Displaying 11-20 letters out of 491 published
Effects of congruence between preferred and perceived learning environments in nursing education in Taiwan: a cross-sectional study.
Correspondence to: Professor Wing P Chan; email@example.com and Professor Chun-Yen Chang;firstname.lastname@example.org Yeh, T-K., Huang, H.M., Chan, W.P., Chang, C. (2016). Effects of congruence between preferred and perceived learning environments in nursing education in Taiwan: a cross-sectional study. BMJ Open, 6, e009925. doi:10.1136/ bmjopen-2015-009925
Dear Editor: Results from this study showed that alignment between perceived and preferred learning environments is associated with better learning outcomes among first year undergraduate nursing students, including their learning achievement, self-efficacy and attitudes towards nursing. Results also found that students preferred a mix of problem- and lecture-based learning. This was a very interesting and timely article, and an excellent read for persons involved in the education of nurses, like myself. As the profession and the environment in which nurses work continue to change, so must the strategies used for nursing education (Rideout, 2001). Here in the Caribbean, we are also moving towards integrating more PBL approaches into our healthcare professional teaching, and evidence is emerging that students want, and appreciate PBL (Shankar and Nandy 2014), combined with an effective learning environment. Despite PBL gaining recognition in nursing and the growing evidence that it is effective in providing student nurses with the requisite skills and knowledge, as the study results show, challenges remain in implementing PBL. The authors' recommendations on how PBL may be improved, including teachers examining students' preferences as well as students' perceptions of the learning environment, are certainly critical in ensuring learning strategies are adapted to students' needs in developing critical thinking (Tiwari, Lai, So, & Yuen, 2005). In addition to these recommendations, however, I would like to suggest that attention be directed to the education system as a whole, not just the educators. The education system is what forms the basis of the learning environment and the perceptions that a student has about their teaching/learning environment are likely to impact their learning outcomes (Lizzio, Wilson & Simons, 2002). System factors, such as expectations of students (i.e., exam performance) as discussed in the article, are likely important in influencing students' teaching preferences. I think the significance of these factors cannot be underestimated and must be considered if teaching and learning are to produce the expected outcomes. Another notable recommendation may also be to explore the role of PBL versus simulation and how this affects students or the acquisition of knowledge and critical thinking. More and more simulation based learning has been proven to be superior to problem based learning in increasing the capacity for critical thinking (Seybert et. al., 2012; Steadman et. al., 2006). Exploring the outcomes of these various teaching/learning methods may help to further understand problem based learning. Terry Campbell Lecturer School of Nursing & Allied Health Professions The College of The Bahamas Nassau, Bahamas
Lizzio, A., Wilson, K., and Simons, R. (2002). University students' perceptions of the learning environment and academic outcomes: implications for theory and practice. Studies in Higher Education, 27(1), 27-52.
Rideout, E. (2001). Transforming nursing education through problem-- based learning. MA: Jones Bartlett Publishing.
Seybert, A., Smithburger, P., Kobulinsky, L., Kane-Gill, S. (2012). Simulation-based learning versus problem-based learning in an acute care pharmacotherapy course. Journal of the Society for Simulation in Healthcare, 7(3), 162-165.
Shankar, R.P., and Nandy, A. (2014). Student feedback on problem- based learning processes. Australasian Medical Journal, 7(12), 522-529
Steadman, R., Coates, W.C., Huang, Y-M., Matevosian, R., Larmon, B., McCullough, L., Ariel, D. (2006). Simulation-based training is superior to problem-based learning for the acquisition of critical assessment and management skills. Critical Care Medicine, 34(1), 151-157.
Tiwari, A., Lai, P., So, M., and Yuen, K. (2006). A comparison of the effects of PBL and lecturing on the development of students' critical thinking. Medical Education, 40(6), 547-556.
Conflict of Interest:
Two opposite interpretations of data about cholesterol, CVD; but good theories of why are missing
Two opposite views: is (or is not) elevated levels of total cholesterol (TC) a primary cause of atherosclerosis and cardiovascular disease (CVD)? If not, what is the primary cause of acquired CVD, how does it relate to cholesterol?
