Polychlorinated dibenzo- p- dioxins and dibenzofurans (EHC 8. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. ENVIRONMENTAL HEALTH CRITERIA 8. POLYCHLORINATED DIBENSO- PARA- DIOXINS AND DIBENZOFURANS. This report contains the collective views of an international group of. United Nations Environment Programme, the International. Labour Organisation, or the World Health Organization. The main objective of the IPCS is to carry out and. Supporting activities include. Other activities carried out by the IPCS include the. Errors and omissions excepted, the. SUMMARY AND RECOMMENDATIONS1. Ambient levels and routes of exposure. Toxicokinetics, biotransformation, and. Health effects. 1. Animals. 1. 1. 4. Humans. 1. 1. 5. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES. ANALYTICAL METHODS. Physical and chemical properties. Analytical methods. Sampling strategy and sampling methods. Extraction procedures. Isomer identification. Other analytical methods. SOURCES OF ENVIRONMENTAL POLLUTION3. Production, synthesis, and use. Industrial processes. This episode puts everyone. The fate of Goryeo comes. VI Diretrizes Brasileiras de Hipertensão. Sociedade Brasileira de Cardiologia; Sociedade Brasileira de Hipertensão; Sociedade Brasileira de Nefrologia. Contamination of commercial products. Chlorophenoxyacetic acid herbicides. Polychlorinated biphenyls (PCBs)3. Chlorodiphenyl ether herbicides. Hexachlorobenzene. Sources of heavy environmental pollution. Industrial accidents. Improper disposal of industrial waste.
Heavy use of chemicals. Other sources of PCDDs and PCDFs in the. Thermal degradation of technical. Incineration of municipal waste. Incineration of sewage sludge. Incineration of hospital waste. Incineration of hazardous waste. Metal industry and metal treatment. Wire reclamation. Fires and accidents in PCB- filled. Pulp and paper industry. Incineration of coal, peat, and wood. Inorganic chlorine precursors. Photochemical processes. Comparison of isomeric pattern and congener. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND. TRANSFORMATIONS. 4. Environmental transport. Soil and sediments. Environmental transformation. Abiotic transformation. Biotransformation and biodegradation. Aquatic organisms. Terrestrial animals. Human data. 4. 4. Adipose tissue. 4. Blood plasma. 5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE5. Water and leachate. Meat and bovine milk. Yusho and Yu- cheng episodes. KINETICS AND METABOLISM OF 2,3,7,8- TETRACHLORODIBENZO- P- DIOXIN (TCDD) AND OTHER PCDDs. Uptake, distribution, and excretion. Studies on guinea- pigs. Studies on hamsters. Studies on monkeys. Metabolic transformation. Studies on mammals. Invivo studies. 6. Invitro studies. 6. Transfer via placenta and/or milk. Matrix effects on the uptake. EFFECTS OF TCDD AND OTHER PCDDs ON EXPERIMENTAL. ANIMALS AND INVITRO TEST SYSTEMS. Invivo studies on mammals. Invitro studies on mammalian cells. Studies on birds. Toxicity of metabolites. Modulation of the acute toxicity. Short- term toxicity. Studies on guinea- pigs. Studies on hamsters. Studies on monkeys. Long- term toxicity. Studies on monkeys. Effects detected by special studies. Wasting syndrome. Hepatotoxicity. 7. Morphological alterations. Hepatic plasma membrane. Biliary excretion. Epidermal effects. Invivo studies. 7. Invitro studies. 7. Effects on the immune system. Histopathology. 7. Humoral- mediated immunity. Cell- mediated immunity. Macrophage function. Effects on the intermediary. Enzyme induction. Studies on rats. 7. Studies on mice. 7. Studies on guinea- pigs. Studies on rabbits. Studies on hamsters. Studies on cows. 7. Studies on chick embryos. Studies on cell cultures. Endocrine effects. Embryotoxicity and reproductive effects. Studies on rabbits. Studies on monkeys. Studies on chickens. Mutagenicity and related end- points. Mutagenicity. 7. 6. Studies on bacteria. Studies on eukaryotic cells. Invivo studies. 7. Interaction with nucleic acids. Cytogenetic effects. Cell transformation. Long- term animal studies on single. Long- term animal studies with mixed. Short- term and interaction studies. Mechanisms of action. Receptor- mediated effects. Impairment of normal cellular regulatory. Endocrine imbalance. Body weight regulation. Plasma membrane function. Impaired vitamin A storage. EFFECTS OF PCDDs ON HUMAN BEINGS - EPIDEMIOLOGICAL. AND CASE STUDIES. Occupational studies - historical perspective. General population studies. Signs and symptoms in humans associated with. TCDD exposure. 