By W. Sven. Champlain College.
So in 1968 he undertook a research study in order to demonstrate that the bactericidal properties of urine were related not so much to acidity or other factors generic 10 mg norvasc fast delivery blood pressure medication used for headaches, but more to the urea concentration in the urine cheap norvasc 5 mg visa blood pressure chart for tracking. In the study, Kaye showed that it was primarily urea levels, rather than organic acids or other factors that were responsible for the antibacterial action of urine: "The results of the present study provide evidence for the role of urea in human urine as an antibacterial agent. They also suggest that within the ranges of concentration commonly achieved in human urine, antibacterial activity is more a function of 127 urea content than of organic add concentration, or ammonium concentration. These experiments demonstrated that supplementation with urea markedly increased the inhibitory quality of the urine. Neter and Clark showed that addition of urea to human urine markedly increased antibacterial activity. And as Kaye demonstrated in his study, by orally ingesting additional urea, we increase the concentration of urea in the system, and consequently increase the antibacterial action of our urine: "Urine collected from volunteers after ingestion of urea demonstrated a 128 marked increase in antibacterial activity, as compared with urine collected before ingestion of urea. Coli strain 14, whereas urine obtained during diuresis supported the growth of this strain. The results of the present study and those of Roberts and Beard and Asscher et al. When we are exposed to foreign organisms which our bodies sense as threatening, our immune system produces a wide variety of antibodies which attack, weaken and destroy the intruders. But 130 numerous research studies have proven that a wide variety of antibodies are also present in our urine when we are fighting disease - and these important antibodies can be reused by the body in urine therapy. As this study in 1962 revealed, urine antibodies are extremely effective disease-fighters and are capable of actively neutralizing or destroying even the aggressive polio virus: Neutralizing activity for the poliovirus was demonstrated in protein concentrates prepared from the urine of a number of normal subjects. The biologic characteristics of the neutralizing activity in the urine resembled those of specific antibody found in blood. This neutralizing substance of the urine has the essential characteristics of antibody. Further studies on the biochemical and physical characterization of this and other urinary antibodies are in progress. This report also revealed that several other types of urine anti-bodies have been found in other research studies:"Antibodies to cholera and typhoid have been found in the unconcentrated urine of normal volunteers immunized with the corresponding vaccine. Antibodies to diphtheria, pneumonia, leptospira and salmonella bacteria have also been found in the urine of immunized or infected individuals. The researchers in this study on polio urine antibodies clearly stated that even minute concentrations of detected or undetected antibodies can control and fight disease: "It is known, however, that the presence of antibody, even in amounts which are not detectable by conventional methods, may prevent disease and detection of virus. It seems likely that antibodies of this type may play a part in the defense against invasion of micro-organisms. The recent outbreaks of food poisoning from contaminated beef and chicken presents an important indication for the use of urine and ureaYour Own Perfect Medicine therapy. Urine therapy is completely safe and applicable to a huge variety of conditions, in addition to being an excellent preventative health treatment. There are many instances when your immune system is dealing with a health threat long before overt symptoms appear. Carmelo Giordano, from the Renal Laboratory, Naples University School of Medicine. Protein is normally broken down into nitrogen and other constituents by both the liver and the kidneys, but when the kidneys malfunction because of infection, damage, etc. However, some researchers, such as Giordano, have discovered that ca urea, (which is produced during protein synthesis and therefore con-The Research Evidence and Case Studies tains nitrogen), can actually play a role in helping kidney patients to use protein more efficiently and to achieve proper nitrogen balance in the body. The study demonstrated that: "If urea was added to the diet, enough synthesis of nonessential amino 134 acids occurred to achieve equilibrium or even positive nitrogen balance. Another report on the role of urea in kidney disease was delivered at an international symposium in Florida in 1968, entitled Urea and the Kidney, In the report, Mackenzie Walser, of the Johns Hopkins University School of Medicine, stated that: "In uremics [kidney patients] on diets containing small amounts of protein, urea apparently provides the principal source of nitrogen for protein synthesis. Further exploration of these findings may yield valuable information in the treatment of renal failure. This study is another research project done on antibodies in human urine and was presented by Dr. Hanson of the Pediatric Clinic of the Karolinska Institute in Sweden at the meeting of the Microbiology Section of the Swedish Medical Society in Stockholm. The report stated that: Human urine contains proteins that have been shown to be identical with serum (blood) immunoglobulin or (antibodies). The report also revealed that: Antibody activity in urine has been demonstrated against several microorganisms including cholera, salmonella, diphtheria, tetanus and polio. There are many other references to urine antibodies in medical literature, a few more of which I will list here.