Goldstein and Brown propose that LDL-C is the essential causative agent of CVD. Ravnskov and his collaborators disagree; they proposed several empirical descriptions of what causes CVD. However, these explanations are not a theory as such term is known in science. In 1956 Sinclair wrote that deficiencies in Essential Fatty Acids (EFAs) are the major cause of CVD. However, the existing data showed that deficiencies of EFAs were extremely rare, perhaps less than 1/100,000 (based on the few reported medical cases). Because CVD is common, if EFA deficiencies were a major contributory factor to CVD, they ought to be common. Sinclair was dismissed or overlooked. In the 1980s I invented technology to accurately measure fatty acids (FA) in tissues. In a plasma sample, prior technology found 20 to 50 chemicals. I found over 400. It means that substances in small quantities such as w3s and trans FA could not be measured accurately because they were superimposed with substances in larger quantities (the technology used, GLC, separates chemicals into peaks and measures the area of the peaks). I found that deficiencies of EFAs were common, and proposed that abnormalities of EFAs are a major factor in CVD, consistent with Sinclair. We do lack, however, a physical/chemistry theory of what causes CVD, and how EFAs or cholesterol contribute to or prevent CVD.
It seems likely that major pathways and regulatory processes involved in lipid metabolism evolved to optimize the body towards some goal (unknown, perhaps longevity, perhaps reproduction, perhaps survival). It seems unlikely that doctors can do better, optimize the body for longevity and other desirable outcomes, by interfering with millions of years of presumably optional evolution (e.g., inhibit cholesterol pathways). Instead, it is more likely that there are factors (currently unknown) that cause CVD, and the body increases cholesterol as a means to prevent rather than cause mortality (or optimize other functions such as brain IQ, resistance to infection, etc.). Thus, while high cholesterol or LDL may in part be associated with heart attacks, creating the appearance that LDL causes CVD, looking at other biomarkers we may find that high cholesterol has protective effects. There are about 20K enzymes and more than 20K chemical reactions that interact with each other and regulate body function. Due to our brain limitations, we rarely look at more than 100 variables concurrently. These variables represent a cross section of the multivariate function of the body. Depending on which variables we look at, and the values of the variables that we ignore (often unknown), relationships can change. Further, we all die. At the start of a clinical trial, death rates (0%) are the same for the experimental group and placebo or control. At 100 years later, they are also the same (100%). In between, there are differences. Depending on the subjects used, the treatments considered, the outcomes and observation time, high levels of LDL-C can be associated with high heart mortality and longevity (because LCL-C is not the major factor in either one).
Current descriptions of potential causes do not provide explicit predictions of the relationships between fatty acids and lipids. One consequence is the frequently changing and inconsistent results of clinical trials and recommendations regarding the role of saturated (SFA), monounsaturated (MUFA) and different types of polyunsaturated fatty acids (PUFA). Ex: should we eat more foods high in MUFAs, like avocados, or should we avoid them? Should we focus on eating some types of SFAs and avoid others, or are they all, biochemically, substantially the same? Is it healthier (e.g., associated with longevity) to eat 0, 1 or 2 eggs per day (and why?). Should we eat a diet low or high in total fat, or on specific types of fats (high in some, low in others)? Should we eat a large meal in the evening and go to sleep shortly afterwards, or a big breakfast, or many small meals during the day? How should we change a diet according to seasons or geographic location? A good theory of disease and aging should answer these questions.
We need conservation and optimization principles in biology similar to those used in Physics (e.g., conservation of energy) from which Physics derives equations of movement that predict arrival times of airplanes or movement of planets. A good theory of cholesterol metabolism and CVD will explain why the body increases or decreases cholesterol production (what is being conserved or optimized), and predict the shape of the relationships among different fatty acids and between fatty acids and cholesterol.
References Goldstein JL, Brown MS. A century of cholesterol and coronaries: from plaques to genes to statins. Cell 2015;161:161???72. doi:10.1016 j.cell.2015.01.036. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6: e010401. doi:10.1136. bmjopen-2015-010401 Sinclair HM. Deficiency of essential fatty acids and atherosclerosis, etcetera. Lancet. 1956 Apr 7;270(6919):381-3. Sinclair, HM. Prevention of coronary heart disease: the role of essential fatty acids. Postgrad Med J. 1980 Aug; 56(658): 579???584. Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93. Siguel E. Essential Fatty Acids in Health and Disease. 1994, P.O. Box 10187, Dept F, Gaithersburg, MD 20898 (book, out of print, new version being prepared) Siguel E, Lerman RH. The Role of Essential Fatty Acids: Dangers in the USDA Dietary Recommendations ("Pyramid") and in Low Fat Diets. Am. J. Clin. Nutrition, 1994; 60:973-79 (let). Siguel, E. A New Relationship between Total/HDL Cholesterol and Polyunsaturated Fatty Acids. Lipids, 1996; 31:S51-6. Siguel. E. A Theory of Health, Disease and Aging (to be published). A biophysical explanation of why cholesterol increases, the mathematical relationship between different types of fatty acids and cholesterol, and propose the primary cause of acquired CVD in Western societies.