8. Skin manifestations. Systemic effects. Neurological effects. Psychiatric effects. Epidemiological studies. Human experimental studies. TOXICOKINETICS OF PCDFs. Uptake, distribution, and excretion. Studies with 2,3,7,8- tetrachlorodibenzo- . TCDF). 9. 1. 2. Studies with other PCDFs. Metabolic transformation. Transfer via placenta and/or milk. EFFECTS OF PCDFs ON ANIMALS1. Studies on rats. 10. Studies on mice. 10. Studies on guinea- pigs. Studies on rabbits. Studies on monkeys. Short- term toxicity. Studies on rats. 10. Studies on mice. 10. Studies on guinea- pigs. Studies on rabbits. Studies on hamsters. Studies on monkeys. Studies on chickens. Chronic toxicity. Studies on monkeys. Effects detected by special studies. Immunobiological effects. Histopathology. 1. Humoral- mediated immunity. Cell- mediated immunity. Enzyme induction. Studies on rats. 1. Studies on mice. 1. Studies on chickens. Studies on cell cultures. Embryotoxicity and reproductive effects. EFFECTS OF PCDFs ON HUMAN BEINGS1. EVALUATION OF HEALTH RISKS FROM THE EXPOSURE TO. CHLORINATED DIBENZO- P- DIOXINS (PCDDs) AND. DIBENZOFURANS (PCDFs). Exposure assessment. Sources of contamination. Routes of exposure. Toxicokinetics of 2,3,7,8- TCDD1. Toxicokinetics of PCDDs and PCDFs. TCDD. 1. 2. 3. 3. Toxic effects 2,3,7,8- TCDD1. Toxic effects of PCDDs and PCDFs. TCDD. 1. 2. 3. 5. Review of species differences. Human health effects. Human body burden and kinetics. General conclusions. EVALUATIONS BY INTERNATIONAL BODIES AND THE CONCEPT. OF TCDD EQUIVALENTS. International evaluations. Methodologies used in assessment of. PCDDs and PCDFs. 1. Individual congeners. Mixtures of PCDD and PCDF congeners and. TCDD toxic. equivalents. FRENCH TRANSLATION OF SUMMARY, EVALUATION, AND. RECOMMENDATIONS. WHO TASK GROUP ON CHLORINATED DIBENZO- p- DIOXINS AND. DIBENZOFURANS. Dr U. G. Ahlborg, Unit of Toxicology, National Institute of. Environmental Medicine, Stockholm, Sweden. Dr J. S. Bellin, Office of Toxic Substances, US Environmental. Protection Agency, Washington, DC, USA. Dr B. Birmingham, Ministry of the Environment, Hazardous Contaminants. Section, Toronto, Ontario, Canada. Professor A. D. Dayan, Department of Health and Social Security. St Bartholomew's Hospital Medical College, London, United. Kingdom (Chairman). Dr A. Greenberg, Department of Health and Social Security. Division of Toxicology and Environmental Protection, London. United Kingdom. Dr R. D. Kimbrough, United States Department of Health and Human. Services, Center for Disease Control, Atlanta, Georgia, USA. Now at the US Environmental Protection Agency Washington. DC, USA). Dr R. Koch, Department of Toxicology, Institute of Hygiene. Gera, DDR. Professor C. Rappe, Department of Chemistry, University of. Umea, Umea, Sweden. Dr S. Safe, Texas A and M University, College Station, Texas. Dr H. Spielmann, Max von Pettenkofer Institute, Bundesgesundheitsamt. Berlin (West). Dr J. Vos, National Institute of Public Health and Environmental. Hygiene, Bilthoven, Netherlands. Representatives. Dr A. Berlin, Health and Safety Directorate, Commission of the. European Communities, Luxembourg. Mrs E. Cox, Department of the Environment, London, United. Miss F. D. Pollitt, Department of the Environment, London. United Kingdom. Secretariat. Dr G. C. Becking, International Programme on Chemical Safety. World Health Organization, Research Triangle Park, North. Carolina, USA (Secretary). Secretariat (contd). Dr H. Hakensson, Unit of Toxicology, National Institute of. Environmental Medicine, Stockholm, Sweden (Temporary. Adviser) (Rapporteur). Dr E. Johnson, International Agency for Research on Cancer. World Health Organization, Lyons, France. Dr S. Tarkowski, Regional Office for Europe, World Health. Organization, Copenhagen, Denmark. NOTE TO READERS OF THE CRITERIA DOCUMENTS. Every effort has been made to present information in the criteria. In the interest of all users of the environmental health. Manager of the International. Programme on Chemical Safety, World Health Organization, Geneva. Switzerland, in order that they may be included in corrigenda, which. Berlin opened the meeting and. Institute and on behalf of. United Kingdom Department of Health and Social Security, who. Becking addressed the meeting on behalf. IPCS (UNEP, ILO, and. WHO). The Task Group reviewed and revised the draft criteria document. Holmstedt, all of the National Institute of. Environmental Medicine, Stockholm, Sweden, and by Professor C. Rappe. of the University of Umea, Umea, Sweden. The. United Kingdom Department of Health and Social Security generously. They do not occur naturally, nor are they. There are 7. 