In some people norvasc 5mg with visa hypertension jnc 7 guidelines, the pains were so acute in their backs and hips that they could not lie in bed buy cheap norvasc 10mg online heart attack jack smack u blue. A few complained of their fesh being sore to the touch, in every part of the body. From these circumstances, the disease was sometimes believed to be a rheuma- tism. This new way of thinking about diseases, requiring careful clinical observa- tion, differentiation, and specifc diagnosis, led naturally to the search for specifc, as opposed to general, causes of illness. Expanding on the concept of careful clinical observation of individuals, epidemiologists in the 1800s observed unusual epidemics and performed con- trolled studies of exposed persons. Epidemiologic theories about the means of transmission of various infectious diseases often preceded the laboratory and clinical studies of the causative organisms. Peter Panum (1820–1885) recorded his observation of an epidemic of measles on the Faroe Islands in 1846. Remarkably, the attack rates among those under 65 years old was near 97%, but older persons were completely spared. This demonstrated that immunity after an attack of natural measles persists for a lifetime. John Snow (1813–1858) performed classic epidemiology of the transmis- sion of cholera in the mid-1850s, nearly 30 years prior to the identifcation of the causative organism. In contrast, the women who were delivered by midwives, who used aseptic techniques (by immersing R1 their hands in antiseptic solution prior to contact with the patient), had © Jones and Bartlett Publishers. His theories were not welcomed by the medical profession, and this, combined with his more liberal political views, resulted in his leaving the hospital in 1849. The Development of Statistics and Surveillance Meanwhile, the felds of probability and political arithmetic, a term coined by William Petty (1623–1687) to describe vital statistics on morbidity and mortality,27 were advancing. Gerolamo Cardana (1501–1576) introduced the concept of probability and described that the probability of any roll of the dice was equal so long as the die was fair. He used inductive reasoning to interpret the mortality trends and noted the ratio of male to female births and deaths, mortality by season, and mortality in persons living in rural versus urban locations. He examined several causes of deaths over time and constructed the frst life tables. Later he attributed many of these deaths to his other activities in the autopsy room. Daniel Bernoulli (1700–1782), the son of Jacques Bernoulli, ana- lyzed smallpox mortality to estimate the risk-beneft ratio of variolation. Edwin Chadwick (1800–1890), an arrogant zealot, managed to institute numerous sanitary reforms when he wasn’t annoying his peers. His 1842 report “to the Poor Law Commission” outlined the cost effectiveness of public health. His report emphasized the understanding that hygiene was closely related to health, but he also linked morality to hygiene and health. He made the following pronouncements: That the formation of all habits of cleanliness is obstructed by defective supplies of water. His careful documentation of deaths was used by John Snow to investigate the 1849–1953 London cholera epidemics. Farr initially disagreed with Snow’s hypothesis that cholera was transmitted by water. However, he was eventually convinced, and his book based on the 1866 epidemic demonstrated that contaminated water was a risk for cholera. Anton van Leeuwenhoek (1632–1723) invented the microscope, and in 1683 he described how materials such as rainwater and human excretions had cocci, bacilli, and spirochetes. Because they were often present in decaying or fermenting materials, some people maintained that they were spontaneously generated from inanimate material. Further, he could pass the disease from one mouse to another by inoculating them with these microorganisms.
Grazing animals spread the bacteria by eating/picking up contaminated dirt or food sources order norvasc 2.5 mg amex blood pressure over 60. Spores have also been found in the guts of insects buy cheap norvasc 5 mg on line untreated prehypertension, although the importance of their role is not yet known. During droughts, when animals graze closer to the ground, more dirt is consumed and the incidence of anthrax appears to increase. Outbreaks have been reported in some domestic animals (mainly pigs) after consuming feeds containing meat and bone meal originating from carcases contaminated with anthrax bacterial spores. Wild carnivores and scavengers become infected through the consumption of infected meat. After feeding on an infected carcase, non-biting blowflies may contaminate vegetation by depositing vomit droplets and subsequently animals feeding on such vegetation then become infected. Although a minor mode of transmission, biting flies may transmit the disease from one animal to another during severe outbreaks. How is the disease Humans can become infected with anthrax by breathing in anthrax spores transmitted to humans? Consumption of undercooked meat from infected animals may cause gastrointestinal anthrax. Acute cases in cattle, sheep and wild herbivores are characterised by fever, depression, difficulty in breathing and convulsions, and, if untreated, animals may die within two or three days. In pigs, anthrax is characterised by swelling of the throat, causing difficulties in breathing and similar characteristics are seen in dogs, cats and wild carnivores. The incubation period of anthrax is typically 3 to 7 days (ranging from 1 to 14 days). Apoplectic – occurs most frequently at the beginning of an outbreak, where animals (mostly cattle, sheep, goats and wild herbivores) show signs of loss of conciousness and sudden death. Signs include fever, ruminal stasis, excitement followed by depression, difficulty in breathing, uncoordinated movements, convulsions and death. Unclotted blood issuing from body orifices, rapid decomposition of the carcase and incomplete rigor mortis are often observed. Chronic anthrax – can be seen in cattle, horses and dogs but occurs mainly in less susceptible species such as pigs and wild carnivores. Characterised by swelling of the throat and tongue and a foamy discharge from the mouth. Recommended action if Contact and seek assistance from appropriate animal health professionals. Diagnosis In animals, anthrax is diagnosed using samples taken from superficial blood vessels or natural openings of dead animals and by examining blood smears on a microscope slide. Artificial media can be used to grow the micro- organism from a dead animal, hides, skin, wool or soil. Livestock In areas prone to anthrax a preventive strategy should be adopted involving thorough surveillance and annual vaccination