawing on local ethnic communities as a research resource; the program at Middlesex reiterated established colonial divisions between basic research and clinical observation. Only the latter came to fruition in the form initially proposed.      	The use of non-European  bodies to advance established research agendas is hardly a novelty in the history of medicine. However, the location of such studies at the heart of elite metropolitan institutions with a general, rather than specialist, remit—university teaching hospitals, not tropical medicine institutes—	In another way, too, U.K. studies of rickets and osteomalacia among Commonwealth immigrants illustrated continuity between colonial medicine and the medical mode that superseded it. Just as colonial medicine stigmatized nonwhite bodies as simultaneously pathological and vulnerable 	Assimilation has, for immigrants, long been equated with health, while resistance—often through the preservation of dietary or religious practices—has been similarly linked to illness.The solution lies in adequate education of Asian women immigrants firstly to speak English and secondly in the elements of child care in this climate.	  The involvement of Asian children may be due to multiple factors, including habitual consumption of a racial diet, lessened exposure to sunshine, failure of immigrants to learn (or to be taught?) that supplementary intake is essential beneath the smoke pall of a northern city, and the hypothetical possibility that a dusky skin requires more ultraviolet radiation than a white skin. The problem of this racial group is circumscribed and ought to be evanescent. 	As this quotation suggests, race was considered a contributory factor, echoing the colonial medical literature both in targeting nonwhite racial traits as unhealthy, and in focusing closely on interactions  between race and climate among dislocated populations. Other researchers had identified the same “problem”: “It seems a reasonable suggestion that the Pakistani, by virtue of his pigmented skin, requires more sunlight than the native Glaswegian to produce the necessary amount of vitamin D.”Lancet was calling for direct observation and supervision of rickets prophylaxis among “young immigrants” by health visitors as a “justifiable extension of preventive medicine in these circumstances.”Lancet article used recent studies comparing the vitamin D content of indigenous and immigrant diets in Glasgow (and discovering near-parity) to argue that “skin pigmentation . . . is likely to be the major intrinsic cause” of late rickets among British Asians, even when taking previous dietary habits into account.	Most articles published during this first wave of “New Commonwealth” immigration focused on the new Asian communities, though often casually likening them to indigenous “problem families.”	Whether or not they accepted such models of racial difference, by the early 1970s researchers across the field were coming to the conclusion that “the combination of dietary habits and social customs among immigrant Asians, including their traditional clothing and their habit of avoiding direct sunlight may be . . . the more important aetiological factors in the production of rickets and osteomalacia.”	However, though the clinical literature focused attention on dietary choices and cultural traditions, and on the imperative need for Asians in Britain to assimilate, the demographics of rickets in British Asian communities 	  They examined 74 adults and children, and found convincing evidence of active rickets or osteomalacia in no less than 35; children between 5 and 15 were most seriously affected. Since all the cases responded rapidly to small doses of calciferol, simple deficiency of vitamin D was apparently responsible. Seeking an explanation for these rather startling observations, the Glasgow workers inquired into the Pakistanis’ dietary habits. Children younger than 5 were receiving welfare foods, which presumably protected them from the disease.Lancet’s leading article discussing it were much cited in further research, this aspect of its findings received little comment or attention—even from G. C. Arneil and his colleagues, authors of the original work. Similarly, evidence that poor housing —rather than modest clothing—might be responsible for elevated levels of osteomalacia and rickets among British Asian women and girls was disregarded.	Although both the study and the prevent Asian rickets remained focused not on the provision of attractive supplements, or fortified staple foods, or brighter dwellings, but on educational programs explicitly designed to change culturally sanctioned behavior and dietary choices, and to encourage assimilation. In an unusually direct letter, replying to questions posed by a Glasgow sixth-form student working on a class project, an L. Willcocks of the Department of Health and Social Services summed up the arguments against fortification as they had emerged over the previous decade; the letter is worth citing at length:      	By the mid-1970s, then, a new category of rickets had joined “clinical,” “radiological,” and “biochemical” rickets: “Asian” (or “Asiatic”) rickets. Sufferers were sought out and actively treated; however, governmental efforts to 	  Regarding supplementation of food by Vitamin “D,” in 1977, the Committee on Medical Aspects of Food . . . set up a Working Party to report on the need for food fortification with Vitamin D in relation to deficiency disease of all ages in the population. . . . The first decision which had to be made was whether fortification should be “universal”  or “selective” (i.e. applied to foods mainly or solely eaten by those at risk). The universal approach was ruled out for a number of reasons, amongst them being that there was a general trend to the view that food should be as “pure” as possible and that there was a segment of the population that has rooted objections to what it sees as “mass medication”—here can be instanced the history of fluoridation in this country. In addition intakes of Vitamin D in excess are known to be harmful and this is a very important factor to be taken into account when the majority of the population in this country do not suffer from a deficiency of the vitamin.		  The point about the danger of excess Vitamin D also of course is relevant when considering the case for fortification on a selective basis. Also the eating habits of those from the Indian sub-continent vary considerably.	Willcocks noted that these arguments had turned COMA against additional fortification, and continued with a revealing discussion of the action to be taken instead:      sic] that they be kept in doors and that their clothes should be such as to cover a considerably greater proportion of their body. . . . Thus the natural process of acculturisation [sic] might well bring about the complete eradication of rickets. . . . We feel that the best way, in all the circumstances, to deal with the problem is by education . . . to increase the awareness . . . of the problem of rickets and vitamin D deficiency and the relatively simple ways the disease can be combated. As I said, sunlight is free and Vitamin D supplements are available under NHS arrangements.	  But . . . dietary sources are not the chief or even the most physiological sources of Vitamin D. In fact the chief source is the ultra-violet component of sunlight, and it can be said to be the source with “all the advantages”: it is free, and is natural and being in the open air has many beneficial side effects. It is indeed held by many that the reason why the appearance of rickets has been confined 	This assumption that assimilation would cure the “Asian rickets” problem was widespread and almost unexamined. While researchers, health workers, and even policymakers might doubt the efficacy of different strategies aimed at encouraging assimilation, none questioned its benefits—at times comparing British Asians unfavorably to West Indian immigrants, whose health was credited to their more rapid acceptance of “a mode of life more like that of European[s].”	In 1981, researchers still commonly assumed a link between assimilation and health, distinctiveness and disease. One group complained:      	  Prolonged residence in the United Kingdom and a long period of exposure to western customs was not associated with a better vitamin D status in the adults. The vitamin D status of this community was still markedly inferior to that of a white control group despite attempts to influence their dietary practices and habitual solar exposure.	The authors of another 1981 article, despite noting suggestively that “the absence of European children [in Glasgow] with nutritional rickets since 1975 . . . is attributable to health education and improved living and social conditions,” still attributed rickets among British Asians to “traditional diet” and sun-avoidance rather than a failure to benefit from those improved social conditions.	