5 positional isomers of PCDDs and. PCDFs. Levels of PCDDs and PCDFs up to 5. For these persons, inhalation and dermal contact are. Data on bioavailability through. The reported half- lives for. The half- life of. TCDD in adipose tissue of the rhesus monkey is about 1 year. The half- life for 2,3,7,8- TCDD has been. Studies on rats have. CDF is more highly retained than is. TCDD. They also appear. None of these populations were randomly sampled. The more. highly chlorinated PCDDs and PCDFs, particularly octa. CDD, are also. present in these samples. Average tissue levels of TCCD tend to. The toxic responses. TCDD induces a wide spectrum of biological effects. A depletion. Not all of these. The most. characteristic toxic effects observed in all laboratory animals are. Chloracne and. related dermal lesions are the most frequently noted signs of. TCDD toxicosis in humans; dermal lesions are also observed in. In contrast, most rodents. TCDD. Many of the toxic lesions are noted. The lowest- observed- effect levels have been reported to be. In two cancer studies in. The incidence of certain hormone- dependent. Thus, it is assumed to be. There are 1. 2 isomers that display higher toxicity, i. CDDs and CDFs with four chlorine atoms. A mixture of two. CDD). has been demonstrated to possess carcinogenic properties in long- term. Arimidex (Anastrozole) Drug Information: Side Effects and Drug Interactions. Serious adverse reactions with ARIMIDEX occurring in less. This may cause difficulty in swallowing and/or breathing; and 3). Common adverse reactions (occurring with an incidence of. The median duration of adjuvant. ARIMIDEX 1 mg and tamoxifen 2. Adverse reactions occurring with an incidence of at least. Table 1. Table 1 : Adverse reactions occurring with an incidence. ATAC trial*Body system and adverse reactions by COSTART preferred term*ARIMIDEX 1 mg(N. In the overall population, angina pectoris was reported. ARIMIDEX arm and 5. ARIMIDEX arm and 3. In women with pre- existing ischemic heart disease. ARIMIDEX and 1. 0% in patients on tamoxifen. In this patient. population, angina pectoris was reported in 2. ARIMIDEX and 1. 3/2. ARIMIDEX and 8/2. Bone Mineral Density Findings. Results from the ATAC trial bone substudy at 1. ARIMIDEX had a mean decrease in. BMD) compared to. Patients receiving tamoxifen had a mean increase in both lumbar spine. BMD compared to baseline. Because ARIMIDEX lowers circulating estrogen levels it. A post- marketing trial assessed the combined effects of. ARIMIDEX and the bisphosphonate risedronate on changes from baseline in BMD and. All patients received calcium and. D supplementation. At 1. 2 months, small reductions in lumbar spine bone. In the primary analysis population for. ARIMIDEX alone), there was no clinically significant change in LDL- C. HDL- C from baseline to 1. In secondary population for lipids. ARIMIDEX+risedronate), there also was no clinically significant change in. LDL- C and HDL- C from baseline to 1. In both populations for lipids, there was no clinically. TC) or serum triglycerides (TG) at. In this trial, treatment for 1. ARIMIDEX. alone had a neutral effect on lipid profile. Combination treatment with. ARIMIDEX and risedronate also had a neutral effect on lipid profile. The trial provides evidence that postmenopausal women. ARIMIDEX should be. National Cholesterol Education Program guidelines for. LDL. elevations. Other Adverse Reactions. Patients receiving ARIMIDEX had an increase in joint. Patients receiving ARIMIDEX had an increase in. The cumulative incidence of new primary cancers was. ARIMIDEX group (1. There were more deaths. ARIMIDEX treatment group. First- Line Therapy. Adverse reactions occurring with an incidence of at least. Table 3. Table 3 : Adverse Reactions Occurring with an. Incidence of at Least 5% in Trials 0. Body system Adverse Reaction*Number (%) of subjects. ARIMIDEX (N=5. 06)Tamoxifen (N=5. Whole body. Asthenia. Pain. 70(1. 4)7. 3 (1. Back pain. 60(1. 