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It is not surprising that they have developed as sep- arate best 500 mg robaxin, unrelated disciplines discount robaxin 500mg free shipping. But physicians and nonmedical biologists have begun to realize that there is much to be gained by integrating these disciplines. Evo- lutionary medicine recognizes that these different perspectives are complemen- tary, and that integrating them will give a richer understanding of health and disease. Understanding evolutionary processes helps to explain our evolved vul- 178 Perspectives in Biology and Medicine Evolution and Medicine nerabilities or susceptibilities to disease and our current burden of disease. Con- versely, since disease has served as an important selection factor in evolution (Haldane 1949a), knowledge of the present patterns of disease gives insights into our evolutionary history. Analysis of the evolutionary causes of diseases may lead to novel strategies to prevent, postpone, or ameliorate them. Understanding both the proximate and ultimate causes of diseases will provide a richer understand- ing of disease. Finally, evolutionary explanations of disease are important because patients often want to know why they have the diseases they have. In the absence of evolutionary explanations, they may fall back on unhelpful folk beliefs, such as the idea that their diseases are punishment for sinful behavior (Bynum 2008). Why Our Evolutionary Heritage Has Left Us Vulnerable to Disease Many diseases cause premature death (death before the end of the reproductive and child-raising periods) or reduced fertility. But most diseases do not affect all members of a population or do not affect everyone to the same degree. Rather, individuals exhibit variation in resistance or response to diseases, just as they exhibit variation in virtually all other traits. At least some of this variation is due to genetic or heritable variation in the population. Heritable variations in resis- tance to these diseases represent variations in fitness; individuals who survive and remain fertile in the face of a disease will on average produce and raise more children than will people who die from or become infertile as a result of the dis- ease. As a disease spreads through a population, natural selection will increase the frequency of alleles that are associated with resistance to it. The alleles associated with resistance to malaria are classic examples of this process. Despite selection for disease resistance throughout our evolutionary history, however, natural selection has clearly not eliminated disease. Evolutionary med- icine helps us understand the limits as well as the power of natural selection in shaping human biology and the reasons—the ultimate causes—for our contin- ued vulnerability or susceptibility to disease. Broadly speaking, there are several important limits to natural selection that contribute to the persistence of disease (Nesse 2005; Perlman 2005). First, there are limitations intrinsic to the process of evolution by natural selection itself. Diseases that cause premature death or reduced fertility will select for and increase the frequency of alleles that are associated with disease resistance. New alleles can enter populations either by mutation or by gene flow from other populations of the same species. Once these alleles enter a popula- tion, their fate is determined by genetic drift (changes in allele frequency due to random sampling in the transmission of alleles from one generation to the next) as well as by natural selection. These other evolutionary processes may counter- act the effects of selection by introducing or increasing the frequency of alleles spring 2013 • volume 56, number 2 179 Robert L. For these and other genetic reasons, ben- eficial alleles—specifically, alleles associated with disease resistance or a decreased risk of disease—may not spread or become fixed in a population. Natural selection increases the frequency of traits that enhance reproductive fitness. If diseases do not decrease reproductive success, there will not be selection for resistance to them. Diseases of aging—diseases that increase in prevalence after the end of our reproductive and child-raising years—are one class of diseases that may not significantly decrease fitness. Evolutionary life his- tory theory and the evolutionary theory of aging provide a framework for understanding and, possibly, postponing these diseases. Even when selection is intense, allele fre- quencies in populations change only gradually over many generations. The other species with which we interact, and especially the pathogens or parasites that infect us and cause disease, constitute an important and rapidly changing component of our environment. Just as our evolutionary ancestors evolved and we are continuing to evolve in- creased resistance to our pathogens, these pathogens have evolved and are evolv- ing to overcome this resistance and to grow in and be transmitted among us. This process of host-pathogen coevolution helps to rationalize the natural histories of infectious diseases and to explain why some infections are relatively benign while others are virulent.