of susceptible animals (usually cattle, sheep and goats). Vaccination is normally carried out 2-4 weeks before the onset of the known period of outbreaks. Any animals showing signs of anthrax must be treated and not used for food until several months after the completion of treatment. The live Sterne vaccine is effective but there is some concern over its ecological effect and possible pathogenicity in some species. Antibiotic treatment (penicillin or tetracycline) can be an option if animals show clinical signs of anthrax but often it is not a practical or feasible method of control. Culling of infected animals and removal of diseased carcases reduces contamination sources. When this is not possible, place the unopened carcases in heavy duty black plastic bags which are sealed and leave in the heat. Carcases infected with anthrax should not be moved, instead they should be disposed of using appropriate methods on site to prevent further environmental contamination. Above all, be alert, vigilant and maintain surveillance particularly during high risk times. Anthrax is a seasonal disease which may reoccur the following year and being prepared for potential outbreaks is vital. This includes early carcase detection along with minimising environmental contamination through proper carcase disposal and decontamination Wildlife species should be monitored for any interaction with livestock (e. Burning surrounding areas of bush to kill spores and disperse unaffected wildlife.
Also buy cheap norvasc 2.5mg on-line blood pressure ranges for dogs, trials of reduction of saturated fat and its partial replacement by unsaturated fats have improved dyslipidaemia and lowered risk of cardiovascular events (103–105) discount 2.5 mg norvasc visa heart attack enzyme test. Disappointingly, several large randomized trials of multiple risk factor interventions, using individual counselling and education, found no reduc- tion in cardiovascular morbidity or mortality (106). These interventions, however, did bring about modest changes in risk factor proﬁles. In a meta-analysis of 18 trials, 10 of which reported clinical data, net changes were seen in systolic blood pressure (−3. It was, however, not possible to determine whether these changes were the result of concurrent drug treatments or regression to the mean. If real, these reductions are important, since even small reductions in major risk factors have been associated with a reduced risk of cardiovascular diseases in long-term, large-scale population studies (107). Observational studies have found that other behavioural modiﬁcations, in particular cessation of smoking, are associated with a reduction in cardiovascular disease mortality (108–112). In men in the United Kingdom, a healthy lifestyle and increased physical activity have been shown to reduce the chances of developing cardiovascular disease (113). While interventions targeted at individuals could be expected to bring about behavioural changes if they are implemented in a supportive environment, evidence for this view is not strong (106–114). However, ﬁscal interventions and legislation on smoking in public places are capable of bringing about widespread and useful reductions in smoking prevalence. Appropriate policies might address: agricultural subsidies for fruits and vegetables; food pricing and avail- ability; labelling of food; public transport; pedestrian- and cyclist-friendly road planning; school health education; and tobacco control measures, including prohibition of advertising and price control. The overall objective should be to make it easy for the population to make healthy choices related to diet, physical activity and avoidance of tobacco. Evidence There is a large body of evidence from prospective cohort studies regarding the beneﬁcial effect of smoking cessation on coronary heart disease mortality (116). However, the magnitude of the effect and the time required to achieve beneﬁcial results are unclear. Some studies suggest that, about 10 years after stopping smoking, coronary heart disease mortality risk is reduced to that of people who have never smoked (109, 110, 117, 118). It has also been shown that cigarette smokers who change to a pipe or cigar (119), and those who continue to smoke but reduce the number of cigarettes, have a greater mortality risk than those who quit smoking (112). A 50-year follow-up of British doctors demonstrated that, among ex-smokers, the age of quitting has a major impact on survival prospects; those who quit between 35 and 44 years of age had the same survival rates as those who had never smoked (120). The beneﬁts of giving up other forms of tobacco use are not clearly established (121–124). General recommendations are therefore based on the evidence for cigarette smoking. Recent evidence from the Interheart study (31) has highlighted the adverse effects of use of any tobacco product and, importantly, the harm caused by even very low consumption (1–5 cigarettes a day). The beneﬁts of stopping smoking are evident; however, the most effective strategy to encourage smoking cessation is not clearly established. All patients should be asked about their tobacco use and, where relevant, given advice and counselling on quitting, as well as reinforcement at follow-up. There is evidence that advice and counselling on smoking cessation, delivered by health profession- als (such as physicians, nurses, psychologists, and health counsellors) are beneﬁcial and effective (125–130). Several systematic reviews have shown that one-time advice from physicians during routine consultation results in 2% of smokers quitting for at least one year (127, 131). Similarly, nicotine replacement therapy (132, 133) can increase the rate of smoking cessation. Nico- tine may be administered as a nasal spray, skin patch or gum; no particular route of administration seems to be superior to others. In combination with the use of nicotine patches, amfebutamone may be more effective than nicotine patches alone, though not necessarily more effective than amfebutamone alone (135, 136). Nortriptyline has also been shown to improve abstinence rates at 12 months compared with a placebo. Both agents have appreciable discontinuation rates because of side- effects (135–137). Data from observational studies suggest that passive cigarette smoking produces a small increase in cardiovascular risk (138–140). Whether reducing exposure to passive cigarette smoke reduces cardiovascular risk has not been directly established. The interventions described above targeted at individuals may be less effective if they are imple- mented in populations exposed to widespread tobacco advertising, sponsorship of sporting activities by the tobacco industry, low-cost tobacco products, and inadequate government tobacco control policies.