2)6. Headache. 47 (9)4. Abdominal pain. 40 (8)3. Chest pain. 37 (7)3. Flu syndrome. 35 (7)3. Pelvic pain. 23 (5)3. Cardiovascular. Vasodilation. Hypertension. 25 (5)3. Digestive. Nausea. Constipation. 47 (9)6. Diarrhea. 40 (8)3. Vomiting. 38 (8)3. Anorexia. 26 (5)4. Metabolic and Nutritional. Peripheral edema. Musculoskeletal. Bone pain. Nervous. Dizziness. Insomnia. 30 (6)3. Depression. 23 (5)3. Hypertonia. 16 (3)2. Respiratory. Cough increased. Dyspnea. 51 (1. 0)4. Pharyngitis. 49 (1. Skin and appendages. Rash. 38 (8)3. 4 (8)Urogenital. Leukorrhea. 9 (2)3. A patient may have had more. Less frequent adverse. ARIMIDEX l mg in either Trial 0. Trial 0. 02. 7 were similar to those reported for second- line therapy. Based on results from. No significant differences were seen between treatment. Table 4 : Number of Patients. Pre- specified Adverse Reactions in Trials 0. Adverse Reaction*Number (n) and Percentage of Patients. ARIMIDEX 1 mg(N=5. NOLVADEX 2. 0 mg(N=5. Depression. 23 (5)3. Tumor Flare. 15 (3)1. Thromboembolic Disease. Adverse reactions reported in greater than. Table 5 : Number (N) and Percentage of Patients with. Adverse Reactions in Trials 0. Adverse Reaction*ARIMIDEX 1 mg(N=2. ARIMIDEX 1. 0 mg(N=2. Megestrol Acetate 1. N=2. 53)n %n %n %Asthenia. Nausea. 41(1. 6)4. Headache. 34(1. 3)4. Hot Flashes. 32(1. Pain. 28(1. 1)3. 8(1. Back Pain. 28(1. 1)2. Dyspnea. 24(9)2. 7(1. Vomiting. 24(9)2. Cough Increased. 22(8)1. Diarrhea. 22(8)1. Constipation. 18(7)1. Abdominal Pain. 18(7)1. Anorexia. 18(7)1. Bone Pain. 17(6)2. Pharyngitis. 16(6)2. Dizziness. 16(6)1. Rash. 15(6)1. 5(6)1. Dry Mouth. 15(6)1. Peripheral Edema. Pelvic Pain. 14(5)1. Depression. 14(5)6(2)5(2)Chest Pain. Paresthesia. 12(5)1. Vaginal Hemorrhage. Weight Gain. 4(2)9(4)3. Sweating. 4(2)3(1)1. Increased Appetite. A patient may have had more. Other less frequent (2% to 5%) adverse reactions. ARIMIDEX l mg in either Trial 0. Trial 0. 00. 5. are listed below. These adverse experiences are listed by body system and are. Body as a Whole: Flu syndrome; fever; neck. Cardiovascular: Hypertension. Hepatic: Gamma GT increased; SGOT. SGPT increased Hematologic: Anemia; leukopenia. Metabolic and Nutritional: Alkaline. Mean serum total cholesterol. L among patients receiving ARIMIDEX. Increases in. LDL cholesterol have been shown to contribute to these changes. Musculoskeletal: Myalgia; arthralgia. Nervous: Somnolence; confusion. Respiratory: Sinusitis; bronchitis. Skin and Appendages: Hair thinning (alopecia). Urogenital: Urinary tract infection. The incidences of the following. These six groups, and the adverse reactions captured in. The results are shown in the table. Table 6 : Number (n) and Percentage of Patients with. Pre- specified Adverse Reactions in Trials 0. Adverse Reaction Group. ARIMIDEX1 mg(N=2. ARIMIDEX1. 0 mg(N=2. Megestrol Acetate. N=2. 53) n(%)n(%)n(%)Gastrointestinal Disturbance. Hot Flushes. 33(1. Edema. 19(7)2. 8(1. Thromboembolic Disease. Vaginal Dryness. 5(2)3(1)2(1)Weight Gain. Post- Marketing Experience. These adverse reactions are. Therefore, it is not. The following have been reported in. 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Containment devices play an important role, especially for individuals who prefer to avoid the risks of interventional treatments, or in whom active treatment is impossible for any reason. Simple clinical interventions. Underlying disease/cognitive impairment. Urinary incontinence, especially in the elderly, has been associated with multiple comorbid conditions including: cardiac failure; chronic renal failure; diabetes; chronic obstructive pulmonary disease; neurological disease including stroke and multiple sclerosis; general cognitive impairment; sleep disturbances, e. However, this is often difficult to assess as patients frequently suffer from more than one condition. In addition, interventions may be combined and individualised, making it impossible to decide which alteration in an underlying disease has affected a patient’s UI. Question. In adults with UI, does improving an associated condition improve UI compared to no correction of that condition? Evidence. There is compelling evidence that there is a higher prevalence of UI in women with type 2 diabetes. One study showed no correlation between earlier intensive treatment of type 1 diabetes mellitus and the prevalence of UI in later life