Conflict of Interest:
I conduct many activities that influence my opinions (e.g., my research, write books or articles or patents, have websites, design foods, lecture about health and disease, health policies). Among other things, I describe the types of fats to eat, exercise, stress management, diets, eating less, periodic fasting, CVD, aging. I am developing a new theory of disease and aging, including lipid metabolism and the cause of cardiovascular disease (CVD). I intend to profit from my intellectual property (IP) (e.g, write articles, web sites, books, patents, lectures, ads, biomarker tests, etc). I wrote a patent to measure fatty acids. I wrote one book on essential and trans fatty acids. I gave talks to corporations, conferences and trade shows, for which I was paid. I may receive compensation from food or other companies. This comment is an extract of books and articles either written or in progress (authorized by the author under the non-exclusive common license CC BY-NC 4.0 requested by BMJ). I criticized the value of the USDA nutrition guidelines, federal nutrition funding, and the National Cholesterol Education Program. I do not consider eggs harmful because they have cholesterol and fat, made my views public, received funding from egg industry. I tell my family to eat eggs and red meat, but avoid processed fat. I do not follow the USDA nutrition guidelines. I proposed a different Food pyramid and nutrition guidelines. These are my opinions based on my research, 20+ years communications with USDA/HHS committees, attendance to professional conferences, lectures I gave, review of published articles.
Reply to: BMJ Open - Conflict of interest between professional medical societies and industry: a cross sectional study of Italian medical societies' websites
Dear Editor, the above-mentioned paper, published on June 3d, 2016 by group.bmj.com, reports the results of a survey performed on 154 professional medical societies (PMS) belonging to FISM, the Italian Federation of Medical Societies. According to the study outcomes, industry sponsorship to PMS are very common both by Pharmaceutical and Medical Devices Companies even if a precise and dedicated regulation is still missing. We deeply feel the need to point out to your attention a critical remark we think should be addressed by the editorial office. First of all the peer review analysis didn't detect a major mistake concerning the Ministry of Health Decree Law of 2004, mentioned by the authors (see Chapter "Methods"- page 2 - line 11-16): This Decree has been rejected by the Supreme Court (Consulta - sentence nr. 328/2006 - registered on 13/10/2006) because of formal flaw and has never been resubmitted for approval. Therefore, it's not true that professional medical societies are regulated by this law that simply doesn't exist anymore. Only recently, the Ministry of Health has been focusing again on professional medical societies accreditation evaluating, with the support of Fnomceo, a panel of criteria identified by FISM and its affiliated medical societies to drive the accreditation procedure. Secondly, we are pleased to tell you about FISM readiness to share with you all the huge work that has been done since 2004 to update professional medical societies' regulations in order to enhance transparency and favour the development of internal ethical codes to better manage financial interactions with the industry. Waiting for your kind reply, Best regards.
Franco Vimercati (President) Francesco Macri (FISM Secretary)
Conflict of Interest:
Risk Management in Personal Protective Equipment trials
We read with great interest the study of Schroeder et al and found it a valuable contribution to a very contemporary topic in emergency and disaster medicine. We would however raise two concerns regarding the study design and research governance.
The authors state that the participants were using the gastight ISOTEMP-4000 chemical protection overall, but notably, no self-contained breathing apparatus (SCBA) was connected. According to the manufacturers specifications the suit is for use with a SCBA only and must only be used by persons who have been fully trained and are familiar with the complete suit equipment and requirements. Failure to do so carries the risk of asphyxiation.
Furthermore, as all participants were supposedly employed by the sponsor, we wonder how explicit the participant information document had addressed the above named safety risk of the personal protective equipment (PPE).
Finally, the local ethics committee had not only approved the study but also waived written consent for the participants. This raises a concern if the committee had independently sought information from the manufacturer regarding the suits correct and safe use. If that would be the case the ethics committee could have missed an important opportunity in its duty of care.