Research results challenged many aspects of this model of pathological cultural distinctiveness/curative assimilation. In 1982, a study concluded:      	  No consistent relationship could be demonstrated between the dietary consumption of vitamin D, phytate, chuppatty flour, fibre, oxalate or meat and the serum 25 hydroxyvitamin D concentration. This supports the view that dietary factors play only a minor role in the aetiology of vitamin D deficiency among Asian immigrants.	But as late as 1986, investigators still felt obligated to test the theory that Asians were racially unsuited, by their darker skins, to the British climate, concluding bluntly that “Indian and Pakistani immigrants have the same capacity as Caucasians to produce vitamin D in response to ultraviolet irradiation.”	By the mid-eighties, the term “Asian rickets” no longer figured in medical indices, and appeared only in the work of a few long-term researchers. Yet through the 1990s, researchers for the Medical Protection Society were still reporting on the dangerous health effects of “Hindu vegetarianism,” and its costs to the NHS. And like these attitudes, rickets also remained in Britain’s Asian communities, despite much-increased outreach and education efforts like Glasgow’s “Stop Rickets” campaign of 1981: “In spite of the extensive medical, social and political attention this condition has received . . . vitamin D deficiency continues to persist in certain Asians in a clinically florid fashion. An effective preventative policy is long overdue.”	By the late seventies and early eighties, the expert medical community that had developed around “Asian rickets” broadly supported the use of supplementation in one form or another as a short-term response to the problem’s persistence.	The case of rickets illustrates the continuation of certain modalities of colonial tropical medicine: the same actors and institutions were involved, and the imperial networks that medicalized culture and race in the former colonies and the New Commonwealth came into play equally in conceptualizing immigrant and ethnic minority health needs at home. Sociologists (and a few historians) have already pointed out that attention to the medical needs of Asian, African-Caribbean, Cypriot, and other minority ethnic groups has come primarily from clinicians and health policymakers—and thus only indirectly reflects those communities’ own perceptions and medical experiences.	Asian immigrants and their doctors were given two choices: rickets and osteomalacia could be “Asian”—in other words, caused by the dietary and dress choices of Pakistani, Bangladeshi, and Indian immigrants and their families—or they could be “English”: caused by the unfortunate climate and northern latitude of the United Kingdom (sometimes in combination with the much-discussed “dusky skin” of these communities). But either way, in the eyes of medical policymakers, the disease could—and therefore should—be cured by assimilative behavioral changes: changes to make British Asians less Asian or more English. And because assimilation could become cure, responsibility for the two diseases was pinned firmly on the affected communities, families, and individuals themselves. This was a clear shift from British policy responses to rickets in the indigenous community before, and especially during, World War II. And it is far from coincidental that this medical discourse on the malign impacts of “alien” culture on individual bodies ran in parallel to a political discourse predicting similarly disastrous results from the interpenetration of the British body politic by “alien” cultural elements. If, in the end, there were no rivers of blood, there were certainly no rivers of (vitamin D– fortified) milk, either.


The goal of this study was to describe how activists engaged in campaigns to change alcohol policies in inner city areas framed alcohol problems, and whether or not their frameworks reflected major models used in the field, such as the alcoholism as a disease model, an alcohol problems perspective, or a public health approach to alcohol problems. The findings showed that activists’ models shared some aspects with dominant approaches which tend to focus on individuals and to a lesser extent on regulating alcohol marketing and sales. However, activists’ models differed in significant ways by focusing on community level problems with alcohol; on problems with social norms regarding alcohol use; and on the relationship of alcohol use to illicit drugs. These groups have developed local and statewide ordinances to limit and regulate alcohol outlets, organized networks to eliminate alcohol billboard advertising, and launched protests against racial and ethnic targeting by alcohol and tobacco companies –4. Howevi.e., the former uses a master frame to portray its honesty, with supporting core frames citing the uncertainty of health risks; and the latter use a master frame of distrust for the industry and core frames citing the substantial health risks of smoking) . Tsmoking) . Cress asmoking)  studied 1.1.alcoholism as an addictive disease model, the alcohol-related problems framework, the personal responsibility and blame model, and the public health framework for addressing alcohol problems.A number of frameworks have been widely used by alcohol policy researchers ,9,12 to The alcoholism as an addictive disease paradigm became the dominant model for conceptualizing alcohol-related problems in the US after World War II. This approach reflects strong anti-prohibitionist sentiment and focuses primarily on the problems of addiction within the individual. In this model, alcoholism is regarded as a loss of control over alcohol in biologically predisposed individuals who experience a myriad of health and social problems as a result of their addiction. Individual alcoholics are believed to be the main source of society’s problems with alcohol, and providing adequate alcoholism treatment is viewed as the main public policy solution for handling alcohol-related problems .Although the alcoholism as a disease model was immensely influential and still shapes some clinical and lay people’s understanding of alcohol problems, by the 1970s, the scientific community began to question the validity of bundling such a wide range of problems under the rubric of alcoholism. As Room  noted, aThe personal responsibility and blame model for alcohol problems was popularized during the wave of citizen activism regarding drinking and driving in the early 1980s. This model targets the individual drinker as deviant and criminal for violating laws and harming others. As Renairman  the result of that, there is very little participation in the children’s schooling. And since there’s not enough money at home, the children often have to look for work instead of going to school. And then their mothers also have to find one or two jobs because welfare doesn’t give enough money. And so I see that alcohol causes all of the disrepair and destruction of the family”. Another respondent from this city talked about the cause-and-effect relationship of alcohol as it relates to husbands who are abusive drinkers. He focused on situations in which a man might “drink up his check”, letting his kids starve and rent go unpaid, which would the cause his spouse to get upset, and be possibly beaten by him.About 10% of the informants mentioned youth drinking issues when defining alcohol-related problems. Most of the comments were references to underage drinking, problems stemming from youth drinking, or youth drinking environments. The kinds of common problems associated with youth drinking included violence or disruptions at parties and accidents related to driving under the influence. A respondent from Baltimore said, “I know we have a problem in terms of use of alcohol by minors. The statistics in that report [Governor’s Blue Ribbon Commission] are pretty startling about use of alcohol by minors; the dangers associated with that use related to drunk driving, drinking, and boating accidents; violence associated with the use of alcohol, including sexual violence”. One informant from Detroit found that alcohol use is a serious problem among African Americans, particularly young people. He described the regular practice of high school students taking their lunch breaks to buy 40-ounce bottles of alcohol, which they consume in parking lots while socializing with friends, with the full awareness of teachers. The drinking continues with students purchasing alcohol on the way home from school and consuming to the point where drinking on one’s porch and leaving the malt liquor bottles behind “becomes a part of [the] culture of the neighborhoods.Models of alcohol problems based on addictive or abusive drinking were widely discussed by informants in the study. More than half (51%) of respondents defined alcohol problems in these terms. Responses describing alcoholism or addiction (30%) emphasized symptoms such as dependence, loss of control, and tolerance. For example, one informant from Detroit stated that “alcoholics. . . are physically and psychologically dependent on alcohol” and defined alcohol as a drug because users build up a tolerance for it and require increasing amounts before they exhibit signs of intoxication. In Los Angeles, an informant