Anveden Berglind I.,Institute of Environmental Medicine |
Alderling M.,Karolinska Institutet |
Meding B.,Institute of Environmental Medicine
British Journal of Dermatology | Year: 2011
Summary Background Previous knowledge of the impact of certain life-style factors on hand eczema is scanty. Objectives To investigate a possible association between hand eczema and life-style factors such as obesity, physical exercise, stress, smoking and alcohol consumption. Methods In a cross-sectional public health survey in Stockholm, Sweden, 27 994 (58%) randomly chosen individuals aged 18-64 years completed a postal questionnaire regarding physical and mental health, social relations, economic status and work. Of these, 27 793 individuals responded to the question regarding hand eczema and were included in the present study. The association between life-style factors and hand eczema was analysed by prevalence proportion ratios (PPR), using a generalized linear model. Results Hand eczema was more common among individuals who reported high stress levels, PPR 1·326 (95% CI 1·303-1·350). There was also a positive dose-response relationship between hand eczema and stress. Hand eczema was less common among individuals reporting high physical exercise, and most apparent in women, PPR 0·781 (95% CI 0·770-0·792). Men who reported high alcohol intake reported hand eczema less often, PPR 0·958 (95% CI 0·930-0·987). Obese individuals reported hand eczema more commonly, PPR 1·204 (95% CI 1·174-1·234). There was a slight increase of hand eczema among smokers, PPR 1·025 (95% CI 1·006-1·044). Conclusions Hand eczema was more common in individuals who reported stress, obesity and smoking. In individuals who reported high physical exercise levels hand eczema was less common. As there appears to be an association between life-style factors and hand eczema it is important to consider life-style factors in clinical practice. © 2011 British Association of Dermatologists.
Jorgensen L.,Karolinska Institutet |
Ahlbom A.,Institute of Environmental Medicine |
Allebeck P.,Karolinska Institutet |
Dalman C.,Karolinska Institutet
Acta Psychiatrica Scandinavica | Year: 2010
Objective: To estimate the incidence rate of schizophrenia and non-affective psychoses from registers, to highlight the importance of including data from out-patient care, and to assess the proportion of persons treated in out-patient care only. Method: Data from out-patient and in-patient psychiatric care in Stockholm and information from several national registers constitute 'The Stockholm Non-Affective Psychoses Study' (SNAPS). Incidence rates based on SNAPS data were calculated and compared to in-patient care incidence rates. Results: The incidence rate was 72/100 000 for non-affective psychoses (age group 18-44) and 28/100 000 for schizophrenia (age group 18-34) in the SNAPS. This was higher compared to in-patient based incidence rates (42 and 13/100 000 respectively). The proportion of individuals with psychosis treated in out-patient care only was 25%. Conclusion: There are substantial differences in the incidence rates of non-affective psychoses and schizophrenia depending on the availability of data. Not including out-patient care will underestimate the incidence rates. © 2009 John Wiley & Sons A/S.
Lindgren P.,Institute of Environmental Medicine |
Jonsson B.,Stockholm School of Economics
European Journal of Health Economics | Year: 2012
Background The economic evaluation of statins has undergone a development from risk-factor-based models to modeling of hard end points in clinical trials with a shift back to risk-factor models after increased confidence in their predictive power has now been established. At this point, we can look back on the historical economic data on simvastatin to see what lesson regarding reimbursement we can learn. Methods Historical data on the usage and sales of simvastatin in Sweden were combined with published epidemiological and clinical data to calculate the social value of simvastatin to the present day and to make projection until projected until 2018. The distribution of the social surplus was calculated by taking the costs born by society and the producer of the drug into consideration. Results The cost of simvastatin fell drastically following patent expiration, although the number of treated patients has continued to grow. Presently, the use of simvastatin is close to cost neutrality taking direct and indirect cost savings from reduced morbidity into account. However, the major part of the social surplus generated comes from the value of improved quality-adjusted survival. Of the social surplus generated, the producer appropriated 20-43% of the value during the on-patent period, a figure dropping to 1% following loss of exclusivity. The total producer surplus between 1987 and 2018 is 2-5% of the total social surplus. Conclusion Only a small part of the surplus value generated was appropriated by the producer. A regulatory and reimbursement approach that favors early market access and coverage with evidence development as opposed to long-term trials as a pre-requisite for launch is more attractive from both a company and social perspective. © 2011 Springer-Verlag.
Rasouli B.,Institute of Environmental Medicine |
Grill V.,Norwegian University of Science and Technology |
Midthjell K.,Norwegian University of Science and Technology |
Ahlbom A.,Norwegian University of Science and Technology |
And 3 more authors.