The second concern relates to the study design. The authors choose to use Level 1 PPE (Gastight suit with SCBA). This is an unusually high PPE level for a medical first responder, as SCBA training is extremely limited in that community. This is attested by the fact that none of the study participants was certified to use a SCBA.
In England and Wales every one of our sixteen ambulance services provides a team of specially trained paramedics (HART- Hazardous Area Response Teams) capable of medical care in the hot zone of CBRN or HazMat incidents. They operate under Level 2 protection but none of these paramedics is trained to perform advanced airway management or endotracheal intubation.
On the "First Receiver" side, our major UK hospitals provide Level 2 suit-ensembles for emergency doctors in order to allow medical care during the decontamination process prior to admission into the emergency department. Using these "Level 2" Powered Respirator Protective Suits (Respirex) avoids complicated SCBA training and annual medical certification of the staff.
We therefore feel that the study might have benefited from a Level 2 PPE setup using Air-Purifying or Powered Air-Purifying Respirators. We are aware that this might not have altered the interesting results this important study provided but it would have been more realistic and probably safer for the participants.
Conflict of Interest:
C-MAC videolaryngoscopy associated with higher force on the maxillary incisors
We read with interest the high-fidelity simulator based study by Nakanishi et al  comparing macintosh direct laryngoscope (DL) with video laryngoscopes (VL) on the force applied to oral structures during intubation attempts by novice physicians. The findings of this study are quite interesting and we wish to raise some important points which would explain the findings. The study revealed that use of DL was associated with greater force applied to the tongue compared with VLs. The classical technique of DL described by MacIntosh  requires upward lifting of the tongue by the laryngoscope blade thereby drawing the epiglottis along with it, aligning the oral, pharyngeal and tracheal axes and improving the visualisation of the larynx. It also recommends the lifting of the laryngoscope handle along the axis of the handle away from maxillary incisors. All of these manoeuvres are bound to increase the pressure and force applied to the tongue, at the same time minimising and avoiding force applied over the maxillary incisors. The study also revealed, in contrast to previously published studies, [3,4] that the C-MAC VL was associated with higher maximum force applied to the maxillary incisor in comparison with DL and Airway Scope (AWS). This can be explained by the incorrect technique often adapted by novice physicians, using maxillary incisors as a fulcrum to lift the epiglottis and other soft tissues in order to improve the laryngeal view without encompassing the rest of the manoeuvres described by Macintosh. The differences in the geometrics - sloping keel of the C-MAC VL blade in contrast to the right angled keel of standard MacIntosh blade also in our opinion contributes to this problem - by decreasing the available clearance to insert the endotracheal tube, introducing the tendency to use maxillary incisors as a fulcrum, thereby applying more pressure on them. Unlike the previously published studies where the force applied on the maxillary incisor was measured using three discrete Flexiforce sensors mounted on the concave surface of the blade, the current study measured the force applied on the implanted sensors in the maxillary incisors of the manikin. We also wish to disagree with the statement that in spite of the force generated on the maxillary incisors with C-MAC VL, it would be safe to use them without the risk of dental injury. Based on our clinical experience, much lower force than 150N may be sufficient to induce dental damage in patients with previous dental instability especially in emergency settings based on our clinical experience. Another surprising finding of the study was the longer time to intubation with the VL in comparison with the DL. Although the authors have not elaborated, this has been well recognised and can be attributed to specific methods of endotracheal tube insertion and issues depending on the design of the VL - e.g. difficulty in advancement of the ETT with channelled VLs. The authors also have not provided information on the use of adjunct airway devices like bougie and their effects on the above finding.
1. Nakanishi T et al. Comparison of the force applied on oral structures during intubation attempts by novice physicians between the Macintosh direct laryngoscope, Airway Scope and C-MAC PM: a high-fidelity simulator- based study. BMJ Open, 2016;6(5):e011039
2. MacIntosh, RR. A new laryngoscope. Lancet, 1943; 1:205.
3. Lee RA et al. Forces applied to the maxillary incisors by video laryngoscopes and the Macintosh laryngoscope. Acta Anaesthesiol Scand, 2012 Feb;56(2):224-9.
4. Pieters B et al. Indirect videolaryngoscopy using Macintosh blades in patients with non-anticipated difficult airways results in significantly lower forces exerted on teeth relative to classic direct laryngoscopy: a randomized crossover trial. Minerva Anestesiol, 2015 Aug;81(8):846-54.