New alleles can enter populations either by mutation or by gene flow from other populations of the same species 500 mg robaxin with amex. Once these alleles enter a popula- tion purchase robaxin 500mg otc, their fate is determined by genetic drift (changes in allele frequency due to random sampling in the transmission of alleles from one generation to the next) as well as by natural selection. These other evolutionary processes may counter- act the effects of selection by introducing or increasing the frequency of alleles spring 2013 • volume 56, number 2 179 Robert L. For these and other genetic reasons, ben- eficial alleles—specifically, alleles associated with disease resistance or a decreased risk of disease—may not spread or become fixed in a population. Natural selection increases the frequency of traits that enhance reproductive fitness. If diseases do not decrease reproductive success, there will not be selection for resistance to them. Diseases of aging—diseases that increase in prevalence after the end of our reproductive and child-raising years—are one class of diseases that may not significantly decrease fitness. Evolutionary life his- tory theory and the evolutionary theory of aging provide a framework for understanding and, possibly, postponing these diseases. Even when selection is intense, allele fre- quencies in populations change only gradually over many generations. The other species with which we interact, and especially the pathogens or parasites that infect us and cause disease, constitute an important and rapidly changing component of our environment. Just as our evolutionary ancestors evolved and we are continuing to evolve in- creased resistance to our pathogens, these pathogens have evolved and are evolv- ing to overcome this resistance and to grow in and be transmitted among us. This process of host-pathogen coevolution helps to rationalize the natural histories of infectious diseases and to explain why some infections are relatively benign while others are virulent. Understanding pathogen evolution and host-pathogen coevolution may suggest strategies for slowing the spread of antibiotic resistance and for reducing the virulence of infectious diseases. The human environment is strongly influenced by cultural beliefs, practices, and artifacts, all of which are subject to rapid change. Disease may result from an inability of natural selection to keep pace with a changing cultural environ- ment—in other words, from a mismatch between the environment in which we now live and the genes we have inherited from our evolutionary ancestors, genes that enabled these ancestors to survive and reproduce in the various environ- ments in which they lived. The increasing prevalence of obesity and hyperten- sion exemplifies the principle that genes that enhanced the fitness of our ances- tors may now increase our risk of disease. In brief, macroevolu- tion constrains microevolution (Stearns,Allal, and Mace 2008). Our macroevolu- tionary history has left us with complex and highly interdependent developmen- tal pathways. Many of our anatomical peculiarities, such as the placement of our trachea in front of our esophagus, which leaves us vulnerable to choking, can be understood as the result of our evolutionary history—in this case, our history as aquatic organisms whose respiration depended on gills rather than lungs. The de- velopment of our respiratory and gastrointestinal systems is now so deeply embed- 180 Perspectives in Biology and Medicine Evolution and Medicine ded in the whole of our development that mutations that might have led to a safer anatomic design would almost certainly have been lethal (Held 2009). Moreover, because of our complex internal organization and our complex interactions with the external world, virtually every gene has multiple phenotypic consequences. Evolution frequently involves tradeoffs or compromises, such that natural selec- tion leads to suites of traits that are not perfect or ideal, but work well enough for survival and reproduction, and are better than the available alternatives. Finally, despite natural selection, survival and reproduction may be con- strained by limitations of environmental resources, in the way originally envi- sioned by Malthus. Availability of nutritional resources is thought to have played a major role in evolution ,and nutritional deficiencies are still important causes of disease and death. Understanding the evolutionary reasons for our susceptibility to disease com- plements the traditional biomedical understanding of the etiology and patho- genesis of disease. Together, these two perspectives on health and disease, the ulti- mate and the proximate causes of disease, can help us understand why we get sick as well as how we get sick, and may provide insights into interventions that might reduce the burden of disease. The distribution of the sickle-cell trait in East Africa and elsewhere, and its apparent relationship to the incidence of subtertian malaria. Darwin and the doctors: Evolution, diathesis, and germs in 19th-cen- tury Britain. Medical education in the United States and Canada:A report to the Carnegie Foundation for the advancement of teaching. Cause and effect in biology revisited: Is Mayr’s proximate-ulti- mate dichotomy still useful? Glucose-6-phosphate dehydrogenase defi- cient red cells: Resistance to infection by malarial parasites. Neither the European Commission nor any person acting on behalf of the Commission is responsible for the use which might be made of the information contained therein. More information on the European Union is available on the internet (http://europa. It is a new paradigm in medicine based on the smart use of technology, coupled with greater participation by patients in the management of their own health, to help prevent disease and promote healthy living. When diseases can be prevented and not only treated, the cost of healthcare will come down, creating a virtuous circle for health policy.