defined alcohol problems as “somebody who is addicted or their life is controlled in a daily acquisition of alcoholic beverages”. An informant from Milwaukee defined alcohol problems in terms of his own experience as an alcoholic, whereby alcohol takes over a person’s life to the point he or she cannot “do anything without alcohol”. A respondent from San Antonio commented on the medical consequences of continual alcohol use and difficulties with withdrawal: “The medical problems that occur from them constantly being exposed to the alcohol is long range. . . . When this person is a alcoholic, it’s hard on detoxification, as opposed to a person who is dependent on a drug like marijuana or dependent on a drug like heroin. The withdrawal symptoms and all the things that person has to go through medically, it could tear you apart. . . . It’s very traumatic when you see somebody that you know going through the withdrawal symptoms of alcohol”.Aside from addiction, some informants (30%) defined alcohol problems in terms of abusive or excessive drinking. Most often informants described intoxication or drinking to the point that it leads to personality changes or social disruption. An informant from Detroit defined alcohol problems as “when there’s a overindulgence which causes the person who’s consuming the alcohol behavior or mood to change. . . [which] could possibly lead to a violent individual or individual with no rationale or whatever”. A respondent from Los Angeles made a similar point: “Alcohol problems is when a person drinks on a continual basis. . . they must have that 6-pack every night or several cocktails. It can also be a problem for even just a weekend drinker. And, it just changes up the person’s whole personality”. In Milwaukee, a respondent defined alcohol problems as “any use above moderation” that impairs judgment or physical actions, or a negative change in behavior because of the abuse of alcohol.A public-health-oriented model of alcohol problems also was widely reflected in responses by informants in the study. Nearly half of those interviewed (46%) discussed one or more issues related to alcohol sales and marketing. Alcohol problems were defined in terms of the overconcentration of alcohol outlets (16%); problems with selling practices and the environment in and around outlets (10%); and challenges with zoning, licensing, and regulating stores (6%). A respondent from Milwaukee focused on the problems of having a high density of alcohol outlets and the problematic selling practices of owners. He mentioned a neighborhood population composed of 63% youth, with almost 30 liquor stores in a 14-block area. He said many business owners knew welfare had been cut in Wisconsin, so they would not take a 6-pack apart and sell single beers at the beginning of the month; however, in the second through fourth weeks, “they know people are going through real hard times, they’ll set up deals and stuff. So they could still make their money and pull you in. . . . And they most definitely try to work with the minors in the neighborhood”. A community leader from Oakland also discussed the problems with outlets, which she said were intensified by the fact that her neighborhood had “five liquor stores within two blocks”. This respondent viewed “alcohol problems as a liquor outlet [includes stores where at least 30 to 40% of sales are in alcohol] and it can be people in bars”. She stated, “I have noticed that whether it’s a momma-and-poppa store on a corner, if they sell alcohol. . . people will go in and buy beverages and come out. And then they’ll stand there and [go] back and forth just getting alcoholic beverages. . . . And then when they get too intoxicated to go about their business. . . they would just either sit down there in front of the store and go to sleep or they stand there and they beg. . . . The fact there they were out there begging was. . . one thing that was bad. . . “cause most of the people in this community are working families or either seniors”. The respondent also mentioned that the families and seniors had to pass youth selling drugs out in front these establishments, litter from the numerous containers of alcohol, and/or people lying or sitting down in the street. A respondent from Los Angeles linked overconcentration with zoning and licensing issues: “Alcohol became a problem when the city planners allowed them to over-saturate it with liquor stores, when the land usage laws were ignored. The city administrators were aware that there was an overconcentration of alcohol. . . but they looked the other way. They haven’t sold any liquor license since 1965; however, liquor stores are popping up all over because the liquor licenses that were sold never expired”.Easy accessibility to alcoholic beverages through high levels of physical availability (12%), attractive pricing (5%), and aggressive sales and promotion (3%) were other important issues voiced by informants in their definitions of alcohol problems. Respondents linked high levels of alcohol availability to heavy alcohol consumption and to a variety of related problems. Echoing these concerns, one informant from Raleigh said, “The major thing is the sheer amount of alcohol that’s sold in our neighborhood is a problem . . . . The fact that more alcohol is sold than any other legal product. . . that’s a real problem because it encourages alcoholism, domestic abuse, trash, filthiness around the neighborhood”. A respondent from Los Angeles said, “Alcohol [is] usually the most available in communities that can least afford it. And when I say the most available, I mean. . . it’s not unusual on some of the main thoroughfares to find 4 or 5 liquor stores within six blocks”. In Detroit, the director of a community-based organization focused on cheap pricing and convenient packaging of alcohol, which “causes the most devastation”. He stated, “It’s the drug that’s legal, it’s the drug that’s most readily available, and the packaging is such that anybody can afford it. There was a time when those little bitty airline bottles of liquor or booze. . . there was a time when the only place you could buy that was a souvenir shop on an airplane. . . . But now they sell it in the stores all day every day, 75 cents, 50 cents. . . . They went from the fifth. . . [to] the pint. Then they went to the pocket pint, which is smaller than a pint, just large enough to slip right into the ol’ back pocket, whip it out whenever you want, to the airline size. In other words, we’re covering all areas of the market. If you got 50 cents, you could walk in here and get a little swigger to shake the hanks off of you”. In addition to expressing concerns about the high quantities and low prices of beverages available in these communities, some informants focused on characteristics of beverages  they believed to be particularly harmful, such as fortified wines, malt liquor, and 40-ounce portions.Alcohol advertising and media images (12%) and alcohol-related billboards (5%) also were defined as alcohol problems within these communities. Informants believed the glamorization of alcohol enticed people, especially vulnerable populations, such as youth and the poor, to drink either to achieve status or popularity or to escape from problems. Advertisements from television and billboards were identified as the major vehicles through which these messages were conveyed, and informants believed their influence was enhanced by subliminal seduction. One informant from Baltimore said, “In this community, we have a lotta kids that are teenagers that are doing the 40-thing. It’s so popular because they got the commercials and they used to have the billboards. . . . And these teenagers can’t wait for somebody to buy them wine coolers or beer or whatever it is, whatever the drink of choice is, like Alize. . . . A few people used to drink it. . . but now because the advertisement has pushed it, people are drinking that more often. . . . The advertisement is what pushed these things. . . and it is so obvious, but nobody realizes it”. A respondent from San Antonio remarked that alcohol billboards were very prevalent in low-income areas and kept alcohol fresh in a user’s mind. He described a big sign that stood over a church and showed a fifth of liquor being poured into a glass over ice. To get the sign removed, activists worked for many months and met with local and state politicians. However, after being removed, it was replaced with another alcohol ad “with a pretty lady holding the bottle”. This respondent was particularly concerned about the message to children who saw billboards in a supposedly safe environment. A respondent from Milwaukee criticized the heavy promotion of alcohol on billboards throughout the community and argued that “subliminal seduction” helps entice consumers to purchase alcoholic beverages. In Oakland, one informant cited as an aspect of alcohol problems “a subliminal level that comes through advertisements or romanticism that comes with the illusions of the freedom that alcohol brings”.Informants in the study were particularly concerned about alcohol promotion activities