Conflict of Interest:
Hazard ratio should be obtained with appropriate formula
We recently read Tian and Xu's article with interest, in which the prognostic value of lncRNA MALAT1 in human cancer was investigated by a meta-analysis. The authors obtained hazard ratios (HRs) by three different methods. In method 2, the HRs were calculated from the total number of events and its P value with the formula: HR=[P0/(1-P0)]/[P1/(1- P1)], where P0 represents a 5-year survival rate in the group with low expression of MALAT1 and P1 represents a 5-year survival rate in the group with high expression of MALAT1. The formula of 95% CI was exp(lnHR+/-1.96*SE), where exp=exponential, lnHR=the natural logarithm HR, and standard error (SE) of HR.
As we known, odds ratio (OR) is obtained by doing logistic regression, whereas HR is obtained from Cox regression model. OR is the ratio of the odds of an event occurring in one group to the odds of it occurring in another group. If the probabilities of the event in each of the groups are P0 (first group) and P1 (second group), then the OR=[P0/(1-P0)]/[P1/(1-P1)]. On the other hand, HR is often treated as a ratio of death probability. In the Cox-model, this can be shown to translate to the following relationship between groups' survival rates : S1(t)=S0(t)HR, where S1(t) represents the survival rate in experimental group and S0(t) represents the survival rate in control group. Therefore, in our opinion, this is a rather mistake to obtain HR by using the OR's formula.
Like the supplement material provided by Tian and Xu's article, take the original data obtained from Dong et al's  study for example, P0=5-year survival rate in the group with the low expression of MALAT1=alive/the total number of events=3/5=0.6, P1=5-year survival rate in the group with the high expression of MALAT1=alive/the total number of events=4/14=0.2857. Therefore, HR=(lnP1)/(lnP0)=(ln0.2857)/(ln0.6)=2.45. However, the HR value was 3.75 in Tian and Xu's article, calculated by the formula of [P0/(1-P0)]/[P1/(1-P1)], which overestimated the death risk of the high expression of MALAT1. In addition, using the different HR values to calculate the 95% confidence intervals (CIs) of HR step by step 4, the 95% CIs of HR were significantly distinct from each other, with HR (95% CIs) of 2.45 (0.60 to 9.95), and 3.75 (0.47 to 29.62), respectively.
In conclusion, the authors have incorrectly used the OR's formula to obtain HR values. It would overestimate the hazard ratio and affect the range of the 95% CIs. It is important to comprehend that HR is an index to assess the time-to-event (survival) outcomes, which obtained from Cox regression model. We should use the appropriate HR formula to transform the survival data provided by the original study.
Funding supported by grants from the National Natural Science Foundation of China (81401466).
1. Tian X, Xu G. Clinical value of lncRNA MALAT1 as a prognostic marker in human cancer: systematic review and meta-analysis. BMJ Open, 2015;5:e008653.
2. Case LD, Kimmick G, Paskett ED, et al. Interpreting measures of treatment effect in cancer clinical trials. The oncologist, 2002;7:181-7.
3. Dong Y, Liang G, Yuan B, et al. MALAT1 promotes the proliferation and metastasis of osteosarcoma cells by activating the PI3K/Akt pathway. Tumour biology: The Journal of the International Society for Oncodevelopmental Biology and Medicine, 2015;36:1477-86.
4. Tierney JF, Stewart LA, Ghersi D, et al. Practical methods for incorporating summary time-to-event data into meta-analysis. Trials, 2007;8:16.
Conflict of Interest:
Re: The need to further examine the role of religion and its association to STD incidentDear Miriam Yonazi,
Thank you for your interest in our article.
You have valid points regarding the limitations of the study. I believe these are addressed in our limitations section, although we did not stress the implicit limitations of the retrospective design using a national register to examine the disease incidence in the cohort.
We used syphilis, gonorrhea and chlamydia as a measure of STD because these data were available to us, and primarily chlamydia infections were estimated suitable as a proxy of HPV infections as described in the article. HPV infections are often asymptomatic and remain undiagnosed, hence we had no valid measure of these infections in the cohort.
Our study does not examine how religiousness is associated with STD, but we used church membership as a predictor of lower incidence of STD. Your proposal of further studies on the relationship between religiousness and STD is very interesting. We have previously found members of religious minorities in Denmark to be more religious than the general Danish population , which in light of this article supports the hypothesis that higher degrees of religiousness are associated with a lower risk of STD. But this hypothesis needs to be tested in future (prospective) studies.