Susceptible age groups: larvae and metamorphs are most commonly affected in North America discount robaxin 500mg otc. Geographic distribution The disease has been reported in North and South America generic robaxin 500mg without prescription, Asia, the Pacific and Europe. How is the disease Horizontal transmission: direct contact, cannibalism, through the water. Movement of ranaviruses into an area will most probably happen by movement of infected amphibians, fish or reptiles or via equipment and other inanimate objects that have been contaminated with ranaviruses. The viruses are highly infectious and capable of surviving for extended periods of time in the environment, even in dried material. Diseased larval amphibians often have swollen bodies and signs of internal and cutaneous haemorrhage. Affected adult amphibians may have reddening of the skin, skin ulceration, bloody mucus in the mouth and might pass blood from the rectum; often there is systemic internal haemorrhaging (which also may be seen in affected fish and reptiles). These signs are all typical of the disease syndrome ‘red leg’: ranaviruses are not the only possible cause of ‘red leg’ in amphibians and other differential diagnoses should be borne in mind. Seasonal variations in disease outbreaks have been reported, with both their prevalence and severity being greater during the warmer months, therefore temperature is considered a likely factor influencing disease outbreaks. Dead animals should be submitted to a suitable diagnostic laboratory for post mortem examination. Surveillance of live animals should be carried out if possible and sick animals submitted for testing. Diagnosis Liver and/or kidney samples from dead animals should be sent to an appropriate laboratory for diagnostic testing. Toe or tail clips from live animals might also be used for diagnosis, but the reliability of these has not been validated. Before collecting or sending any samples from animals with a suspected disease, the proper authorities should be contacted. Samples should only be sent under secure conditions and to authorised laboratories to prevent the spread of the disease. Although ranaviruses are not known to be zoonotic, routine hygiene precautions are recommended when handling animals. Also, suitable precautions must be taken to avoid cross contamination of samples or cross-infection of animals. Ideally any site containing a reasonable population of amphibians should be monitored for sick and dead animals as a matter of course. If sick or dead animals are found, they should be tested for ranavirus infection so that the site’s ranavirus status can be determined. People coming into contact with water, amphibians, reptiles or fish should ensure where possible that their equipment and footwear/clothing has been cleaned and fully dried before use if it has previously been used at another site. To properly clean footwear and equipment: first use a brush to clean off organic material e. Ideally, different sets of footwear should be used at the site than are used by staff at home. Biosecurity measures should be increased to reduce the chance of spread if disease is confirmed. Livestock It is important to reduce the chance that livestock moving between sites (especially those travelling from known infected sites) will carry infected material on their feet or coats. Foot baths can be used and animals should be left in a dry area after the bath for their feet to fully dry before transport. Wildlife Do not allow the introduction of amphibians, reptiles or fish without thorough screening and quarantine for ranavirus. This screening may still not pick up all subclinically infected individuals but will reduce the risk of actively infected animals being introduced to the site. Humans must ensure that all biosecurity measures described above are Humans followed to prevent introduction of the infectious agent into previously uninfected areas. The disease has been shown to cause significant population declines of common frog Rana temporaria in the United Kingdom, apparently following virus introduction from North America. Ranavirus infection might be implicated in declines elsewhere, but data are lacking. There are potential economic losses due to potential risk of disease spread to fish. An insect-borne viral disease that primarily affects animals but can also affect humans. The virus is mostly transmitted by the bite of infected mosquitoes, mainly of the Aedes species, which acquire the virus when feeding on infected animals.

Four separ- ate studies failed to show any relationship between egg con- sumption (the main source of dietary cholesterol) and serum 98 cholesterol buy cheap robaxin 500 mg online. Blood cholesterol for practical purposes has no predictive 100 value for the risk of a future heart attack in the individual generic 500 mg robaxin, and manipulation of blood cholesterol with diet or drugs has no effect on overall mortality, though it may significantly 101 increase the risk of cancer death. First, it implied that a cholesterol level, say, of 210 is more dangerous than a level 200. Thirdly, it implied that it is desirable for people to strive to have their cholesterol reduced to or below 200 mg/dl. The fact is that there is no evidence that moderate drinking leads to dangerously high blood pressure and that it is linked to stroke of any kind. Similarly, in a study of 87,500 nurses, the risk of stroke was lower at all levels of drinking than in teetotal- 106 lers. The general protective effect of alcohol against heart 107 disease is well documented in many studies, both in men and women, yet health promotionists find it somewhat embarrassing to mention it. A double brandy before going to bed, or a half-bottle of a good wine with lunch a day could be better preventive medicine than all the cholesterol guidelines combined. There is no doubt that the Spaniards, the French, the Italians or the Greeks enjoy their cuisine, their drinks and F amour. The simplistic reasoning behind this idea could be sketched as follows: in Mediterranean countries the mortality from coronary heart disease is lower, much lower, than in Britain. As often happens with single- issue fanatics, they conveniently forget that people in the Mediterranean region do not on average live any longer than the British; they simply die of something else, or, to be pre- cise, something else appears on their death certificates. The life expectancy at birth for English men in 1988 was 73 years, the same as in France or Italy. The Chinese population has been presented as an example of what could be achieved in the Western countries as regards blood cholesterol. Chinese peasants were said to have very low blood cholesterol levels and very low mortality from 108 heart disease. What we were not told was how long they live, but nearly half of all their deaths were from cancer. There was little difference in overall mortality in those with the lowest cholesterol and those with the highest cholesterol. The test for any dietary guru is to ask him this simple question: if you are really so concerned about heart disease prevention, do you eat Japanese food yourself and do you recommend it to your friends? The truth is that the hypothesis of the caus- ation of heart disease is unproved, untestable because unfalsi- fiable, extremely complex, on occasions misinterpreted and 113 some of it contradictory. A glimpse into the workings of expert committees was provided by Nevin Scrimshaw: Reviewing personal experience as a participant in dozens of expert, technical, and advisory committees over the past 20 years, I am impressed that the most dogmatic and out- spoken committee members on any issue may turn out subsequently to have been mistaken on that issue. There have also been occasions when a strong and persistent dis- senter has been proved to be right. We need constantly to remind ourselves that neither individuals nor committees are infallible, and that all scientific issues need to be 117 addressed with some humility. A warning not to take official dietary guide- lines too seriously was given by two nutrition specialists in 11 an article in The Lancet. Improbable arguments were put forward to implicate fat and sugar in death, such as comparing fat and sugar consumption 121 in Britain 200 years ago with the present. That the lon- gevity and the health of people had dramatically improved during the same interval did not seem to enter the equation. At one point the experts simply invented the fact that in Japan, mor- 123 tality from heart disease was progressively increasing and in China, used as an example of how low one could get in the national cholesterol level, heart disease was among the 124 three leading causes of death. The old cholesterol canard was revived and it was urged that nowhere in the world should one eat more than 300 mg of cholesterol a day. Once they passed puberty they could forget meat as their brain development was complete. The horror of salt was again reiterated and as a throw-away 128 it mentioned that salt could cause stomach cancer. The new lower limits for recommended intake of fat, satu- rated fat and cholesterol were set at 15 per cent, nought per cent and nought per cent, respectively. Yet it was the dietary propaganda of the same experts which had advocated polyunsaturates in the first place. The report called on every institution worthy of its name to employ all possible means to disseminate the message. The ministry of health in countries where the government controls the radio and television should take steps to ensure 98 Lifestylism that other sections of the mass media. It is also recommended that governments recruit specialists in behavioral manipulation who can assess the 130 best way of amplifying the community action.