targeted at vulnerable populations, such as ethnic minorities, low-income groups, or youths (7%). Leaders believed targeting poor or other disadvantaged neighborhoods with excessive advertising and alcohol sale venues, while excluding more powerful and affluent communities from these tactics, was inherently unjust and led to higher rates of alcohol problems and worse social conditions in poorer areas. One respondent from Oakland said, “We’re not upper class. We’re semi lower income. That the alcohol industry targets us big time. They make it quite easy and available to buy your one can of poison. . . . You know that strong shit that they’re out of their mind with one bottle of it, you know. That malt liquor stuff. . . . What an easy target is someone that you know maybe not got a lot of education, that may not have a job, and they set them up for addiction. . . . And they’re starting younger and younger and younger and younger as the years go by”.Although few contemporary studies have focused on community and neighborhood problems related to alcohol use, respondents in this study were keenly aware of these problems. More than two-thirds discussed alcohol problems in terms of the impact of alcohol use on broader community life. Within this category, the largest proportion of respondents (28%) suggested alcohol use or related issues  were problematic because they had negative effects on the community as a whole and/or could be considered a social problem. For example, one of the activists in Los Angeles stated, “We look at alcohol problems like any other social problem. It has social groups, and we would say that there is a number of different social conditions that create the substance abuse problem; specifically, the alcohol problem in the communities that we work in, which are mostly Latino. So we don’t look at it as an individual issue. We see a tremendous social problem in that it involves thousands and tens of thousands of people, and I’m not just talking about people that abuse, but the people that are victims of domestic violence or economic [problems]”. A number of the informants also defined alcohol problems in terms of the nuisances  and anti-social behaviors  associated with public drinking and its effects on community life. Many of these themes were stated by a respondent from Milwaukee who said, “I define an alcohol problem with people who are either walking up and down the streets, in clearly intoxicated stages; carrying bottles of alcohol. . . whistling or being loud and rude to people; urinating; defecating in public, which happens around here; leaving their bottles; being passed out on your steps. Some drunk drivings you’ll see up and down the street here. Accidents, people vomiting, that’s the outward appearances of an alcohol problem here in this immediate neighborhood”.A number of activists (14%) defined alcohol problems in terms of the impact of alcohol use on crime in their communities. The most common crimes attributed to alcohol were robbery or stealing; crimes associated with lack of inhibition, such as bar fights and violent confrontations; and prostitution. One informant, a police officer from Los Angeles, described some of these issues: “Ninety percent of the females we arrested were involved with alcohol at the time of arrest, where they’re either inebriated or involved with consuming. . . . And then the people. . . trying to make dates with these girls—most of ‘em are under the influence, so it lowered their inhibitions to go after things like that. . . . Most of the fights that occurred at the bars was abuse of alcohol. People just lose their tempers and [are] out of control and then. . . we have an apparent homicide. All related to this alcohol situation”. An informant from Raleigh focused on neighborhood theft as an issue: “I define it when I see people that are intoxicated hanging around on the streets, not working. At the day care, people break in cars the minute they park ‘em out there. . . . We’ve had several break-ins in the mornings when parents drop children off. I consider that a problem because they have to support their habits and they are not working, so they go out to do whatever they need to do. We’ve had several break-ins in the day care, too”.Some leaders interviewed (10%) expressed concerns about the impact of alcohol use on local community economies, especially those related to depressed housing values and the lack of economic development in poorer communities. For example, one interviewee from Raleigh stated he was focused on the family “trying to climb out of poverty” who lives on the same block and sees their property value “go to hell” and “who have a 8- or 10-year-old kid that they don’t think they can let play in his own neighborhood”. A respondent from Los Angeles suggested that alcohol consumption, sales, and distribution create environmental problems, such as the focus on alcohol outlets to the exclusion of other types of businesses: “I think a lot of that [lack of commercial development] has to do with people saying, ‘Oh, there’s a lot of liquor stores in the two-block radius. I’m not putting my Starbuck[s] or my Borders Books [there].’” From a related perspective, some informants (8%) described how questionable alcohol marketing and sales tactics or problematic drinking styles were concentrated in poorer or ethnic minority communities, as compared with those in middle-class or suburban environments. Other structural problems  were mentioned, but with less frequency. A somewhat higher percentage of respondents (6%) voiced concerns about the exposure of youth to adverse social conditions in communities as a result of alcohol use or sales and marketing.Another major issue raised by respondents defining alcohol-related problems was the interrelationship between alcohol use and the social environment (23%). Some leaders interviewed believed permissive social norms (8%), the tendency to ignore or rationalize problems associated with drinking (7%), and the belief that drinking is necessary for recreation or fun (3%) contribute to drinking problems. One respondent from Oakland said, “I can’t speak for other cultures. . . but I can tell you about Latino culture. If you’re going to have a party for a child, if you want everyone to have a good time, the children, the adults. . . many times you would include liquor. You would bring alcohol to the party, and for me, that––well, some years back––that would be very normal. . . . I would see that there would be a birthday or a baptism, and you’d have the piñata for the child, but there would always be liquor. I think that is something that we have to educate our community about. . . because I think that [at] a party for children, there doesn’t necessarily have to [be] liquor there. Although the children won’t drink the alcohol. . . from the time they see this, they grow up seeing it as something normal”. An informant from San Antonio said he does not define alcohol problems from the standpoint of being an alcoholic, but in terms of people overdrinking for recreational purposes: “I just think people use alcohol to an excess. . . . It’s just that people think that alcohol is a way to have fun. And that’s where the misconception is, and the misuse starts”. In addition to these issues, a few respondents defined alcohol problems in terms of the disrespectful behavior of drinkers (2%), as a reflection of spiritual problems (2%), and as a potential danger to the broader social fabric (1%).In defining alcohol problems, some informants focused on drug-related issues (17%). Some viewed alcohol use as particularly harmful because it leads to illicit drug use and abuse. For example, an informant from Detroit, a police officer, defined alcohol as an abused drug that leads to the abuse of other drugs: “Alcohol is like the gateway. It’s the formation, the start of, the beginning [of] problems into other substance abuse”. He described the progression from 40-ounces of alcohol to cigarettes and cigars, then on to marijuana, and eventually to heroin and cocaine. This abuse leads to the loss of jobs due to inebriation, inability to function, or failure to pass drug screening tests. Other responses focused on the fact that alcohol is a legal drug (9%) that can be as dangerous as or more easily abused than illegal drugs. These responses often described the joint use of drugs and alcohol or the physical proximity of drug dealing to alcohol outlets. An informant from Baltimore stated, “All of our open-end drug markets are located next to alcohol outlets. . . . Alcohol is the single most abused drug in our neighborhood. It is abused by those persons who are manically depressed. People who are self-medicating [with] alcohol who also use other substances. Crack users kick their high, so to speak, by using malt liquor and malt liquor that is 5 to 6 times higher in potency than the average malt liquor. . . . The illegal drugs are not as abused as alcohol”.3.2.After defining alcohol-related problems, informants were asked to describe which alcohol problems they viewed as most important in their community. The respondents mentioned many of the themes described in the previous section; however, substantial and significant differences were found with respect to the prevalence of themes ranked as the most important problems relative to the themes used to define alcohol problems . Probablp < 0.10) and domestic violence as among the most important alcohol problems as they were to include these factors in their problem definition.A substantial divide also was found between the percentage of informants defining alcohol problems in terms of negative drinking consequences for individuals or families (44%) and the percentage ranking these issues as the most important problems (15%). Moreover, significantly more informants defined alcohol problems as self-medication (14%) and family problems (27%) than saw those as among the most important problems . In addition, fewer respondents ranked health problems, job problems, low morale, and idleness as the most important problems than included these factors as part of their definition of alcohol problems, although these differences were not statistically significant. However, informants were as or more likely to regard youth alcohol-related problems , and the proportion regarding drugs as an important problem was 17%, compared with 10% who included drugs as a factor in defining alcohol problems. Respondents were four times more likely to view lack of alcohol education as important rather than to define alcohol problems in those terms (9% versus 2%). A similar trend was found with respect to alcohol outlet regulation and youth concerns. The only major negative discrepancy between defining versus ranking alcohol problems occurred with regard to respondents mentioning general community problems (28% versus 12%). However, this should be considered in conjunction with the finding that a higher percentage of respondents ranked crime and lack of alcohol education among the most important issues than mentioned them in defining alcohol problems.3.3.p = 0.016) were significantly more likely than were those from other cities to define alcohol problems in terms of alcohol addiction and abuse, while respondents from Oakland (p = 0.021), Raleigh (p = 0.007) and Baltimore (p = 0.023) were significantly more likely than were those from other cities to define these problems in terms of community issues. In addition, respondents residing in Detroit (p = 0.010), San Antonio (p = 0.003) and Baltimore (p = 0.008) were more likely than were others to mention socio-cultural issues when defining alcohol-related problems. Religious leaders were significantly more likely to define alcohol problems in terms of alcohol sales and marketing (p = 0.021) and drug problems (p = 0.000) than were other informants.The analyses explored whether significant differences existed between how alcohol problems were defined and how they were ranked by respondents in different communities and by informants who played different types of roles in community leadership. Because differences existed in the distribution of types of activists across different cities , regressp = 0.013) and informants living in Baltimore (p = 0.001) were more likely than were others to describe alcohol abuse and alcohol addiction as important alcohol problems, and professional activists (p = 0.32) and residents of Raleigh (p = 0.0000) were more likely than were others to view community-level problems in this manner.In terms of ranking alcohol-related problems, politicians (Although few overall differences were found with respect to how respondents from different areas or in different roles framed alcohol-related problems, the findings suggest that framing processes may be nuanced according to different community contexts or policy goals. For example, respondents in both of the cities that emphasized community-level problems were engaged in policy changes regarding alcohol outlets, and respondents in communities that emphasized the socio-cultural context of alcohol abuse and addiction were engaged in fighting media images of alcohol.4.The findings from this study illustrate that activists engaged in efforts to change alcohol policies in local communities expressed some of the same conceptualizations as did those characterizing the dominant models for framing alcohol problems. Their definitions of alcohol problems reflected some of the assumptions associated with the alcoholism as a disease model, the alcohol problems perspective, and the public health model of alcohol problems. The only model that had little support was the individual responsibility and blame model, described in the drunk driver reform movement. However, the findings also showed the emergence of other significant frameworks not described in the literature. These models focused on the impact of alcohol use on the broader community and neighborhood context, on problems in the normative context of alcohol use, and on problems linking alcohol use with illicit drug use.When the respondents were asked to rank problems in terms of their importance, the community model of alcohol problems and public health model emerged as the most dominant, followed by the alcohol problems perspective, normative problems and drug problems related to alcohol, and finally models based on alcoholism as a disease or abusive drinking.As described previously, the goal of the study was to describe the frameworks used by leaders engaged in campaigns to change alcohol policies in inner city areas, and to examine their diagnostic framing in order to better understand how social movements form. Social movement theorists have argued that the framing process mirrors the goals and strategies of activists seeking social change ,11. GiveIn fact, the adverse impact of alcohol at the community and neighborhood level appears to be one of the most salient ways of framing alcohol problems for citizen groups interested in social activism in inner city communities. Based on interviews in this study, the public use of alcohol was perceived to have very negative consequences in areas with high levels of crime, poverty, blight, drug use, and other social problems. A previous analysis from this study  showed tet al. [The findings from the present study suggest that expanded frameworks of alcohol problems that encompass neighborhood- and community-level effects might be most useful for developing prevention approaches that relate to the experiences of people living in disadvantaged neighborhoods. As described in recent research on alcohol policy , 22, theet al.  on alcoh


Verbascum thapsus) has a large number of synonyms and old local “nick names” which connect the plant with mycobacteria. A strong history of medicinal use has been uncovered for the treatment of tuberculosis, tubercular skin disease, leprosy, and mycobacterial disease in animals. Here, we examine problems encountered in treating such diseases today, the historical and scientific links between mullein and pathogenic bacteria, and the possibility that this common weed could harbour the answer to beating one of the world's biggest infectious killers.Common mullein weed ( It has killed ancient Egyptians and Iron Age British settlers as well as John Keats, D. H. Lawrence, and Vivien Leigh. Throughout history, it has left its mark on our ancestors as “phthisis”, “consumption”, and the “white plague”. But far from being a disease of the past, Tuberculosis (TB) is now killing almost 5000 per day, or one person about every 20 seconds . The WorMycobacteria are notoriously tough micro-organisms. Their intrinsic resistance to many antibiotics can be largely attributed to the unique structure of the cell envelope, which is rich in high molecular weight fatty acids and peptidoglycan cross-linkage . PermeabThree of the four first-line antibiotics listed above work by directly or indirectly affecting the synthesis of the mycobacterial cell wall and this remains an area of pharmaceutical interest . The thrUp to half of pharmaceutical agents prescribed today contain at least one ingredient derived from plants —an indicVerbascum thapsus, or common mullein.  