 Thygesen LC, Hvidt NC, Juel K, et al. The Danish Religious Societies Health Study. Int J Epidemiol, 2012; 41:1248-55
Conflict of Interest:
Typographical error in first sentence
We have noted that there is an error in the Introduction in the first sentence. It reads "...lymphocytes undergo a malignant change and multiple uncontrollably" It should be "multiply" not "multiple".
Conflict of Interest:
Re:RE: Community-Linked Maternal Death Review (CLMDR) to measure and prevent maternal mortality: a pilot study in rural Malawi
We thank Levis K. Nyavanda for his interest in our work and his letter in response to our article. We agree that Health and Demographic Surveillance Systems (HDSS) can provide accurate data on births and deaths in settings such as Mchinji, Malawi where our study was set. Our community-linked maternal death review (CLMDR) intervention however did not rely on such a complex and expensive system to identify deaths. In our study we compared the maternal mortality ratio estimated from the number of maternal deaths identified by the community and facility maternal death review teams and the total population size of the district and estimated crude birth rate, to that observed from a cluster randomised trial in the same site that did involve a HDSS. We do not propose that our CLMDR system could act as a replacement for a HDSS, but rather we aimed to highlight its comparable robustness. We are unsure what Nyavanda means when he states "the Community-Linked Maternal Death Review (CLMDR) on its own could not predict accurate verbal autopsy information through a prospective cohort study without case controls and multinomial regression models". Who would the "case controls" be? And would the multinomial regression models be used to predict different causes of maternal deaths (these being the multinomial outcomes?) using information from the verbal autopsy? Our CLMDR system is intended to identify individual deaths and investigate and respond to the social, as well as clinical and health systems factors that contribute to these deaths so as to prevent future deaths from occurring. Aggregating the verbal autopsy data could be done to useful effect at macro-level, as it has been done in previous work . However rapid analysis tools for verbal autopsy tend to be optimized for population-level reporting and would not necessarily be an appropriate approach in the immediate local situations CLMDR seeks to improve. Aggregation could also be done without the use of multinomial regression models - indeed with relatively few deaths from each cause such models would likely be underpowered as well as be unnecessarily complex and incomplete given likely lack of data on all important social and system factors for each case.
We agree that the CLMDR process requires local adaptation in each new context in which it is introduced, and encourage such adaptation. We also thank Nyavanda for his suggestions for "additional stages" - we kindly note however that the community training stage is already an integral part of the CLMDR intervention - indeed the volunteer community teams require training in the process before it can start in their community - and the community are already encouraged to be a focal point for providing reliable information about the context of the maternal deaths. As we state in our paper the community CLMDR teams identified 43 (83%) of the maternal deaths, including 4 that happened at the district hospital but were overlooked by the pre-existing facility-based system. CLMDR also encourages integration of community and facility data.
1. Fottrell E, Osrin D, Alcock G, Azad K, Bapat U, et al. Cause-specific neonatal mortality: analysis of 3772 neonatal deaths in Nepal, Bangladesh, Malawi and India. Arch Dis Child Fetal Neonatal Ed, 2015; 100(5):F439-47.
Conflict of Interest:
Association between sexually transmitted disease and church membership. A retrospective cohort study of two Danish religious minorities
Korup and colleagues aimed to investigate the incidence of sexually transmitted diseases among Danish Seven-day Adventists (SDAs) and Danish Baptists as a proxy for cancers related to sexual behaviour. The authors use a retrospective cohort design with a cohort comprised of 3119 SDA females, 1856 SDA males, 2056 Baptist females and 1467 Baptist males and came with the conclusion that there is significant lower incidence of sexually transmittable diseases, mostly including human papillomavirus, which may partly explain the lower incidence of cancers of the cervix, rectum, anus, head and neck.
It is not clear why the authors selected SDAs and Baptists in this study. I would suggest that the authors use a comparative case study method to get an in-depth examination of SDAs and Baptists, as well as Catholics, who are generally against the use of condoms in sexual relationships. It will be interesting to also understand whether the studied population is involved in oral sex and the types of prevention methods used. Another interesting area is to examine the prevalence among married couples, given that some countries have observed an increased incidence of STDs in married couples.
Conflict of Interest: