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Head and neck cancers are largely caused by smoking, alcohol and HPV virus (oral sex).Possible is there a (small) familial factor in this large (altough) retrospective trial, so not conclusive on this familial effect.Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE studyA large study in France confirms thisConclusion:To our knowledge, the ICARE study is the first population-based case–control study in France and one of the largest in the world which investigates the role of risk factors other than tobacco and alcohol consumption in the occurrence of oral cavity cancer. Strengths of this study include large sample size allowing us to perform analyses by subsite, and detailed data about family history of cancer and personal medical history.BackgroundThe aim of this study was to evaluate the role of family history of cancer and personal history of other medical conditions in the aetiology of the oral cavity cancer in FranceMethodsWe used data from 689 cases of cavity squamous cell carcinoma and 3481 controls included in a population-based case–control study, the ICARE study. Odds-ratios (ORs) associated with family history of cancer and personal medical conditions and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression and were adjusted for age, gender, area of residence, education, body mass index, tobacco smoking and alcohol drinking.ResultsPersonal history of oral candidiasis was related to a significantly increased risk of oral cavity cancer (OR 5.0, 95% CI 2.1-12.1). History of head and neck cancers among the first-degree relatives was associated with an OR of 1.9 (95% CI 1.2-2.8). The risk increased with the number of first-degree relatives with head and neck cancer.ConclusionA family history of head and neck cancer is a marker of an increased risk of oral cavity cancer and should be taken into account to target prevention efforts and screening. Further studies are needed to clarify the association between oral cavity cancer and personal history of candidiasis.Peer Review reportsBackgroundOral cavity cancer (International Classification of Diseases 10th revision (ICD-10) codes C00-C08 [1]) is an important public health burden with an annual worldwide incidence estimated at approximately 263,000 cases, and mortality at 127,000 [2]. Among developed countries, France has the highest age-standardized incidence rate for males (7.6/100,000) and one of the highest for females (1.5/100,000) [3]. As is the case for the other sites of upper aerodigestive tract (UADT), tobacco and alcohol consumption are the main risk factors for oral cavity cancer [4, 5].Besides the role of human papilloma viruses (HPV) 16 and 18 in the aetiology of UADT cancers, few other conditions such as herpetic infection [6–11], candidiasis [6, 10, 11], warts [6, 9–11], and gastro-oesophageal reflux [7] have been investigated. The results of the epidemiological studies on the role of these medical conditions in the occurrence of UADT cancers are contradictory and the underlying mechanisms are not complete elucidated.Other risk factors, such as genetic polymorphism in genes involved in the metabolism of tobacco and alcohol carcinogens and DNA repair seems to play a role in the development of UADT cancers [12–19]. Few epidemiological studies considered the risk of UADT cancers in relatives of subjects with cancer history [20–26]. Familial clustering of UADT cancers may indicate that genetic factors play a role in the process of carcinogenesis, but may also reflect a tendency of relatives to have similar behaviour towards tobacco and alcohol. Limited data are available on the combined effect of family history, and tobacco and alcohol consumption [20, 23, 26]. The literature is contrasted about whether the cancer risk varies according to UADT subsite, gender, type of affected relative (parents, siblings), and their cancer site.The present work aimed to investigate the role of family history of cancer and personal medical history in the aetiology of oral cavity cancer in France using data from a large case–control study, the ICARE study.MethodsICARE studyThe ICARE study (Investigation of occupational and environmental CAuses of REspiratory cancers) is a multicentre population-based case–control study on lung and upper aerodigestive tract cancers carried out from 2001 to 2007 in 10 French administrative areas (“départements”) covered by a general cancer registry. This study was set up to explore the role of lifestyle, environmental and occupational risk factors in lung and UADT cancers. The study design has been described in details elsewhere [27].Briefly, all newly diagnosed primary oral cavity, pharynx, larynx, sinusal cavities, trachea and lung cancers were selected. Only histologically confirmed cases aged 75 or younger at interview, identified between 2001 and 2007, and residing in one of the 10 départements, were eligible. Clinical and anatomo-pathology reports were reviewed to determine topography and histological type of the tumours according to the International Classification of Diseases for Oncology [28]. All histological types were included.Controls were selected from the general population by random digit dialling [29]. The controls were frequency-matched to the cases by age, gender and area of residence (“département”). Additional stratification ensured that controls were representative of the population of the “département” in terms of socio-economic status based on the last job held.Present analysisThe present analysis included all ICARE controls and only the cases with oral cavity cancer (ICD-10 codes C01-C06).Among the 1316 oral cavity cancer cases identified as eligible, 196 could not be reached, 81 were deceased and 71 were too sick to be interviewed. Of the 968 cases who were contacted, 176 refused to participate and 792 (81.8%) answered the questionnaire. We focused only on the cases with squamous cell carcinoma (772 subjects, 97.5% of all cases with oral cavity cancer).Of 4673 eligible controls, 4411 were contacted, and 3555 (80.6%) agreed to participate.Data collectionTrained interviewers administered a detailed standardised questionnaire during face-to-face interviews. If the subject was too sick to be interviewed, a shortened version of the questionnaire was used to interview him or a next-of-kin. Among the 772 subjects with squamous cell carcinoma of the oral cavity, 689 (89.2%) filled a complete questionnaire and 83 (10.8%) a shortened questionnaire. Among controls, 3481 (97.9%) filled a complete questionnaire and 74 a shortened questionnaire (2.1%). As the shortened version of the questionnaire did not contain information about family history of cancer and medical conditions, the present analysis was based on 689 cases with squamous cell carcinoma and 3481 controls, all with a complete questionnaire.The complete questionnaire consisted of the following items: socio-demographic characteristics (age, gender, birth country, education level, marital status), residential history, personal medical history, family history of cancer, detailed tobacco and alcohol consumption (quantity, duration, type of product, age at starting, time since cessation), non-alcoholic beverage consumption (coffee, tea), anthropometric variables (height, weight at interview, two years before and at age 30), detailed lifelong job history and occupational exposures.To ascertain personal medical history, study participants were asked if, throughout their lives, they had ever had (“yes, no, or don’t know”) any of the following diseases: tuberculosis, chronic bronchitis, asthma, recurrent rhinitis, nasal polyps, recurrent nose bleeds, recurrent sinusitis, gastro-oesophageal reflux (heartburn or regurgitation), herpes, candidiasis, and warts. If the answer was “yes”, the subjects were asked to specify the age at first occurrence, the treatment and if the diagnosis was made by a doctor. Subjects reporting having ever had herpes, candidiasis or warts were asked to specify the location: lip and genitals for herpes, oral cavity and genitals for candidiasis, and hands, feet and head and neck for warts.To ascertain the family history of cancer, subjects were first asked to give the year of birth of their biological mother and father, and of their full brothers or sisters (“brother or sister having the same mother and the same father than you”). Then, they were asked for each of these relatives if she/he had ever had a cancer (“yes, no or don’t know”). If the answer was “yes”, the subjects were asked to specify the age at cancer diagnosis and if possible the type of cancer. No verification of the cancer diagnosis in the relatives was performed.Statistical analysisWe used unconditional logistic regression models to calculate odds ratios (OR) and their 95% confidence intervals (95% CI). All p-values were derived from two-sided statistical tests.All logistic regression models controlled for age (≤ 50, 51–59, 60–69, ≥ 70 years), gender, area of residence, education level (primary or less, vocational secondary, general secondary and university), BMI two years before the interview (categorical, according to the classification of the World Health Organization [30]: < 18.5, 18.5-24.9, 25.0-29.9, ≥ 30 kg/m2). Previous analyses of our data showed that the variables that best characterize the association between tobacco and alcohol consumption and oral cancer risk were smoking status, smoking duration, daily quantity of tobacco smoked and daily quantity of alcohol drinking [31]. To control for smoking, we used smoking status (never, current, former), average daily quantity of tobacco smoked (1–19, 20–39, ≥ 40 grams), and duration of smoking (1–30, 31–40, > 40 years) [32]. Average daily quantity of alcohol drinking in quartiles (never, < 0.6, 0.6-2.0, 2.1-4.5, > 4.5 standard glasses) was included in the models to adjust for alcohol drinking. The quantity of pure alcohol contained in a standard glass (15 cl of wine, 30 cl of beer, 5 cl of spirits, 10 cl of aperitif, and 30 cl of cider) is the same for each type of alcoholic beverage.We analysed the risk of oral cavity cancer related to the personal medical history using two variables: all medical conditions self-reported by the subjects and medical conditions reportedly diagnosed by a doctor. The date of interview was used as the date of reference for both cases and controls. This date was close to the date of diagnosis of the cases since cases were interviewed on average within three months of diagnosis.The family history of cancer was evaluated separately for mothers, fathers, brothers and sisters, and then among all first-degree relatives taken together. We analysed the risk of oral cavity cancer related to the cancer site among relatives: all sites together, head and neck (including oral cavity, pharynx, larynx, nasal cavity and sinuses) and non-head and neck cancers. Because a high number of cancers in family members were reported non-specifically as “cancer of the head and neck”, we chose to group the locations of head and neck cancers to reduce potential inaccurate reporting of cancer subsites. We nevertheless performed some analyses for family history of specific head and neck cancer sites among all first-degree relatives.We also conducted analyses stratified by tobacco and alcohol consumption. We also performed the same analyses using a more restricted definition of the oral cavity excluding base of tongue (C01), lingual tonsils (C02.4), soft palate (C05.1) and uvula (C05.2), since these subsites are often included in the oropharynx. In addition, seven subsites (base of the tongue, mobile tongue, floor of the mouth, gums, soft palate, hard palate, and other parts of the oral cavity) were compared for family history of cancer and personal history of other medical conditions using unconditional polytomous logistic regression.Statistical analyses were conducted using STATA software version 10.0 (StataCorp, Texas, USA).ResultsAmong the 689 cases, the most common tumour location was floor of the mouth (188 cases, 27.3%), followed by mobile tongue (162 cases, 23.5%) and base of the tongue (130 cases, 18.9%). Less frequent tumour locations were: other parts of the oral cavity (81 cases, 11.7%), soft palate (74 cases, 10.7%), gums (37 cases, 5.4%), and hard palate (17 cases, 2.5%). The analysis using the restricted definition of oral cavity involved 485 cases.The main characteristics of cases and controls are presented in Table 1.Table 1 Main characteristics of cases and controlsFull size tableMen represented more than two-thirds of subjects in both cases and controls. Cases were younger (mean age around 57 years) than controls (mean age around 59 years) (p < 0.001).Compared with controls, cases had a lower education level (p < 0.001), a higher consumption of tobacco (p < 0.001) and alcohol (p < 0.001), and a lower BMI two years before the interview (p < 0.001).Personal medical conditionsStatistical analysis showed significant positive associations between the risk of oral cavity cancer (C01-C06) and chronic bronchitis (OR 1.7, 95% CI 1.2-2.4) (Table 2). Histories of tuberculosis and candidiasis overall were associated with an increased risk of oral cavity cancer (ORs 1.6), but the results did not reach statistical significance. Among candidiasis locations, oral candidiasis was associated with an increased risk of oral cavity cancer (OR 5.0, 95% CI 2.1-12.1). Significant inverse relations were observed between the risk of oral cavity cancer and recurrent rhinitis (OR 0.6, 95% CI 0.4-0.9), nasal polyps (OR 0.3, 95% CI 0.1-0.9), and gastro-oesophageal reflux (OR 0.5, 95% CI 0.4-0.7). Herpetic lesions were not related to the risk of oral cavity cancer, regardless of the location of the herpes. The risks associated with a history of skin warts were reduced, but the results did not reach statistical significanceTable 2 Risks of oral cavity cancer associated with personal medical conditionsFull size tableBecause high prevalence of oropharyngeal candidiasis has been described in subjects with head and neck cancer undergoing radio/chemotherapy [33, 34], we also conducted analysis after excluding subjects declaring candidiasis at the time of interview or at the time of diagnosis of another cancer; the association between oral cavity cancer risk and oral candidiasis remained practically unchanged (OR 6.0, 95% CI 2.2-16.4). Oral candidiasis may also constitute an early manifestation of the cancerous disease. When we excluded all subjects reporting a history of oral candidiasis near the current cancer (up to two years before the cancer diagnosis), the association between oral cavity cancer and oral candidiasis remained significant (OR 3.7, CI 95% 1.3-10.1).We calculated the ORs for oral candidiasis in strata of tobacco and alcohol consumption. The OR was slightly higher in ever smokers (OR 5.6, 95% CI 2.0-15.2) than in never smokers (OR 4.3, 95% CI 0.5-41.7), but the interaction between tobacco smoking and oral candidiasis was not significant (p-value for interaction = 0.14). Oral candidiasis was associated with an elevated risk of oral cavity cancer in drinkers of more than 2 glasses/day (OR 3.9, 95% CI 1.0-14.8) but not in drinkers of 2 glasses/day or less (OR 1.1, 95% CI 0.2-23.8), although the ORs were not statistically different (p-value for interaction = 0.50).When the analysis was restricted to medical conditions that the subjects reported as diagnosed by a doctor, similar results were observed, except for the association between bronchitis and oral cavity cancer which became weaker and non-significant (OR 1.2, 95% CI 0.9-1.6) (data not shown).Family history of cancerThe associations between family history of cancer and risk of oral cavity cancer are presented in Table 3.Table 3 Risks of oral cavity cancer associated with family history of cancer among first-degree relativesFull size tableHistory of cancer in general, and of head and neck cancer in particular, among fathers, were associated with a slightly elevated risk of oral cavity cancer, but the results were not statistically significant (OR 1.3, 95% CI 0.9-1.6, and 1.5, 95% CI 0.9-2.4, respectively).History of head and neck cancer among mothers was significantly associated with an elevated risk of oral cavity cancer (OR 5.2, 95% CI 1.2-23.9). This OR was higher than that observed for fathers. When cancer history among siblings was analysed, after adjustment for the number of sisters and brothers, we observed a significant association between the risk of oral cavity cancer and history of cancer of any type (OR 1.4, 95% CI 1.1-1.9). History of head and neck cancer among siblings was associated with an increased risk of oral cavity cancer (OR 2.3, 95% CI 1.2-4.2). Analysis by type of sibling showed a significantly increased risk only among subjects having brothers with a history of head and neck cancer (OR 2.6, 95% CI 1.2-5.8); history of head and neck cancer among sisters was not significantly associated with an increased risk of oral cavity cancer (OR 1.7, 95% CI 0.6-4.2).When we analysed the relationship between cancer history among all first-degree relatives and oral cavity cancer risk, we observed significant association for history of head and neck cancer (OR 1.9, 95% CI 1.2-2.8). A family history of any type of cancer slightly increased the risk of oral cavity cancer, but the results were not statistically significant (OR 1.2, 95% CI 0.9-1.5). The risk associated with first-degree relatives’ history of cancer (any type and head and neck) increased with the number of affected relatives.Analysis by type of head and neck cancer in first-degree relatives showed significantly increased risks of oral cavity cancer in subjects with family history of oral cavity cancer (OR 3.5, 95% CI 1.1-11.2) and of “head and neck cancer” (not specified) (OR 1.8, 95% CI 1.1-2.9). A family history of pharyngeal, laryngeal, and sinonasal cancer was associated with non-significantly elevated risks of oral cavity cancer (OR 4.6, 95% CI 0.5-44.8 for history of pharyngeal cancer; 1.6, 95% CI 0.6-4.4 for history of laryngeal cancer; and 1.7, 95% CI 0.3-8.8 for history of sinonasal cancer). However, few subjects reported a specific location of head and neck cancer in first degree relatives (26 oral cavity, 5 pharynx, 35 larynx, and 11 nasal cavity/sinuses cancer).Analysis stratified by gender of first-degree relatives showed that history of head and neck cancer among female relatives (mothers and sisters) was not significantly associated with the risk of oral cavity cancer (OR 2.3, 95% CI 0.9-5.4), although the result was borderline significant. Conversely, history of head and neck cancer in male relatives (fathers and brothers) was significantly associated with the risk of oral cavity cancer (OR 1.9, 95% CI 1.2-3.3). However, these ORs did not differ significantly (p-value of test of comparison of ORs = 0.91).We found a stronger association between the risk of oral cavity cancer and family history of head and neck cancer in subjects aged 45 or more (OR 2.3, 95% CI 1.5-3.4) compared to subjects aged less than 45 (OR 1.3, 95% CI 0.3-6.7), although the ORs were not statistically different (p-value for interaction = 0.46).Analysis by cancer site among first-degree relatives (Table 4) showed elevated ORs among subjects having a family history of lung, oesophagus, cervix and corpus uteri, brain and nervous system cancer, but the results were not statistically significant (OR 1.4, 95% CI 0.9-1.9; 1.5, 95% CI 0.7-3.3; 1.7, 95% CI 0.9-3.1; 2.0, 95% CI 0.9-4.8 respectively).Table 4 Odds ratios for oral cavity cancer risk related to family history of selected cancers in first-degree relativesFull size tableWhen we stratified by tobacco smoking and/or alcohol drinking (Table 5), significantly increased risks of oral cavity cancer related to family history of any type of cancer were observed only in smokers and/or moderate to heavy drinkers. Significantly elevated risks of oral cavity cancer associated with family history of head and neck cancer were seen for both never and ever smokers and for light and moderate to heavy drinkers. However, the increase in risk was small and not significant for never smokers who were also light drinkers.Table 5 Risks of oral cavity cancer related to family history of cancer in first-degree relatives stratified by tobacco smoking and alcohol drinkingFull size tableAnalyses restricted to intraoral cavityWhen the analyses were limited to intraoral cavity (C02.0-C02.3, C02.8, C02.9, C03, C04, C05.0, C05.8, C05.9, C06), the results were similar to that observed for oral cavity globally (C01-C06). Thus, family history of UADT cancer among first-degree relatives was associated with an OR of 1.7 (95% CI 1.1-2.7), personal history of oral candidiasis with an OR of 4.9 (95% CI 1.8-13.3), gastro-oesophageal reflux with an OR of 0.6 (95% CI 0.4-0.8), recurrent rhinitis with an OR of 0.6 (95% CI 0.4-0.9), and nasal polyps with an OR of 0.3 (95% CI 0.1-0.9).Analyses by subsiteWe assessed the risk of oral cavity cancer by anatomical site of the oral cavity (base of tongue, mobile tongue, gum, floor of mouth, hard and soft palate, and other parts of oral cavity) for personal medical conditions and for family history of cancer using a polytomous regression. We did not find any difference between subsites for any variable of interest (tests of comparison of odds ratios non-significant) (data not shown).DiscussionTo our knowledge, the ICARE study is the first population-based case–control study in France and one of the largest in the world which investigates the role of risk factors other than tobacco and alcohol consumption in the occurrence of oral cavity cancer. Strengths of this study include large sample size allowing us to perform analyses by subsite, and detailed data about family history of cancer and personal medical history.The ICARE study was conducted in collaboration with the cancer registries, allowing us to recruit cancer cases in all healthcare establishments in the selected areas. The control group was population-based and common for both pathologies (lung and UADT cancers), which explains the significantly different distribution of age and area of residence between oral cavity cancer cases and controls. However, the large number of subjects in each category allowed for satisfactory adjustment for these variables.The results of the epidemiological studies are contrasted concerning the role of candidiasis in the occurrence of oral cavity cancer, Thus, history of oral candidiasis was associated with an increased risk of oral cavity and oropharyngeal cancer in one study [11], with a reduced risk of oral cavity cancer in another study [7], whereas other authors found no association [6]. Our results have shown that personal history of oral candidiasis was associated with an elevated risk of oral cavity cancer. The increase in cancer risk with oral candidiasis may be explained by the production of endogenous nitrosamines by Candida albicans[35]. These nitrosamines act on the normal epithelium leading to oral dysplasia and further development of oral carcinoma. Nevertheless, some authors suggested that Candida albicans have only an indirect role and that the possibility of their involvement exist in conjunction with other etiological factors such as tobacco smoking [36]. In our study, the risk of oral cavity cancer associated with history of candidiasis was slightly higher in smokers than in never smokers, but the ORs were not significantly different. Other studies showed that Candida albicans may metabolize ethanol into its carcinogenic metabolite, acetaldehyde and, accordingly, candidiasis may be associated with elevated acetaldehyde levels in the oral cavity [37, 38]. Consistent with this mechanism, we found a significantly elevated risk of oral cavity cancer associated with history of candidiasis in moderate to heavy drinkers but not in light drinkers. However, the interaction of oral candidiasis with alcohol drinking was not statistically significant. Also, chronic infections, specifically chronic hyperplastic candidiasis, may trigger cell proliferation, inhibit apoptosis, interfere with cellular signalling mechanisms and up-regulate tumour promoters [39, 40]. In our study only 14 cases and 80 controls reported prior candidiasis and the results should be confirmed by other studies, especially with medical conditions validated by a doctor.In agreement with previous studies [7, 8, 11], we did not find a significant association between the risk of oral cavity cancer and history of herpetic infection. Conversely, only one case–control study [10] found an increased risk of oral cavity and oropharynx cancer associated with this infection and two case–control studies [6, 9] found a decreased risk.Cutaneous warts are caused by different types of HPV, notably 2, 4, 7 and 57, whereas genital warts are caused mostly by HPV types 6 and 11 [41]. Three studies [6, 8, 11], like ours, did not find any association between history of warts (any location) and the risk of oral cavity cancer, whereas one study found a reduced risk of UADT cancer associated with feet, genital and head and neck warts [7].We found an inverse association between the oral cavity cancer risk and history of rhinitis and nasal polyps. These pathologies often have an allergic origin, and several studies found a decreased risk of head and neck cancer associated with a history of allergies [42–45]. The inverse association between allergies and cancer may be explained by an overactive immune function in allergic subjects that effectively detects and eradicates malignant cells, toxins or pathogens from the body [46, 47]. However, we did not find any association with the history of asthma, another allergies-related condition.We found also an inverse association between oral cavity cancer risk and history of gastro-oesophageal reflux but we cannot point to any specific mechanism. The possibility that this result is due to the chance may not be ruled out. Unlike our results, a recent case–control study [7] did not find any association between oral cavity cancer risk and gastro-oesophageal reflux.After controlling for main confounding factors, we observed a higher risk of oral cavity cancer among subjects having first-degree relatives with head and neck cancer history, compared to subjects without such a family history. The risk increased with the number of affected relatives. On the other hand we did not find a significant relationship between the risk of oral cavity cancer and family history of non-head and neck cancers. Several studies [20, 22, 23, 26] reported similar results.Early age of onset may be a feature of hereditary forms of cancer. Higher family risks for many cancers were found when the cancer subjects were diagnosed at an early age [48, 49]. Concerning the association between the risk of oral cancer and family history of head and neck cancer, no clear pattern emerges from epidemiological studies: some of them found a stronger association in younger subjects compared to older subjects [20, 21, 23], others found a contrary result [22, 26], but the differences in risk with age of onset were never significant. Similarly, in our study the interaction of family history of head and neck cancer with age was not significant, although the OR was somewhat higher in older subjects.Familial clustering of cancer cases could be explained by genetic polymorphism in genes involved in the metabolism of tobacco and alcohol carcinogens and DNA repair [12–19], but may also reflect a tendency of relatives to have similar behaviour concerning alcohol and tobacco.In our study, associations between oral cavity cancer risk and family history of cancer were observed among smokers and/or drinkers of >2 glasses/day only. Conversely, an increased risk of oral cavity cancer associated with a family history of head and neck cancer was also observed in non-smokers and light drinkers, but the risk increased with the exposure. Our results are similar to those of other studies on oral/pharyngeal or head and neck cancer [20, 23, 26].The differential ability of subjects to metabolize carcinogens when exposure to tobacco and/or alcohol occurs may explain the higher risk of oral cavity cancer observed in our study among smokers and drinkers having a family history of UADT cancer. Nevertheless, we did not observe an increased risk of oral cavity cancer in subjects having a family history of other cancers related to smoking and/or alcohol drinking (e.g. lung, oesophagus, liver, pancreas), suggesting that other genetic factors might explain these findings.When the analyses were limited to intraoral cavity (C02.0-C02.3, C02.8, C02.9, C03, C04, C05.0, C05.8, C05.9, C06), excluding the sites usually attached to oropharynx (C01, C02.4, C05.1, C05.2), the results were similar to that observed for oral cavity C01-C06. We did not find any difference between subsites base of the tongue, mobile tongue, gums, floor of the mouth, soft palate, hard palate, and other parts of the mouth for any variable of interest.Some limitations of our study can be discussed. The subjects self-reported their own medical history and family history of cancer. Thereby, recall bias could not be ruled out and it is possible that the cases had a higher motivation to recall their personal and family medical history than the controls. Nevertheless, two studies have shown that subjects in case–control studies are able to report accurately family history of common types of cancer among first-degree relatives, with little observable recall bias [50, 51]. In addition, family history of cancer sites other than head and neck was not associated with an increased risk of oral cavity cancer in this study, suggesting that no major recall bias concerning cancer in general has affected our results.With regards to oral candidiasis, a possible explanation would be that cases with oral cancer are more prone to recall previous oral lesions than controls. However, no association was found with labial herpes, another oral condition, suggesting that differential recall between cases and controls is unlikely to explain our results. Moreover, when we limited the medical conditions to those reportedly diagnosed by a doctor, the results were similar. Medical treatments were also collected and those reported for candidiasis were consistent with this pathology. So, we think that misclassification of candidiasis is unlikely to explain our results.Information about other known risk factors for oral cavity cancer such as diet, human papilloma virus (HPV) or dental health was not collected, and residual confounding cannot be excluded. Nevertheless, no association between diet, HPV infection or dental health and family history of cancer has ever been shown in the literature. Also, the possibility of residual confounding for the main risk factors may not be ruled out.We have no way to assess whether cases included in our study differed according to past medical conditions and family history of cancer from cases that could not be included. Nevertheless, the distribution of included cases by age, gender and cancer subsite was very similar to that of all oral cancer cases diagnosed in France [52], suggesting that no major selection bias occurred. We excluded from analysis all subjects with shortened questionnaires because information on medical conditions and family history of cancer was not available. However, these subjects were comparable in age, gender, and tobacco and alcohol consumption to subjects with complete questionnaires.ConclusionThis study showed that family history of head and neck cancer is related to an increased risk of oral cavity cancer, and suggested an association with personal history of oral candidiasis. From a public health point of view, these factors should be taken into account to target prevention efforts and screening.References1.World Health Organization: International Classification of Diseases 10th Revision. 2007, Geneva: World Health OrganizationGoogle Scholar2.Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM: Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. 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J Natl Cancer Inst. 1994, 86: 1600-1608. 10.1093/jnci/86.21.1600.CASArticlePubMedGoogle Scholar50.Kerber RA, Slattery ML: Comparison of self-reported and database-linked family history of cancer data in a case–control study. Am J Epidemiol. 1997, 146: 244-248. 10.1093/oxfordjournals.aje.a009259.CASArticlePubMedGoogle Scholar51.Love RR, Evans AM, Josten DM: The accuracy of patient reports of a family history of cancer. J Chronic Dis. 1985, 38: 289-293. 10.1016/0021-9681(85)90074-8.CASArticlePubMedGoogle Scholar52.Ligier K, Belot A, Launoy G, Velten M, Bossard N, Iwaz J, Righini CA, Delafosse P, Guizard AV: Descriptive epidemiology of upper aerodigestive tract cancers in France: incidence over 1980–2005 and projection to 2010. Oral Oncol. 2011, 47: 302-307. 10.1016/j.oraloncology.2011.02.013.ArticlePubMedGoogle ScholarPre-publication historyThe pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2407/13/560/prepubDownload referencesAcknowledgementsICARE study was supported by the French National Research Agency (ANR), the French Agency for Food, Environmental and Occupational Health and Safety (ANSES), the French Institute for Public Health Surveillance (InVS), the Foundation for Medical Research (FRM), the Foundation of France, the Agency for Research on Cancer (ARC), the French Ministry of Work, Solidarity and Public Function (Direction Générale du Travail), and the Ministry of Health (Direction Générale de la Santé). L. Radoï was supported by the French National Cancer Institute (InCA), grant n° 2009–349 for this work.Author informationAffiliationsCentre for Research in Epidemiology and Population Health (CESP), Inserm U1018, Epidemiology of Occupational and Social Determinants of Health Team, F-94807, Villejuif, FranceLoredana Radoï, Sophie Paget-Bailly, Diane Cyr, Gwenn Menvielle, Annie Schmaus, Matthieu Carton & Danièle LuceUniversity Versailles St-Quentin, F-78035, Versailles, FranceLoredana Radoï, Sophie Paget-Bailly, Diane Cyr, Gwenn Menvielle, Annie Schmaus, Matthieu Carton & Danièle LuceCentre for research in Epidemiology and Population Health (CESP), Inserm U1018, Environmental Epidemiology of Cancer Team, F-94807, Villejuif, FranceFlorence Guida, Sylvie Cénée, Marie Sanchez & Isabelle StückerUniversity Paris-Sud, UMRS 1018, F-94807, Villejuif, FranceFlorence Guida, Sylvie Cénée, Marie Sanchez & Isabelle StückerCalvados Cancer Registry, F-1400, Caen, FranceAnne-Valérie GuizardHérault Cancer Registry, F-34298, Montpellier, FranceBrigitte TrétarreInserm U1085, Irset, Faculté de Médecine, Campus de Fouillole, BP 145, 97154, Pointe-à-Pitre, Guadeloupe French West IndiesDanièle LuceCorresponding authorCorrespondence to Danièle Luce.Additional informationCompeting interestThe authors declare that they have no conflict of interest.Authors’ contributionsDL and LR conceived and designed the current study and drafted the manuscript; LR and DC analyzed the data; DL and IS are the principal investigators of ICARE, conceived the study, designed the questionnaire, and coordinated the original collection of the data. AS, DC, SC, MS, AVG and BT contributed to data collection and quality control; SPB, FG, GM, MC contributed to the statistical analysis. All authors participated to data interpretation and critical revision of the manuscript. All authors read and approved the final manuscript.Rights and permissionsReprints and PermissionsAbout this articleCite this articleRadoï, L., Paget-Bailly, S., Guida, F. et al. Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE study. BMC Cancer 13, 560 (2013). Family history of cancer, personal history of medical conditions and risk of oral cavity cancer in France: the ICARE studyDownload citationReceived18 January 2013Accepted03 November 2013Published28 November 2013http://DOIhttps://doi.org/10.1186/1471-2407-13-560Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkKeywordsFamily historyMedical conditionsOral cavity cancerRisk factorsCase–control studyDownload PDFBMC CancerISSN: 1471-2407Contact usSubmission enquiries: Access here and click Contact UsGeneral enquiries: [email protected] more on our blogsReceive BMC newslettersManage article alertsLanguage editing for authorsScientific editing for authorsPoliciesAccessibilityPress centerSupport and ContactLeave feedbackCareersFollow BMCBMC Twitter pageBMC Facebook pageBMC Weibo pageBy using this website, you agree to our Terms and Conditions, Privacy statement and Cookies policy. 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This answer may contain sensitive images. Click on an image to unblur it.Three points on confirmed death figures to keep in mind:All three points are true for all currently available international data sources on COVID-19 deaths.the actual total death toll from COVID-19 is likely to be higher than the number of confirmed deaths – this is due to limited testing and problems in the attribution of the cause of death; the difference between reported confirmed deaths and total deaths varies by countryhow COVID-19 deaths are recorded may differ between countries (e.g. some countries may only count hospital deaths, whilst others have started to include deaths in homes)the reported death figures on a given date does not necessarily show the number of new deaths on that day: this is due to delays in reporting.→ We provide more detail on these three points in the section ‘Deaths from COVID-19: background‘.Two tips on how you can interact with this chartAdd any other country to this chart: click on the Add country button to compare with any other country.View this data on a world map: switch to a global map of confirmed deaths using the ‘MAP’ tab at the bottom of the chart.Total confirmed deaths: how rapidly have they increased compared to other countries?Data explorerHow do rates compare when we adjust for population?Explore for yourself in our Coronavirus Data ExplorerCharts which simply show the change in confirmed deaths over time are not very useful to answer the question of how the speed of the outbreak compares between different countries. This is because the outbreak of COVID-19 did not begin at the same time in all countries.This chart here is designed to allow such comparisons.The trajectory for each country begins on the day when that country had 5 confirmed deaths.This allows you to compare how rapidly the number of confirmed deaths increased after the outbreak reached a similar stage in each country.The grey lines in the background help you to see how rapidly the number of confirmed deaths is increasingThese lines show the trajectories for doubling times of 1, 2, 3, 5, and 10 days. If the slope that a country is on is steeper than a particular grey line, then the doubling time of confirmed cases in that country is faster than that. For example, there are several countries for which the slope was steeper than the ‘…every 2 days’ line – this means their death count doubled faster than every two daysHow you can interact with this chartClicking on any country in the chart highlights that country. If you click on several countries you can create a view in which you can compare several countries.Any country you might not see immediately you can find via the ‘Select Countries’ in the bottom left. Just type the name in the search box there.To focus on the countries you highlighted click on ‘Zoom to selection’.What is the daily number of confirmed deaths?Related charts:Data explorerHow do deaths compare when we adjust for population? What if we look at the 3, or 7-day average?Explore for yourself in our Coronavirus Data ExplorerDaily covid deaths regionWhich world regions have the most daily confirmed deaths?Daily confirmed deaths by regionThe previous charts looked at the increase of total confirmed deaths – this chart shows the number of confirmed deaths per day.Why is it helpful to also look at the three-day rolling average of daily confirmed deaths?For all global data sources on the pandemic, daily data does not necessarily refer to deaths on that day – but to the deaths reported on that day.Since reporting can vary very significantly from day to day – irrespectively of any actual variation of deaths – it is helpful to view the three-day rolling average of the daily figures. Below the chart you find the link to the rolling three-day average view.→ We provide more detail in the section ‘Reported new cases on a particular day do not necessarily represent new cases on that day‘.Another tip on how you can interact with this chartBy pulling the ends of the blue time slider you can focus the chart on a particular period. If you bring them together to one point in time then the line chart becomes a bar chart – this of course only makes sense if you compare countries (that is what the Add country button is for).Daily confirmed deaths: are we bending the curve?Related chart:Data explorerHow do rates compare when we adjust for population? What if we look at the 3, or 7-day average?Explore for yourself in our Coronavirus Data ExplorerThis trajectory chart shows whether countries make progress on bringing down the curve of new deaths.To allow comparisons between countries the trajectory for each country begins on the day when that country first reported 5 daily deaths.By default this chart is shown on a logarithmic vertical axis. We explain why in the next section. If you are not familiar with logarithmic axes we recommend you also look at this chart on a linear axis. The visual representation on these different axes can look very different.This chart is shown on log axis, but you can switch to a linear axisThe default view on a logarithmic y-axis is helpful to compare the growth rates between countries: on a logarithmic axis the steepness of the line corresponds to the growth rate. [Here is an explanation for how to read logarithmic axes.]But in this chart – as in many of our charts – you can switch to a linear axis – just click on ‘LOG’.Daily confirmed deaths: when did countries bend the curve?Confirmed covid 19 deaths total vs daily v241 850x600Click to open interactive versionRelated chart:Covid deaths daily vs total per millionHow does this comparison look when when we adjust for population?Daily vs. Total confirmed COVID-19 deaths per capitaThis chart shows the number of daily confirmed deaths (on the y-axis) plotted against the total number of confirmed deaths (on the x-axis).Plotting the data in this way allows us to see when different countries bent the curve.How you can interact with this chartClicking on any country in the chart highlights that country. If you click on several countries you can create a view in which you can compare several countries.Any country you might not see immediately you can find via the ‘Select Countries’ in the bottom left. Just type the name in the search box there.Weekly and biweekly deaths: where are confirmed deaths increasing or falling?Why is it useful to look at weekly or biweekly changes in deaths?For all global data sources on the pandemic, daily data does not necessarily refer to deaths on that day – but to the deaths reported on that day.Since reporting can vary very significantly from day to day – irrespectively of any actual variation of deaths – it is helpful to look at changes from week to week. This provides a slightly clearer picture of where the pandemic is accelerating, slowing, or in fact reducing.The maps shown here provide figures on weekly and biweekly deaths: one shows the number of deaths in the previous seven or fourteen days (the weekly or biweekly total); the other shows the growth rate over this period.Three tips on how to interact with these mapsBy clicking on any country on the map you see the change over time in this country.By moving the time slider (below the map) you can see how the global situation has changed over time.You can focus on a particular world region using the dropdown menu to the top-right of the map.Weekly covid deaths v157 850x600Click to open interactive versionBiweekly covid deaths v133 850x600Click to open interactive versionWeekly growth covid deaths v167 850x600Click to open interactive versionBiweekly change covid deaths v131 850x600Click to open interactive versionGlobal comparison: where are confirmed deaths increasing most rapidly?Location How long did it take for the number of total confirmed deaths to double?Belize doubled in4 daysBahamas doubled in5 daysAruba doubled in7 daysParaguay doubled in11 daysUganda doubled in11 daysNamibia doubled in12 daysGambia doubled in12 daysRwanda doubled in14 daysVietnam doubled in15 daysNepal doubled in15 daysSuriname doubled in15 daysMorocco doubled in18 daysShow moreCountries with less than 5 confirmed deaths are not shown. Deaths from the Diamond Princess cruise ship are also not shown since these numbers are no longer changing over time.Data source: ECDC. Download the full dataset.Simply looking at the total or daily number of confirmed deaths does not allow us to understand or compare the speed at which the toll is rising.The table here shows how long it has taken for the number of deaths to double in each country for which we have data. The table also shows how the total number of confirmed deaths, and the number of daily new confirmed deaths, and how those numbers have changed over the last 14 days.A tip on how to interact with this tableYou can sort the table by any of the columns by clicking on the column header.World maps: Confirmed deaths relative to the size of the populationWhy adjust for the size of the population?It can be insightful to know not just how many have died compared to how many people actually live in that country.For instance, if 1,000 people died in Iceland, out of a population of about 340,000, that would have a far bigger impact than the same number dying in the USA, with its population of 331 million.1 The death count in more populous countries tends to be higher – here you can see this correlation.This is why the two maps below show the deaths per million people of each country’s population.Three tips on how to interact with these mapsBy clicking on any country on the map you see the change over time in this country.By moving the time slider (below the map) you can see how the global situation has changed over time.You can focus on a particular world region using the dropdown menu to the top-right of the map.Total covid deaths per million v264 850x600Click to open interactive versionNew covid deaths per million v256 850x600Click to open interactive versionDeaths and cases: our data sourceOur World in Data relies on data from the European CDCIn this document and the many embedded and linked charts we report and visualize the data from the European Center for Disease Prevention and Control (ECDC).2 We make the data used in our charts and tables downloadable as a complete and structured .csv file here.The European CDC publishes daily statistics on the COVID-19 pandemic. Not just for Europe, but for the entire world. We rely on the ECDC as they collect and harmonize data from around the world which allows us to compare what is happening in different countries. The European CDC data provides a global perspective on the evolving pandemic.The European Centre for Disease Prevention and Control ECDC provides three statistical resources on the COVID-19 pandemic:COVID-19 DashboardSituation reportsThe daily data tablesThe ECDC makes all their data available in a daily updated clean downloadable file. This gets updated daily reflecting data collected up to 6:00 and 10:00 CET.The European CDC collects and aggregates data from countries around the world. The most up-to-date data for any particular country is therefore typically available earlier via the national health agencies than via the ECDC. This lag between nationally available data and the ECDC data is not very long as the ECDC publishes new data daily. But it can be several hours.Deaths from COVID-19: backgroundWhat is counted as a death from COVID-19?The attribution of deaths to specific causes can be challenging under any circumstances. Health problems are often connected, and multiplicative, meaning an underlying condition can often lead to complications which ultimately result in death.This is also true in the case of COVID-19: the disease can lead to other health problems such as pneumonia and acute respiratory distress syndrome (ARDS).So, how are deaths from COVID-19 recorded? What is and isn’t included in these totals?As is standard in death reporting, countries are asked to follow the ‘cause of death’ classifications from the WHO’s International Classification of Diseases guidelines.3 However, countries also typically provide their own guidance to practitioners on how and when COVID-19 deaths should be recorded.Let’s take a look at two concrete examples of national guidance: the United States and the UK. Both provide very similar guidelines for medical practitioners on the completion of death certificates. The US CDC’s Vital Statistics Reporting Guidance can be found here; the UK Government guidance is found here.4Both guidelines state that if the practitioner suspects that COVID-19 played a role in an individual’s death it should be specified on the death certificate. In some cases, COVID-19 may be the underlying cause of death, having led to complications such as pneumonia or ARDS. Even when it’s the underlying and not the direct cause, COVID-19 should be listed.5Although confirmed cases are reliant on a positive laboratory confirmation of the COVID-19 test, a laboratory diagnosis may not be required for it to be listed as the cause of death. In the UK guidelines, for example, it makes clear that practitioners should complete death certificates to the best of their knowledge, stating that “if before death the patient had symptoms typical of COVID19 infection, but the test result has not been received, it would be satisfactory to give ‘COVID-19’ as the cause of death, and then share the test result when it becomes available. In the circumstances of there being no swab, it is satisfactory to apply clinical judgement.”This means a positive COVID-19 test result is not required for a death to be registered as COVID-19. In some circumstances, depending on national guidelines, medical practitioners can record COVID-19 deaths if they think the signs and symptoms point towards this as the underlying cause.The US CDC guidelines also make this clear with an example: the death of an 86-year-old female with an unconfirmed case of COVID–19. It was reported that the woman had typical COVID-19 symptoms five days prior to suffering an ischemic stroke at home.Despite not being tested for COVID-19, the coroner determined that the likely underlying cause of death was COVID–19 given her symptoms and exposure to an infected individual.Why are there delays in death reports?Just as with confirmed cases, the number of deaths reported on a given day does not necessarily reflect the actual number of COVID-19 deaths on that day, or in the previous 24 hours. This is due to lags and delays in reporting.Delays can occur for several reasons:after a death certificate has been completed, inspection by post-mortem or laboratory testing may be required to verify the cause of death;death certificates are then either automatically or manually coded: it is often the case that COVID-19 deaths are always manually coded (this is the case in the USA);there can be significant delays in this coding process, particularly when there is a large increase in the number of deaths (this can be as long as 7 days in the US);these figures are then collected in national registration statistics and reported to international sources.This delay in reporting can be of the order of days – and sometimes as long as a week. This means the number of deaths reported on a given day are not reflective of the actual number of deaths which occurred on that day.Total death figures are likely to be higher than confirmed deathsWhat we know is the total number of confirmed deaths due to COVID-19 to date. Limited testing and challenges in the attribution of the cause of death means that the number of confirmed deaths may not be an accurate count of the true total number of deaths from COVID-19.The European Center for Disease Prevention and Control (ECDC) – our data source on deaths – publishes daily updates of confirmed deaths due to COVID-19.In an ongoing outbreak the final outcomes – death or recovery – for all cases is not yet known. The time from symptom onset to death ranges from 2 to 8 weeks for COVID-19.6 This means that some people who are currently infected with COVID-19 will die at a later date. This needs to be kept in mind when comparing the current number of deaths with the current number of cases.What does the data on deaths and cases tell us about the mortality risk of COVID-19?To understand the risks and respond appropriately we would also want to know the mortality risk of COVID-19 – the likelihood that someone who catches the disease will die from it.We will look into this question in more detail further below in this article and explain that this requires us to know – or estimate – the number of total cases and the final number of deaths for a given infected population. Because these are not known, we discuss what the current data can and can not tell us about the risk of death.AcknowledgementsWe would like to acknowledge and thank a number of people in the development of this work: Carl Bergstrom, Bernadeta Dadonaite, Natalie Dean, Jason Hendry, Adam Kucharski, Moritz Kraemer and Eric Topol for their very helpful and detailed comments and suggestions on earlier versions of this work. Tom Chivers we would like to thank for his editorial review and feedback.And we would like to thank the many hundreds of readers who give us feedback on this work every day. Your feedback is what allows us to continuously clarify and improve it. We very much appreciate you taking the time to write. We cannot respond to every message we receive, but we do read all feedback and aim to take the many helpful ideas into account. Thank you all.CitationReuse our work freelyYou can use all of what you find here for your own research or writing. We license all charts under Creative Commons BY.All of our charts can be embedded in any site.CitationOur articles and data visualizations rely on work from many different people and organizations. When citing this entry, please also cite the underlying data sources. This entry can be cited as:Max Roser, Hannah Ritchie, Esteban Ortiz-Ospina and Joe Hasell (2020) - "Coronavirus Pandemic (COVID-19)". Published online at Our World in Data. Retrieved from: 'Coronavirus Pandemic (COVID-19) - Statistics and Research' [Online Resource]BibTeX citation@article{owidcoronavirus,author = {Max Roser, Hannah Ritchie, Esteban Ortiz-Ospina and Joe Hasell},title = {Coronavirus Pandemic (COVID-19)},journal = {Our World in Data},year = {2020},note = {Coronavirus Pandemic (COVID-19) - Statistics and Research}}EndnotesHere is for our visualization for the population of Iceland and the US. Any other country can be added to this chart.Established in 2005 and based in Stockholm it is an EU agency with the aim to strengthen Europe’s defense against infectious diseases.World Health Organization. International statistical classification of diseases and related health problems, 10th revision (ICD–10), Volume 2. 5th ed. Geneva, Switzerland. 2016.National Center for Health Statistics. Guidance for certifying deaths due to COVID–19. Hyattsville, MD. 2020.The WHO, in its ICD documentation defines the underlying cause of death as “a) the disease or injury which initiated the train of morbid events leading directly to death, or b) the circumstances of the accident or violence which produced the fatal injury”.World Health Organization (2020). Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19). Available online at: https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.p

Well, at least it makes one a stupid liar.But yes, it’s a ruse to hide trans phobia.Ignorant is when we don’t know any better.Stupid is when we do.- - - - - — - - -In response to others:Prior post:“… we should be in an era where a woman can look like Tiffany Moore and Jessica Yaniv. take their word at their womanhood …”Regardless of someone’s presentation or self-identification, it’s illegal to assault or batter or rape someone, it is not okay to assault or batter or rape someone so long as you claim a certain identity or make a certain presentation.- - - - - - - - - -Prior post:“… No, just common sense and the fact that this question is being asked shows that there's some awakening …”Nope, 20+ years of prohibitions against discrimination in access to public toilets have recorded ZERO assaults under the guise of supposed permission for men to enter women’s spaces.- - - - - - - - - -Prior post:“… hmmm…you think a man would never pretend to be a woman (isn’t this what “trans” means?) for the chance to sexually access women? Check this out: [ The Guardian ] Transgender prisoner who sexually assaulted inmates jailed for life …”Keep researching.There are other reports, and only by multiple similar reports from different sources do we get a glimpse of the possible truth here - The Guardian, BBC, Independent, The Telegraph, Mirror, Daily Mail, The Times, Sky, Metro, The Economist, and so on.We do not see a man pretending to be trans* sex/gender woman in order to gain access to women.We see a legal system and prison system act capriciously, releasing a known predator.And we see unreliable incendiary inaccurate reporting ( specifically misdating rape ).There are many reports, nicely summed up by Snopes Did a Male Rapist Who Identifies as Female Transfer to a Women's Jail and Assault Female Inmates?, with references.The most important thing isthe person is a predator.The least important thing iswhether or not they are male in disguiseor trans* sex/gender female.- - - - -That you think:“… man … pretend to be a woman (isn’t this what “trans” means?) …”… says that you do not understand or respect what it is to be trans* sex/gender.So the opening question:“… Is it trans-phobic to believe some men will lie about being women to get into women's spaces? …”… is lost on you, directly.But indirectly, your answer reveals, that:“… Yes, it is trans-phobic to believe some men will lie about being women to get into women's spaces …”- - - - -The background, the general frame of the question is discussions of laws prohibiting trans* sex/gender people from using the publicly accessible toilets, changing rooms, lockers of their self-identified sex/gender.The alignment of your find with the question is that this perpetrator may have used female guise to gain the trust of women, and attacked them.The misalignment of your find, regarding the general framing of anti-discrimination laws, is that:this person’s rapes are reported to have been when using males names, and not in a place where they would have been physically prohibited being by any law regardless of their other-identified or self-identified sex/gender,reported and confessed assaults, not rapes, happened when using female self-identification AND being improperly housed by a faulty legal and prison system, decisions that were reversed when presented with more-complete information.- - - - -The opening question really deals with three separate arenas:Would some men lie about being women in order to get into women’s places?In what places would women be at risk?Is it trans-phobic to believe #1.In practice, in the US, in places with more than 20+ years experience with ordinances that prohibit discrimination against trans* sex/gender people’s legally equal access to publicly accessible sex/gender segregated facilities, there has been no report of assaults, battery, rape by trans* sex/gender women or by males pretending to be women.And, you found a convicted criminal who assaulted, battered, raped, is probably trans* sex/gender, definitely has no appropriate social and medical support throughout their life, and was improperly handled by a recalcitrant legal and prison system.So I answer the opening question’s 3 arenas with:Yes there are probably some people who have lied in order to gain access to women’s places ( the sex/gender of the person submitted is unresolved ).Women are at risk regardless because the places where the reported assault, battery, and rape were perpetrated are either not public, or were mishandled by the authorities.Yes, it is trans phobic to assign the behavior of assault, battery, and rape to being trans* sex/gender.My general understanding is that bad cases make bad law, that is, trying to pre-punish innocent people for the misbehavior of unrelated other people is bad law.Thanks for exploring this.- - - - - - - - - -Prior post:“… You are also correct in saying I “do not respect trans”, because I certainly do not. The idea that a fundamental component of a person’s nature can be decided subjectively is not only plainly wrong, but is conceptually deadly …”“… decided …”?!?We all self-identify ( not “decide” ) our own sex/gender,usually around age 3,presumably when we become self-aware of the sex/gender of our own biological brain,you do,I do,cis* sex/gender people do,trans* sex/gender people do,we all do,legally equally,it’s a legally-equal-recognition-support-and-protection thing where all of us are legally equal under equal law.Most of us identify with, and think with, our own biological brain.If someone identifies with, and thinks with, their genitals … well, that explains a lot.So far, we’ve witnessed:trans* or inter* or ambiguous genetics, XXY, XYX, and so on, mixed genetics, and genetics opposite the person’s sex/gender, XY females, XX males,trans* or inter* or ambiguous gonads, people with both an ovary and a testes, or neither, and so on,trans* or inter* or ambiguous genitals, people with both vagina and penis, an intermediate thingy, or neither, and so on,trans* or inter* or ambiguous hormones, presence/absence, and receptivity/resistance, especially XY females who naturally get pregnant and give birth unassisted, and XX males who live long happy lives with no adverse symptoms, see ambiguous genetics,trans* or inter* or ambiguous endocrine systems, brain sex/gender versus body sex/gender, see ambiguous hormones.Science and medicine observe.Science and medicine do not dictate.There are born-girls who get a penis at 12 years old ( look stuff up ).There are girls born with a clitoris so big that doctors diagnose a penis.There are boys born with penises so small that doctors diagnose a clitoris.It is estimated that 2% to 20% of any population has ambiguities in their sex/gender traits, more so in culturally and or geographically isolated populations. ( See Anne Fausto-Sterling and supporting references )Only ~12% of any population is observed to have only female-traits or only male-traits, the rest of us are mosaics by any trait criteria. ( See Daphna Joel, Luba Vikhanski and supporting references )The concept of sexuality, specifically so-called hetero sexuality as averse to homo sexuality, was not invented until recently, in the mid-1800s, before that, there was just “sexuality”, period, so “norm” is a false, invented, non-existent thing anyway ( See Hanne Blank and supporting references ).Like Asperger’s autism and Kanner’s autism, electronic communication is permitting and encouraging awareness across heretofore isolated personal experiences, and more and more people are self-identifying as non-conforming in spite of presumptions and expectations of science, medicine, society, and religion.If we pay attention long enough, we’ll probably witness and experience every possibility beyond our imaginations.How many supposedly cis* sex/gender people even have any medical examinations reporting on the above often hidden and asymptomatic variables for themselves?“… Why would I? …” they might respond, “… I have no symptoms, nothing’s wrong …”.Correct, the majority of people with trans and anomalies and ambiguities are asymptomatic.Yet, people hold on to their precious prejudices and misbeliefs in their own purity and perfection, with absolutely no substantiation ( I love the stories of KKK members who find that they are descendants of Jews, for example ).But if we ask, we may find one, just one person in our community who might have the opportunity to share that they are an XX male ( yes, across sex/gender of female-to-male ), or someone may know of someone in the family who had an operation as a baby to “complete” their development ( meaning: to remove ambiguities as listed above, to transition them, oh my, as a newborn baby because they were across sex/gender of female-to-male when they were born ).Some folks might say“… cool,. you’re trans* sex/gender … wanna get some lemonade and sit and chat? …”Some may say“… no you are not, no one can be, that’s mentally insane …”… and for them to think of themselves as the opposite gender probably would be a mental issue because they are not the opposite gender.So … what are trans* sex/gender people actually all about?Read on …- - - - -Let’s explore some deeper understanding, and let’s all teach ourselves what the phrase “trans* sex/gender” means to those who self-identify, and can accurately and appropriately be referred to, using those terms.Again and again, I will repeat this and expand this until this is old news that everyone knows well and understands implicitly and teaches to their children.For those willing to learn what being ANY sex/gender is, and for those unaware of, or with presumptions of what being trans* sex/gender is all about, here’s a summary, please note how many “SAME” definitions there are for cis* sex/gender and trans* sex/gender people alike, and please watch and read autobiography videos, movies, posts, blogs, and books for more.What trans* sex/gender people are actually all about is …In the womb before birth, our various endocrine subsystems develop their sex/gender under hormone presence, hormone absence, hormone receptivity, and hormone resistance, SAME for everyone, yet where our brain, and our gonads / genitals, which develop at different times, may develop different sex/gender from each other, all naturally, all in the womb, all before birth.Birth-certificate-witness-doctors can only see our genitals, and they diagnose, they assign, and they register, our sex/gender for us accordingly, SAME for everyone.However, we all self-identify our own sex/gender around 3-years-old according to our own growing self-awareness of the sex/gender of our own brain ( we need no review of our birth certificate assignment, no understanding of future reproductive sexual correlates, no DNA test, no Bible, no liberal indoctrination, no peer pressure ), SAME for everyone.And, if our brain is a different sex/gender than our genitals, then some of us change our sex/gender assignment through new legal registration with our federal, state, and local self-governance — and that's the SAME and equal for all of us, the SAME for cis* sex/gender people, and the SAME for trans* sex/gender people alike.A transition process, if any, is personally variable, and may or may not include any of the following, some of which have absolutely no impact or effect on the sex/gender of one’s body, including the ability to eventually procreate ( to parent our own child ):Presenting as one’s own self-identified sex/gender - hair, shoes, clothes, makeup, and so on, SAME for everyone,Changing one’s name, SAME for everyone,Registering one’s own self-identified sex/gender with any territorial self-governance ( no surgery necessary in the US ), SAME for everyone,Participating in sex/gender-specific activities as one’s own self-identified sex/gender, SAME for everyone,Puberty blockers, to delay the puberty of an averse sex/gender until the person is of legal age and psychological confidence to make a decision either way, puberty or transition, note that most people do not express any self-agency over their own body’s development.Hormones ( now we enter the realm of possible interference with reproduction ), note that anyone can receive hormone treatments for many reasons, so even this is , SAME for everyone,Surgery, including:top ( secondary sex/gender endocrine subsystems ),bottom ( primary sex/gender endocrine subsystems ),face and voice ( safety, as well as self-identity, especially for trans* sex/gender females ).We can all search the web and our local libraries and educate ourselves with something new and so important to understand, try these search keywords ( click on them to get started ):in womb brain sex/gender development for reports of 20+ years settled and continuously evolving science, biology, medicine, endocrinology, psychiatry, and law, the same for cis* sex/gender people and trans* sex/gender people alike.age of trans* sex/gender self awareness for self-testimony on self-identification, legally equal, the same for cis* sex/gender people and trans* sex/gender people alike.Spack trans* sex/gender thrive for the applied life-saving endocrinology support for people worthy of equal happiness, equal participation, equal success in our society, in their own society.register sex/gender SSA and sex/gender visa passport to see how to register our own self-identified sex/gender with our Social Security Administration at the federal, state, and local level, and secure national and international visa and passports that accurately present our own self-identified sex/gender identification, again, same for cis* sex/gender people and trans* sex/gender people alike.trans* sex/gender 101 and trans* sex/gender stories books autobiographies for expansive exploration of real people’s experience, testimony, and references, and to connect us with the wonderful and challenging worlds of people who have incredible and inspirational stories to share.And let's all watch and listen to trans* sex/gender people's own stories on TED and YouTube.… and PLEASE let's all grow some informed empathy.And our own confusion about trans* sex/gender people will be relieved as quickly as we learn new things.Look stuff up with me — let's all enjoy learning.And never forget to treat others with the dignity and respect that they would like, equivalent to what we would like for ourselves.These are life lessons, life saving lessons, for ourselves, and for our parents and grandparents, for our siblings, children, friends, neighbors, folks we work with, and so on.No more second class citizens, ever, please — thank you.Please spend some time pursuing the search terms I offer, especially at your local library.There’s a whole world of information awaiting your engagement.I recommend reading a book.“Becoming Nicole, The Transformation of an American Family” book by Amy Ellis Nutt, 2015:… father Wayne and mother Kelly Maines … question their long-held views on gender and identity, to accept and embrace Wyatt's transition to Nicole, and to undergo an emotionally wrenching transformation of their own that would change all their lives forever … the story of a mother whose instincts told her that her child needed love and acceptance … father … to become a vocal advocate … four years reporting this immersive account of an American family … - Becoming Nicole: The Transformation of an American FamilyThank you for exploring this.- - - - - - - - - -Note from Quora Moderation, Your comment violates our policies “… I get the impression that if you were to suddenly think you were a woman, then you would have to consider yourself in ...” Your answer was deleted. Here’s the “offending” post:, read and decide for yourself.I get the impression that if you were to suddenly think you were a woman, then you would have to consider yourself insane.And that would be true, since you are not a woman ( I presume by your Quora name ).Therefore you assume that anyone else who self-identifies as the opposite sex/gender from what they were other-identified as when babies must be mentally insane, too.I’m asking you to go beyond the limits of your own personal imagination, and learn the reality of other people’s experiences being different, and legitimate.- - - - -Prior post:“… I have [ no ] interest in immersing myself in gender ideology …”Yet you comment and expound on it incessantly nonetheless.And inaccurately.And it’s not an “… ideology …”It’s law.You yourself are legally equally recognized as the sex/gender that you self-identify, legally equally as anyone else is legally equally recognized as the sex/gender they self-identify.Same same.You have the individual right, protected by the US Constitution ( presumably you are US ), but other countries also have governments that are instituted to secure their resident’s individual rights, too.- - - - -The way we think about biological sex is wrong | Emily Quinn - Did you know that almost 150 million people worldwide are born intersex -- with biology that doesn't fit the standard definition of male or female? (That's as many as the population of Russia.) At age 10, Emily Quinn found out she was intersex, and in this wise, funny talk, she shares eye-opening lessons from a life spent navigating society's thoughtless expectations, doctors who demanded she get unnecessary surgery -- and advocating for herself and the incredible variety that humans come in.Prior post:“… Yes, INTERSEX people exist. This fact however can best be understood as a birth defect …”Why?Many inter* sex/gender people are fully functional, no disease, no suffering, no averse symptoms, as I already wrote.“… birth defect …” is an assessment telling about the observer’s criteria, and says nothing about the person being observed.According to the Roman Catholic Church, being female is a birth defect such that Church doctrine states that women cannot interpret scripture, it’s a happenstance of their birth defect.The medical establishment performed hysterectomies on women who were hysterical in their view, so removing the female parts should eliminate the hysteria, hence the name “hysterectomy”.Seriously.Medical support services are evolving beyond“… doctor as god …”to “… doctor as servant and consultant,patient is the decision maker, the one in control …”As I wrote:Science and medicine observe.Science and medicine do not dictate.- - - - -Prior post:“… A man claiming to be a woman is suffering [ from a ] type of dysphoria …”No.It is estimated that only a minority of trans* sex/gender people experience body sex/gender discomfort.Being trans* sex/gender and experiencing body sex/gender discomfort are not mutually inclusive.- - - - -Anorexia and Napoleon are not appropriate analogies for sex/gender, as neither is on the human hormone sex/gender spectrum from female-to-male, in the womb, before birth, where the sex/gender of our various endocrine subsystems develop, naturally, and can sometimes develop across ( trans ) the female-to-male sex/gender spectrum in one person.All a trans* sex/gender person is saying is that their brain sex/gender is at a different place on that female-to-male spectrum, sex/gender wise, compared to their body’s sex/gender.You claim it’s a mental delusion requiring mental therapy, but you have no basis for such a claim.No mental therapy of any type has ever convinced a person that they are not the sex/gender that they self-identify as, and you probably could testify that no one could convince you that you yourself are the opposite sex/gender, so why do you think that other people can be so convinced?No talk therapy, no hypnosis therapy, no religious indoctrination therapy, no conversion therapy, no behavioral modification therapy, no psychoanalytic therapy, no temporal electroshock therapy, no lecture with the fact therapy, no psychotropic drug therapy has ever shown any efficacy in changing someone’s sex/gender self-identification.But one shot - ONE SHOT - of the hormones of the sex/gender a trans* sex/gender person self-identifies as instantly relieves - INSTANTLY RELIEVES - whatever body sex/gender discomfort they may be experiencing, providing proof that body sex/gender discomfort is a body thing, nto a mental thing, and that trans* sex/gender self-identification is accurate as your own presumably cis* sex/gender self-identification.There’s nothing about being trans* sex/gender that would constitute a “mental illness” in and of itself. The American Psychological Association has a pretty good write up about why being trans* sex/gender is not a mental illness on their website. To quote them:A psychological state is considered a mental disorder only if it causes significant distress or disability. Many transgender people do not experience their gender as distressing or disabling, which implies that identifying as transgender does not constitute a mental disorder. For these individuals, the significant problem is finding affordable resources, such as counseling, hormone therapy, medical procedures and the social support necessary to freely express their gender identity and minimize discrimination. Many other obstacles may lead to distress, including a lack of acceptance within society, direct or indirect experiences with discrimination, or assault. These experiences may lead many transgender people to suffer with anxiety, depression or related disorders at higher rates than nontransgender persons.According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), people who experience intense, persistent gender incongruence can be given the diagnosis of "gender dysphoria." Some contend that the diagnosis inappropriately pathologizes gender noncongruence and should be eliminated. Others argue that it is essential to retain the diagnosis to ensure access to care. The International Classification of Diseases (ICD) is under revision and there may be changes to its current classification of intense persistent gender incongruence as "gender identity disorder."Thanks for exploring this.But please, don’t respond until AFTER you have explored the search terms I suggest, and read additional references that you have yet to incorporate into your lack of interest in immersing yourself in sex/gender experiences, testimony, science, and medicine, but which you write about nonetheless.- - - - - - - - - -Question added by Colleen Prinssen 428 Answers 192 Questions “… Is it trans-phobic to believe some men will lie about being women to get into women's spaces? (Is it transphobic to believe some men will lie about being women to get into women's spaces?) …” #957606020 · Thank · Report · 9 Jan 2020 6:31 AM.