vs. Few controlled studies have used the occurrence of UI as a primary outcome, or were powered to assess the occurrence of statistically significant UI, or worsening rates against placebo. In most cases, it is therefore not possible to be sure that a drug causes UI. In patients with existing UI, particularly the elderly, it may be difficult or impossible to distinguish between the effects of medication, comorbidity or ageing on UI. Although changing drug regimens for underlying disease may be considered as a possible early intervention for UI, there is very little evidence of benefit . There is also a risk that stopping or altering medication may result in more harm than benefit. Question. In adults with UI, does adjustment of other (non- incontinence) medication improve UI compared to no change in treatment? Evidence. Structured literature review failed to identify any studies addressing whether adjustment of specific medications could alter existing symptoms of UI. Also, there is little evidence relating to the occurrence or worsening of UI in relation to prescription of any specific drugs. Summary of evidence. LEThere is very little evidence that alteration of non- incontinence medication can cure or improve symptoms of urinary incontinence. Recommendations. GRTake a drug history from all patients with urinary incontinence. AReview any new medication associated with the development or worsening of urinary incontinence. C4. 1. 1. 3. Constipation. Several studies have shown strong associations between constipation and UI. Constipation can be improved by behavioural, physical and medical treatments. Question. Does treatment for constipation improve UI? Evidence. Two, large, cross- sectional population- based studies . An observational study comparing women with UI and women with pelvic organ prolapse (POP) to controls found that a history of constipation was associated with both prolapse and UI . One RCT found that a multimodal intervention in elderly patients, involving assisted toileting, fluid intake, etc., reduced the occurrence of UI and constipation, while behavioural therapy appeared to improve both . However, there is no evidence to show whether or not treating constipation improves UI, although both constipation and UI appear to be improved by certain behavioural interventions. Summary of evidence. LEThere is a consistent association between a history of constipation and the development of urinary incontinence and pelvic organ prolapse. There is no consistent evidence in adults that treatment of constipation alone improves urinary incontinence. Recommendation. GRAdults with urinary incontinence who also suffer from constipation should be given advice about bowel management in line with good medical practice. C4. 1. 1. 3. 3. Research priority. Does the normalisation of bowel habit improve UI in patients who are constipated? Containment. Containment is important for people with UI when active treatment does not cure the problem, or when it is not available or not possible. Some individuals may prefer containment rather than undergo active treatment with its associated risks. This includes the use of absorbent pads, urinary catheters, external collection devices, penile clamps for men and intravaginal devices for women. Studies of catheter use are not specific to patients with non- neurogenic UI. Detailed literature summaries can be found in the current ICUD monograph . A useful resource for health care professionals and patients can be found at: http: //www. Question. For adults with UI, is one type of containment device better than another? Evidence. One RCT involving elderly women in care comparing management with pads to indwelling urethral catheter found no difference in dependency level or skin integrity score at six months . Use of an external sheath was compared with indwelling catheterisation over 3. RCT involving elderly men resident in hospital . A short- term (two weeks) crossover RCT in men with UI found that disease specific Qo. L was better when using an external sheath and more men preferred it, compared to pads . For men with light UI, a randomised crossover trial found that a leaf- shaped type of pad was preferred to rectangular pads . A series of three crossover RCTs examined performance of different pad designs for differing populations . For women with light UI, disposable insert pads (within washable pouch pants) were most effective. In adults with moderate/severe incontinence, disposable pull- up pants were more effective for women, whilst for men disposable diapers were more effective during the day and washable diapers at night. Question. For men or women with UI, is one type of catheter or external collection device better than another? Evidence. A Cochrane review summarised three RCTs comparing different types of long- term indwelling catheters and found no evidence that one catheter material or type of catheter was superior to another . A systematic review of non- randomised studies found no differences in UTI outcome or UUT changes between use of suprapubic or urethral catheter drainage; however, patients with suprapubic catheters were less likely to have urethral complications . For people using intermittent catheterisation, a Cochrane review found no evidence that one type of catheter or regimen of catheterisation was better than another . However, there is recent evidence from a narrative review suggesting that in certain populations using single- use catheters may reduce urethral trauma and UTI . A Cochrane review summarising five trials comparing washout policies in adults with indwelling urinary catheters found inconsistent evidence of benefit . There was no difference in outcome at twelve months in women with SUI between vaginal pessary alone; pelvic floor muscle training (PFMT) alone; and vaginal pessary + PFMT, although vaginal pessary was inferior to PFMT at three months for bother from UI. Summary of evidence. LEPads are effective in containing urine. Hinge- type penile clamps are more effective than circular clamps to control stress urinary incontinence in men. Vaginal devices may improve stress urinary incontinence in women in selective groups. Recommendations. GREnsure that adults with urinary incontinence and/or their carers are informed regarding available treatment options before deciding on containment alone. A*Suggest use of disposable insert pads for women and men with light urinary incontinence. A*In collaboration with other healthcare professionals with expertise in urinary incontinence, help adults with moderate/severe urinary incontinence to select the individually best containment regimen considering pads, external devices and catheters, balancing benefits and harms. A*Choice of pad, from the wide variety of different absorbent materials and designs available, should be made with consideration of the individual patient’s circumstance, degree of incontinence and preference. B* Recommendation based on expert opinion. Research priority. To develop methods for assessing the best method of containment for individual adults with UI. Lifestyle interventions. Examples of lifestyle factors that may be associated with incontinence include obesity, smoking, level of physical activity and diet. Modification of these factors may improve UI. Caffeine reduction. Many drinks contain caffeine, particularly tea, coffee and cola. Anecdotal evidence of urinary symptoms being aggravated by excessive caffeine intake has focused attention on whether caffeine reduction may improve UI. However, a cross- sectional population survey found no statistical association between caffeine intake and UI . Lack of knowledge about the caffeine content of different drinks has made the role of caffeine reduction in alleviating UI difficult to assess. Question. In adults with UI, does caffeine reduction improve UI or Qo. L compared to no caffeine reduction? Evidence. Four studies were found on the effect of caffeine reduction on UI . They were of moderate quality and the results were inconsistent. The studies were mainly in women, so results can only be cautiously generalised to men . One RCT showed that reducing caffeine intake as an adjunct to behavioural therapy resulted in reduced urgency but not reduced UI compared to behavioural therapy alone . Another RCT found that reducing caffeine had no benefit for UI . A further interventional study in the elderly showed borderline significance for the benefit of reducing caffeine intake on UI . In a large prospective cohort study there was no evidence that caffeine reduction reduced the risk of progression of UI over two years . However, it is also possible that heavy physical exercise may aggravate UI.
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