Compliance bias occurs because in general discount 2.5 mg norvasc with amex blood pressure cuff cvs, patients who are compliant with therapy do better than those who are not regardless of the therapy purchase norvasc 5 mg on line heart attack 18 year old male. Compliant patients may have other characteristics such as being more health-conscious in their lifestyle choices, which lead to better outcomes. Studies of screening tests often compare a group of people who are in a screening program with people in the population who are not in the screening program. Therefore, the screened group is more likely to be composed of people who are more compliant or health-conscious, since they took advantage of the screening test in the ﬁrst place. This will make it more likely that the screened group will do better since they may be the healthier patients in general. This bias can be avoided if patients in these studies are randomized before being put through the screening test. One way to test for this bias is to 316 Essential Evidence-Based Medicine Fig. Screening Performed Onset Detectable Symptomatic Death Rapidly progressive - Curable Not curable detected too late; no survival benef t Slowly progressive - Detected in curable symptomatic phase; survival benefit Very slowly growing tumor (missed) - not detected; patient reassured, no actual survival benefit, but, survival appears longer have two groups of patients, one that is randomized to receive the screening test or not and the other group that has a choice of whether to get screened or not. Effectiveness of screening Another problem with screening tests revolves around their overall effectiveness. For example, consider the use of mammograms for the early detection of breast cancer in young women. Women aged 50–70 in whom the cancer is detected at an early stage do appear to have better outcomes. The use of mammogra- phy for screening younger women (age 40–50) is still controversial. In studies of this group, it made very little difference in ultimate survival if the woman was screened. Early detection in this population resulted in a large number of false positive tests requiring biopsy and unnecessary worry for the women affected. It also resulted in an increased exposure to x-rays among these women and increased the cost of health care for everyone in the society. For example, in the case of using mammograms to screen for breast cancer in women at age 40, we can make the spreadsheet as in Table 28. Screening 40- to 50-year-old women for breast can- cer using mammography Screened Not screened Total population 1000 1000 Positive mammogram 300 – Biopsies (invasive procedures) 150 – New breast cancers 15 15 Deaths from breast cancer 5–8 7–8 Source: From:D. On the beneﬁt side, there is the prevention of at most three deaths per 1000 women screened. This means that 333 women must be screened to prevent one death from breast cancer. The test must be accurate and able to detect the target condition earlier than without screening and with sufﬁcient accuracy to avoid producing large numbers of false positive and false negative results. Screening for and treating persons with early disease must be effective and should improve the likelihood of favorable health outcomes by reducing disease-speciﬁc mortality or morbidity compared to treating patients when they present with signs or symptoms of the disease. Only if the ther- apeutic intervention is extremely dramatic, which most aren’t, is there likely to be no question about its efﬁcacy. Look for potential confounding factors during the process by which subjects are recruited or identiﬁed for inclusion in a study of screening. Innate differences between the screened and not-screened groups should be aggressively sought. Frequently these differences are glossed over as being insigniﬁcant and they often are not and can lead to con- founding bias. The beneﬁcial outcomes that the results refer to should be important for the patient. Persons who are labeled with the disease and who are really disease-free will at least be inconvenienced and may require additional testing that is not benign. Early treatment may result in such severe side effects that patients may 2 Agency for Healthcare Research and Quality. This should be done with 95% conﬁdence intervals to demonstrate the precision of that result. Different strategies may result in different outcomes either in ﬁnal results or patient suffering, depending on the prevalence of disease in the population screened and the screening and veriﬁcation strategy employed. These can be done using focus groups or qualitative studies of patient populations.
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