Diabetes Care | Year: 2013
OBJECTIVEdTo investigate the association between smoking habits and risk of autoimmune diabetes in adults and of type 2 diabetes. RESEARCH DESIGN AND METHODSdWe used data from the three surveys of the Nord-Trondelag Health Study, spanning 1984-2008 and including a cohort of 90,819 Norwegian men (48%) and women (52%) aged20 years. Incident cases of diabetes were identified by questionnaire and classified as type 2 diabetes (n = 1,860) and autoimmune diabetes (n = 140) based on antibodies to glutamic decarboxylase (GADA) and age at onset of diabetes. Hazard ratios (HRs) adjusted for confounders were estimated by Cox proportional hazards regression models. RESULTSdThe risk of autoimmune diabetes was reduced by 48% (HR 0.52 [95% CI 0.30-0.89]) in current smokers and 58% in heavy smokers (0.42 [0.18-0.98]). The reduced risk was positively associated with number of pack-years. Heavy smoking was associatedwith lower levels of GADA (P = 0.001) and higher levels of C-peptide (964 vs. 886 pmol/L; P = 0.03). In contrast, smoking was associated with an increased risk of type 2 diabetes, restricted to overweight men (1.33 [1.10-1.61]). Attributable proportion due to an interaction between overweight and heavy smoking was estimated to 0.40 (95% CI 0.23-0.57). CONCLUSIONSdIn this epidemiological study, smoking is associated with a reduced risk of autoimmune diabetes, possibly linked to an inhibitory effect on the autoimmune process. An increased risk of type 2 diabetes was restricted to overweight men. Copyright © 2013 by the American Diabetes Association.
News Article | December 3, 2016
Scientists at the Karolinska Institute in Sweden have just released new findings on the mesothelioma risk posed by various different jobs and its relationship to the country’s 1982 asbestos ban. Surviving Mesothelioma has just published a new article on the findings. Click here to read it now. Of the 280 occupations analyzed in the newly-published study, 24 of them were found to carry an elevated risk for malignant mesothelioma. “Among men, increased risks of mesothelioma of the pleura were observed in male-dominated occupations, with the greatest elevation of risk among plumbers,” writes Nils Plato, a Chemical Engineer with the Institute of Environmental Medicine at the Karolinska Institute. According to the report in Epidemiology and Health, as of 2009, the ban on asbestos instituted in 1982 had yet to show any “clear effect” on the number of mesothelioma diagnoses in the country. “Because mesothelioma takes decades to develop, it can decades for an asbestos ban to impact incidence of the disease,” says Alex Strauss, Managing Editor of Surviving Mesothelioma. “This study is a clear argument for ‘sooner is better than later’ when it comes to banning asbestos.” Although 58 countries have now banned asbestos because of its link to mesothelioma, the US has yet to do so. To read more about the results of the Swedish study, including some surprising careers that carried a mesothelioma risk among women, see Swedish Mesothelioma Rates Unaffected By Asbestos Ban, now available on the Surviving Mesothelioma website. Plato, N, et al, “Occupations and mesothelioma in Sweden: updated incidence in men and women in the 27 years after the asbestos ban”, September 20, 2016, Epidemiology and Health, eCollection 2016, http://www.e-epih.org/journal/view.php?number=863 For nearly ten years, Surviving Mesothelioma has brought readers the most important and ground-breaking news on the causes, diagnosis and treatment of mesothelioma. All Surviving Mesothelioma news is gathered and reported directly from the peer-reviewed medical literature. Written for patients and their loved ones, Surviving Mesothelioma news helps families make more informed decisions.
Discacciati A.,Institute of Environmental Medicine |
Wolk A.,Institute of Environmental Medicine
Recent Results in Cancer Research | Year: 2014
The etiology of prostate cancer (PCa) is still largely unknown and the only well-established risk factors are those that are non-modifiable (age, race, and family history). Therefore, the identification of lifestyle and dietary factors which might prevent PCa development and progression is of paramount importance from a public health point of view. Accumulating evidence indicates that obesity may have a dual effect on PCa: an increased risk of aggressive PCa and a decreased risk of localized PCa. Both occupational and leisure time physical activity have been observed to be associated with a reduced PCa risk. Different dietary factors including coffee have been examined in several epidemiological studies, but results have been mostly inconsistent. However, these inconsistencies can be, at least partly, explained by the fact that the majority of those studies examined total PCa risk only and, in addition, they did not take into account the different genetic characteristics within the study populations. Therefore, the future epidemiological studies should focus on the analysis of PCa subtypes separately in order to examine possible etiological heterogeneity of PCa in relation to some exposures. In addition, differences in the genetic characteristics of the study participants should be taken into account to explore the possibility of gene-environment interactions. © 2014 Springer-Verlag Berlin Heidelberg.
Wallin A.,Institute of Environmental Medicine |
Orsini N.,Institute of Environmental Medicine |
Wolk A.,Institute of Environmental Medicine
British Journal of Cancer | Year: 2011
Background:During the last decade, the epidemiological evidence on consumption of meat and risk of ovarian cancer has accumulated.Methods:We assessed the relationship between red and processed meat consumption and risk of ovarian cancer with a dose-response meta-analysis. Relevant prospective cohort studies were identified by searching the PubMed and EMBASE databases through 21 January 2011, and by reviewing the reference lists of retrieved articles. Study-specific relative risk (RR) estimates were combined using a random-effects model.Results:Eight cohort studies were included in the meta-analysis. The summary RR for an intake increment of 100 g per week was 1.02 (95% confidence interval (CI), 0.99-1.04) for red meat and 1.05 (95% CI, 0.98-1.14) for processed meat. For an intake increment of four servings per week, the summary RR of ovarian cancer was 1.07 (95% CI, 0.97-1.19) for red meat (100 g per serving) and 1.07 (95% CI, 0.97-1.17) for processed meat (30 g per serving).Conclusion:Results from this dose-response meta-analysis suggest that red and processed meat consumption is not associated with risk of ovarian cancer. Although a lower consumption of red and processed meat may offer protection against other types of cancer, other interventions are needed to reduce the risk of ovarian cancer. © 2011 Cancer Research UK All rights reserved.
Tsinganou E.,Institute of Environmental Medicine
German medical science : GMS e-journal | Year: 2010
Human intestinal spirochetosis (IS) is a condition defined histologically by the presence of spirochetal microorganisms attached to the apical cell membrane of the colorectal epithelium. Intestinal spirochetes comprise a heterogeneous group of bacteria. In humans, Brachyspira aalborgi and Brachyspira pilosicoli predominate. Prevalence rates of IS are low where living standards are high, in contrast to poorly developed areas where IS is common. Homosexuals and HIV-infected individuals are at high risk of being colonized. Clinical significance in individual cases has remained unclear up to now. A review of the literature assumes that invasion of spirochetes beyond the surface epithelium may be associated with gastrointestinal symptoms which respond to antibiotic treatment (metronidazole), whereas individuals lacking this feature may be mostly asymptomatic. Of unknown reason, homosexual and HIV-positive men as well as children are more likely to be symptomatic irrespective of invasion. Rare cases of spirochetemia and multiple organ failure have been reported in critically ill patients with IS.
Kaminskyy V.,Institute of Environmental Medicine |
Zhivotovsky B.,Institute of Environmental Medicine
Journal of Internal Medicine | Year: 2010
Kaminskyy V, Zhivotovsky B (Karolinska Institutet, Stockholm, Sweden). To kill or be killed: how viruses interact with the cell death machinery (Symposium). J Intern Med 2010; 267: 473-482. A virus (from the Latin virus meaning toxin or poison) is a small infectious agent that can only replicate inside the cells of another organism. Viruses are found wherever there is life and have probably existed since living cells first evolved. Viruses do not have their own metabolism and require a host cell to make new products. The range of structural and biochemical (i.e., cytopathic) effects that viruses have on the host cell is extensive. Most viral infections eventually result in the death of the host cell. The causes of death include cell lysis, alterations to the cell's surface membrane and various modes of programmed cell death. Some viruses cause no apparent changes to the infected cell. Cells in which the virus is latent and inactive show few signs of infection and often function normally. This causes persistent infection and the virus is often dormant for many months or years. Some viruses can cause cells to proliferate without causing malignancy, whereas others are established causes of cancer. Human organisms use a genetically controlled cell death programme that prevents the spreading of viral infection and kills the virus. Between 19 and 21 November 2009, with sponsorship from the Journal of Internal Medicine, the Swedish Research Foundation and the Swedish Cancer Society hosted a conference in Stockholm entitled: 'To kill or to be killed. Viral evasion strategies and interference with cell death machinery'. Four comprehensive reviews from this conference are presented in this issue of the Journal of Internal Medicine. These reviews include descriptions of: the modulation of host innate and adaptive immune defenses by cytomegalovirus; the impact of gamma-chain family cytokines on T cell homoeostasis in HIV-1 infection and the therapeutic implications; approaches to killing tumours by depriving them of the mechanisms for detoxification; and viral strategies for the evasion of immunogenic cell death. © 2010 Blackwell Publishing Ltd.
Frostegard J.,Institute of Environmental Medicine
BMC Medicine | Year: 2013
Atherosclerosis, the major cause of cardiovascular disease (CVD), is a chronic inflammatory condition with immune competent cells in lesions producing mainly pro-inflammatory cytokines. Dead cells and oxidized forms of low density lipoproteins (oxLDL) are abundant. The major direct cause of CVD appears to be rupture of atherosclerotic plaques. oxLDL has proinflammatory and immune-stimulatory properties, causes cell death at higher concentrations and contains inflammatory phospholipids with phosphorylcholine (PC) as an interesting epitope. Antibodies against PC (anti-PC) may be atheroprotective, one mechanism being anti-inflammatory. Bacteria and virus have been discussed, but it has been difficult to find direct evidence, and antibiotic trials have not been successful. Heat shock proteins could be one major target for atherogenic immune reactions. More direct causes of plaque rupture include pro-inflammatory cytokines, chemokines, and lipid mediators. To prove that inflammation is a cause of atherosclerosis and CVD, clinical studies with anti-inflammatory and/or immune-modulatory treatment are needed. The potential causes of immune reactions and inflammation in atherosclerosis and how inflammation can be targeted therapeutically to provide novel treatments for CVD are reviewed. © 2013 Frostegård; licensee BioMed Central Ltd.