Ireland has a relatively low number of native vascular plant species, at 815 . During Mullein has grown wild throughout Ireland for centuries—on walls, wasteland, quarries, and roadsides. It can grow to heights of up to two metres, with a round woolly stem, broad basal leaves, and yellow flowers which bloom from June to September  4, 26]., 26.4, 2 The first English language herbals—written as far back as the sixteenth century—also point to mullein as a TB remedy and praise it's soothing and expectorant properties. Culpeper advises that mullein will help a persistent cough, tumours, or inflammations of the throat , while GMycobacterium in general. While revising historical remedies, we must consider our modern day understanding of microbiology. It is now possible to prove that diseases which were once believed to be completely unrelated are in fact caused by the same pathogen. Mycobacteria are an example of this—causing a variety of infections in humans and animals  have long been known to possess expectorant and demulcent properties—these are now attributed mainly to its mucilagenous constituents and saponins [Verbascum species endemic to Turkey have activity against the Mycobacterium smegmatis model [Verbascum species—both from whole plant [As already outlined, the mulleins (saponins . Althougsaponins  while exis model . In partle plant –53 and sle plant –56 (TablVerbascum species belong) harbour the chemotaxonomic markers of verbascoside, aucubin, and catalpol [Verbascum species are examples of this. The hydrolysis products of aucubin and catalpol, and aucubin itself, have been shown to have antimicrobial activity [Staphylococcus aureus, including drug resistant strains [As a family, the Scrophulariaceae (to which catalpol . The latcatalpol . Plants activity , 70. Veractivity  but is p strains . One pos strains . Further strains .Saponins are also a major chemical constituent of mullein. This diverse class of compounds are derived from a 30-carbon precursor and perform a range of biological actions. While previous studies have shown weak antimicrobial activity and often only at low cell density , 75, somVerbascum species have been shown to contain a diverse range of compounds, and similar compounds have been shown to have antimycobacterial properties, the two have yet to come together in a comprehensive study. Thorough in-vitro screening of the bioactivity of mullein extracts against mycobacteria is required, such as that carried out by Turker and Camper against other respiratory pathogens. When dealing with the spectrum of animal- and human-related mycobacterial diseases, continued laboratory screening of herbal extracts should be encouraged. It would appear that a member of the Scrophulariaceae which was once known as “bullock's lungwort” and has now been proven to be rich in lipophilic molecules is an ideal place to mine for potential anti-TB agents. However, while It is clear that many of mullein's historical uses, synonyms, anecdotes, and local “nick names” connect this plant with mycobacteria. Of course, the historical links between mycobacteria and mullein may be coincidental. A large number of medicinal uses have been recorded for this plant while its synonyms are almost as numerous. While this is common for a traditional medicinal plant, numerous connections to one pathogen—recorded throughout history and across the world—are not. Whether the link is coincidental or rooted in true antimycobacterial actions, it merits investigation. An ancient plant, an ancient infection, an ancient link, and a modern-day cure?


Researchers are exploring various ways to control the stubborn biofilms that bacteria form on medical devices and in many persistent infections.  David Davies stood at the hospital bedside of his great-aunt, who had recently had all her toes amputated to try to prevent persistent wounds from spreading. It didn't work; doctors would later amputate both of her feet, and she never returned to her independent life. As Davies thinks back to this episode from his high-school days, “I remember wondering ‘How come, in this era of antibiotics, was it not possible to treat what was obviously, to me, an infection?’”Even today, such nonhealing wounds are common in people with late-stage diabetes like Davies' great-aunt, who have poor circulation, as well as in people with compromised immune systems. Davies, now an associate professor at Binghamton University, says that many doctors treat these debilitating wounds as a problem with the patient, rather than a sign of infection. “There's no excuse for it,” he says.Wounds are just one example of the huge impact of bacterial biofilms. The United States National Institutes of Health says that 80% of chronic infections are biofilm related. Unlike the more familiar “planktonic” lifestyle, in which bacteria float or swim freely, in biofilms they surround themselves with a complex polymeric matrix, better known as “slime.” As it grows thicker, the film often includes many bacterial species and the matrix develops a complex structure. Traditional antibiotics are often ineffective. “We thought we had it all figured out,” Davies says, but the past 20 years have shown that researchers are still in the “dark ages” when it comes to understanding and controlling bacteria.Pseudomonas aeruginosa lung infections that haunt cystic fibrosis patients and for recurrent middle ear infections of Haemophilus influenzae. But biofilms are also prime suspects in a long list of other “itises,” including endocarditis, prostatitis, and conjunctivitis.As biofilms, bacteria routinely foul industrial equipment and medical devices like catheters and implants, where they form dense layers that cling tightly to the artificial surfaces. They also occur naturally within us, most familiarly as dental plaque. In addition, biofilms are increasingly blamed for recurrent and chronic infections. The case is clear for the Researchers have learned much in recent years about the mechanisms that let bacteria establish a beachhead on a surface and work together to form a highly structured matrix that nourishes and protects them. The films are easily seen by electron microscopy on foreign surfaces like catheters. However, definitively establishing a role for biofilms in a particular disease—or in chronic wounds like those of Davies' great-aunt—is difficult, in part because traditional culture and assay techniques work best for planktonic forms. Even as the evidence comes in, however, many researchers are actively seeking unique vulnerabilities of the biofilm state, hoping to control these stubborn films wherever they occur.The usual defenses often fail against bacteria that have formed biofilms. The slimy matrix protects bacteria from assaults such as those by immune cells. In addition, bacteria in a biofilm are 10–1,000 times more resistant to antibiotics than in their planktonic form.“There's no simple explanation why biofilms are more resistant to antibiotics,” says George O'Toole of Dartmouth. He suggests that resistance is a natural part of adaptation to life on a surface. Although people like to think that we invented antibiotics to disrupt microbial processes, most were adapted from naturally occurring chemicals that the bacteria have evolved to resist. “Almost every antibiotic that's out there is derived from another microbe,” O'Toole says. “Bacteria and fungi have been dealing with this biological warfare for millions or billions of years.”At first, researchers attributed the resistance mainly to the complex slime that the bacteria secrete. The slime does present a barrier to immune cells like phagocytes. However, experiments show that many antibiotics, as well as nutrients and waste products, readily diffuse through the water-rich matrix.The slow metabolism of biofilm cells also contributes to their resistance. The bacteria in the film are relatively quiescent and divide only rarely. Antibiotics such as the penicillins, which need to be incorporated in the cell wall, are only effective against actively dividing cells. However, other antibiotics work just as well against quiescent cells, because they target basic cellular processes such as metabolism or protein or DNA synthesis. For reasons that are still being clarified, even these antibiotics are less effective against biofilms.Because biofilms, once formed, are so hard to eradicate, many researchers—and makers of medical devices—have tried to stop them from forming in the first place. A biofilm starts when a few pioneer cells use specialized chemical hooks to adhere to a surface. These pioneers help to make a target surface more attractive to subsequent cells, which eventually mature into a complex, structured film .Makers of medical devices, such as catheters, frequently try to prepare the device surfaces to disrupt the initial adhesion. For example, they may alter the physical characteristics or chemical properties of the surface, such as its hydrophobicity, to make it harder for these first pioneers to stick. “Overall, these approaches haven't been very successful,” asserts Phil Stewart. Stewart heads the Center for Biofilm Research at Montana State University in Bozeman. One reason for this lack of success is that surfaces immersed in bodily fluids develop a coating of bio-friendly material. Once the original surface is even partially covered, bacteria have a place to stick.Some researchers are going beyond simple surface treatments to incorporate biologically active agents into the surfaces of medical devices. Some naturally occurring proteins, like lactoferrin, interfere with bacterial adhesion. In addition, surfaces impregnated with antibiotics can delay biofilm growth, although this technique has the important downside of encouraging resistant bacteria. These surface treatments are directly useful only for human-made devices, but they also provide a testing ground for possible treatments for medical biofilms.Researchers are also exploiting the unique biochemistry of bacteria in biofilms, such as a lack of iron or oxygen. Once a biofilm is established, however, it develops a complex structure in which different cells occupy distinct environments. This diversity, both physiological and genetic, is an important part of biofilms' stubbornness, say Pradeep Singh of the University of Washington. First, “the cells are experiencing different environmental conditions, so their physiology is by nature different. The guys on the outside have very different physiology from the guys on the inside, so if you have a treatment or a target or a drug that affects one, the other may not be affected.” Levels of acidity, oxygen, and iron, for example, vary widely through the film.As the cells grow in these varying environments, they diverge genetically as well. In one study of biofilm growth, Singh says, “if we started with genetically identical population of cells, after five or ten days we'd find that population had actually diversified and was more like an old-growth forest than an monoculture of cells.” Like the forest, Singh suggests, the diversity of the biofilm could be a key element of its robust response to antibiotics and other assaults.The diversity clearly lets biofilms recover rapidly. Researchers speak of a small population of cells, called “persisters,” that for one reason or another survive an immune or antibiotic attack. Afterwards, says Bill Costerton of the University of Southern California, “if you are a persister, you wake up in a puree of the guts of your neighbors that contains every molecule you ever needed.” These well-fed survivors can rapidly reestablish the film once the assault is over, he says. “Biofilms have a regrowth rate that is truly phenomenal.”Dealing effectively with this diversity may require a shift from the traditional single-antibiotic approach to bacteria. “If you look at a lot of other treatment regimens for other diseases—cancer, HIV—it's almost always a cocktail of drugs targeting different aspects of the disease process,” says Dartmouth's O'Toole. Combining antibiotics with other compounds that disrupt the formation or survival of the film might render the bacteria more susceptible to antibiotics—and could reduce antibiotic resistance, as well.As bacteria arrange into a biofilm, the expression of scores of genes increases or decreases compared to their level in the planktonic form, raising hopes for targeting the biofilm-related pathways. Although many of the changes are still not understood, those involved in interbacterial signaling are especially promising. Indeed, for several species, researchers have identified signaling chemicals that perform in “quorum sensing,” which induces an abrupt change in phenotype when the density of nearby cells  exceed a threshold level.At first, quorum sensing seemed to be a critical pathway for forming biofilms, although the precise pathways differ somewhat between species. Recent results, however, show that mutant bacteria that can't do quorum sensing can sometimes form biofilms nonetheless. “The whole quorum sensing thing is still kind of shaking out,” says Montana State's Stewart. Although he suspects that disrupting quorum sensing will remain an important tool, Stewart says, “my read at this point is it's not as simple as ‘they have to be able to communicate to build a biofilm.’”In addition, Washington's Singh says that the bacteria from the lungs of cystic fibrosis patients who have longstanding biofilm infections are often mutants that can no longer perform quorum sensing. He suspects that once a biofilm is established, the chemical signals could serve as a beacon for the immune system. In their ongoing battle to evade detection, the bacteria may evolve to suppress quorum sensing when it is not helpful.Once biofilms develop, their most obvious distinguishing feature is the slime they secrete, which both holds the cells together and helps protect them . This riAnother strategy exploits viruses called phages that target bacteria. Phages tend to be highly specific, targeting particular species and even strains of bacteria. This specificity can be useful, especially for systemic treatments, because it can avoid disrupting natural, beneficial populations of bacteria, such as those in the gut. These beneficial bacteria often occur in biofilms themselves, and can naturally suppress more troublesome strains.P. aeruginosa, Escherichia coli, Staphylococcus aureus, and S. epidermidis) are responsible for a large fraction of infections. Researchers in the former Soviet Union have used phage to treat infections for decades and have developed cocktails that attack a spectrum of organisms. In this country, there are both practical and regulatory challenges to introducing active viruses into patients, but that may be changing.However, doctors might need to know which specific organisms causing an infection in order to choose a phage to treat it. This may not be as difficult as it seems, since a few organisms (such as “My sense is that increasingly the US community is open to the potential of using phage,” says Jim Collins of Boston University. With colleague Timothy Lu, Collins has used synthetic biology to alter natural viruses, adding genes for enzymes that attack the slime. The phage first hijack the bacterial machinery to replicate themselves, then break the cells open to release not just the copies, but the enzyme. Compared to the phage alone, this engineered phage “was about 100 times more effective” at disrupting a laboratory biofilm, Collins says.Rodney Donlon heads a team at the US Centers for Disease Control and Prevention aiming to reduce infections in medical devices. He says that the engineered phage is “very interesting,” although the genetic engineering of the virus could raise further concerns about its release into the environment. Still, Donlon emphasizes that phage naturally only attack bacteria. “They will not infect human or plant cells.” But the phage are not without problems, such as the release of toxins when the cells split open or immune responses to the viruses like those that have dogged gene therapy trials.Donlon has explored phage for devices, incorporating them into coatings on catheters. In what Donlon describes as a “proof of principle,” these coatings suppress the growth of biofilms in laboratory tests. Interestingly, they appear to remain active even after exposure to bodily fluids.Since each biofilm is different, however, researchers may need to tailor their approach to a particular species and matrix—or a combination. To overcome this problem, Binghamton's Davies looked at the final stage of the life cycle of biofilms: autodispersal. In this stage, regions of the film spontaneously disperse as cells dissolve the matrix by secreting enzymes and revert to their planktonic form.Davies' team found a signaling molecule that initiates autodispersal. As in quorum sensing, this signal induces a profoundly different behavior above a threshold concentration. The chemical signals are completely different, however, and instead of causing films to coalesce, it causes them to break up.One of the most tantalizing aspects of this molecule is that it appears to be universal across bacterial species. Although the enzymes required to degrade the matrix differ between species, the same signaling molecule triggers the process. Davies' team has identified the molecule and verified that a synthesized version induces dispersal even in films that are below the threshold density, and works even in multispecies biofilms.For widespread infections like those in cystic fibrosis, instantaneously releasing billions of bacteria in their planktonic form could cause even worse problems than the film. But for localized infections, like those in the sinus or middle ear, Davies thinks his dispersion-inducer could make intractable infections vulnerable to traditional antibiotics, or even to normal immune response. “Most infections are very localized, and it's not easy for the cells to really get very far from the site of the biofilm infection,” he says. At a more personal level, Davies hopes that the dispersal agent could help millions of people with nonhealing wounds, like those of his aunt.In fact, recent results show biofilms in many chronic wounds, says Randall Wolcott, who heads the Southwest Regional Wound Care Center in Lubbock, Texas. “Six months from now, I think the wound-care community will fully accept biofilm as a major barrier to healing.”Although worried about being branded as “one of those alternative-medicine types,” Wolcott has been exploring anti-biofilm therapies. “I watched so many people die, in their forties and fifties, a piece at a time,” he says. “I'd just had enough.” Overall, he says, “biofilm disease kills more people than cancer.”For wounds that don't respond to standard-of-care wound treatment, including mechanical removal of damaged tissue, Wolcott adds as many as six or seven agents to kill bacteria and disrupt the biofilms. He also uses phages, which qualify as natural substances and has occasionally seen “wounds that have been present for years go on to heal up in weeks.”These ongoing studies show the potential for treatments directed at biofilms, especially in combinations that counter the natural diversity of the biofilm populations. “We know how to manage biofilms,” says Wolcott. “We just need to bring it into medicine.”


Schistosoma parasites are disease-producing trematodes, or “blood flukes”, that infect an estimated 207 million people worldwide PLoS Neglected Tropical DiseasesSchistosoma haematobium, S. mansoni, or S. japonicum, can cause chronic disability By way of background, it should be recognized that any infection with the major species that affect humans, i.e., average health impact of schistosomiasis that determines the clinical and public health commitment to treat or prevent schistosome infection.How debilitating is it for an average person to have schistosomiasis? This is an important question, and one that has not been well answered in the past. It is particularly relevant that we have an accurate disability estimate because in the Global Burden of Disease (GBD) program's disability-adjusted life year (DALY) ranking system S. mansoni and S. japonicum) or bladder cancer, hydronephrosis, or renal failure (S. haematobium) occurred In past decades, the day-to-day impact of schistosomiasis was often minimized as “asymptomatic”, except when certain schistosomiasis-specific pathologies such as advanced hepatosplenomegaly, intestinal bleeding  is not the solution to obtain probabilistic data for life-path analysis, “. . . mainly because [experts] often do not think in the ways required by economic evaluation . . .” S. japonicum–related disease outcomes. The authors also note that there were some significant gaps in the available data for certain infection-related outcomes, and these, therefore, could not be included. Variation of the outcomes by location and by treatment status also could not be provided, pointing the way to areas where future research can be done. In addition, the problem of fairly redistributing the currently aggregated DALY values for anemia, malnutrition, etc., needs to be further assessed for multiple infections In terms of limitations, it must be noted that the current analysis is restricted only to PLoS Neglected Tropical DiseasesThis paper's message should urgently reach the directors of the GBD initiative. This program, now headquartered at the University of Washington, is presently undertaking an extensive revision of the 1996 GBD report Critics have argued that if we take the same approach for all diseases, it would result in similar increases in disability weights and in DALY scores for all the NTDs, with no significant change in their rankings among the global disease “league tables”


Sir,, how (what) to tell to the patient, how (what) we should tell to the caregivers, the time, the extent and in how many steps we should reveal it.I read the article “The doctor's dilemma: Truth telling” with gre


On 29–30 November 2007, just days before the United Nations Climate Change Conference began in Bali and Al Gore and Rajendra Pachauri received the 2007 Nobel Peace Prize for their work on climate change, the U.S. Institute of Medicine (IOM) held a workshop to highlight gaps in scientific understanding about the environmental and human health effects of transportation fuels. The transportation sector’s use of fuel is expected to grow more quickly than demand for energy in any other sector between 2005 and 2030, Scott Nauman, manager of economy and energy in the ExxonMobil Corporate Planning Department, told conference attendees. Therefore, new transportation fuels are key players among the innovative technologies being investigated and developed to help countries throughout the world cut greenhouse gas emissions.As worldwide transportation fuel use rises, the emissions and carbon dioxide emitted by burning these fuels will also rise, pointed out Samuel Wilson, acting director of the NIEHS. “We want to add ‘minimizing the human health impact’ . . . to the criteria for developing alternative fuels,” he said.According to Michael Wang, a vehicle and fuel systems analyst at the U.S. Department of Energy Argonne National Laboratory, biofuels are considered the most promising alternative for reducing petroleum use and decreasing greenhouse gas emissions from transportation. Electricity is also expected to grow as a source for plug-in hybrids, as is hydrogen. The idea of producing transportation fuels from coals “has generated some interest lately because they can be produced domestically,” Wang says, but their carbon emissions are “pretty high.”The main biofuel currently being developed for transportation in the United States is ethanol from corn via distillation, and its production is increasing rapidly. According to the Energy Information Administration, the percentage of the U.S. gasoline pool represented by ethanol rose from 1.27% in 2000 to 2.85% in 2005. However, John Regalbuto, director of the National Science Foundation’s Catalysis and Biocatalysis Program, predicts that hydrocarbon-based “green gasoline,” “green diesel,” and “green jet fuel” will represent a significant fraction of new biofuels by 2022. When produced via catalysis from materials such as switch-grass and waste wood products, the performance of these renewable biofuels are “essentially the same” as their conventional counterparts, he says. However, their manufacture involves intermediates such as hydroxymethylfurfural and ionic liquid solvents that require further study in terms of health effects.Additives also affect the emissions of transportation fuels, as well as these fuels’ impact on the environment, stressed Serap Erdal, an assistant professor at the University of Illinois–Chicago School of Public Health. Uncertainty over which additives will be added to new fuels and how the complex mixtures will behave in the environment makes it very hard to predict potential health effects, agreed the experts amassed at the IOM meeting. In the United States, for example, ethanol has only recently been used as an additive to make gasoline burn more efficiently. But in Brazil, where ethanol has been used as a fuel for nearly 30 years, it has become clear that, compared with gasoline, the sugarcane-derived fuel produces much higher emissions of formaldehyde, a known human carcinogen, and acetylaldehyde, a suspected human carcinogen, said Paolo Saldiva, a professor of medicine in the University of São Paolo’s Department of Pathology. However, he said that the health effects of exposure to these compounds via air emissions are unclear.What is indisputable is that key decisions leading to the development of new fuels will be made before the requisite health effects data are available, so “we need to get going as soon as possible . . . to collect baseline data,” said Dan Greenbaum, president of the Health Effects Institute, which published a report summarizing the health effects of exposure to 21 mobile source air toxics in November 2007. Added Erdal, “There is a critical need to institute public health surveillance so that we are already collecting data and are able to detect changes as they take place.”