Topic: Suppression of data by Canadian pharmaceutical companies and its effects

Please read all instructions before writing this essay and ensure to follow the instruction.

Essay topic: Suppression of data by Canadian pharmaceutical companies and its effects
Links for material:

Assignment 2 Steps (satisfy the formatting, APA, and rubric handouts, on Moodle and reviewed in class, as well):
1. Using your approved or revised essay topic, clearly refine your critical analysis of your pharmaceutical policy challenge within the scope of the course.
2. Compile your required 8-10 peer-reviewed sources, optional grey literature, and other optional sources.
3. Before you start to write your paper, write your notes on how you will contextualize your policy challenge by discussing its background with reasonable scope and definition. Compile your notes on the present status of the policy challenge. Review your literature with a critical lens.
4. Prepare your introduction, thesis statement, and subheadings for your paper.
5. Prepare at least your first subheading body paragraphs. If you have space for the start of your second subheading of body paragraphs, begin writing these paragraphs.
6. On your sixth and final page of this assignment, draft your plan for the remainder of your paper’s subheadings, arguments, and sources, as well as your planned conclusion and future directions based on your research.
7. See rubric and handouts to ensure that you have met all requirements
1. Title page (does not count toward page count): Project title, student name, student #, course name/code, professor’s name, , and the due date of the assignment.
2. Introduction (1/2 page): In a single paragraph of approximately 10 sentences, follow the rubric to draft your introduction.
3. Subheadings and body paragraphs (4.5 pages): Provide at least your first subheading, along with arguments and critical analyses of your chosen policy challenge.
4. Proposed continuation of paper (1 page): Provide your planned continuation and development of your paper’s second half and conclusion/future directions. Ensure that your proposed arguments are supported by peer-reviewed literature. Be sure that your planned continuation of your paper is well thought out and flows smoothly from your first subheading. This must be completed in paragraph form.
5. References (does not count toward page limit): APA format, per OWL Purdue APA website, online.
4. Assignment Form from syllabus

First Nations Health in Canada:
A Program Evaluation of the Environmental Threats to Health by the X Institution

Student’s First and Last Names
Student Number
Course Code: Course Full Name
Course Director’s Name
Due Date

This is the introduction to my paper. Your first sentence will introduce your topic in a concise, yet clear manner. Your second and third sentences will describe the context of your topic. Your third, fourth, and fifth sentences will narrow your introduction to the issues that you have identified as most poignant to discuss in this paper and their significance. Your sixth sentence will be your thesis statement – a clear roadmap to the structure of your paper. Here is an example you may modify for your use: In this paper, I will be analyzing the issue of ______ by considering the themes of ______ and _______. Your introduction is to be no more than half a page, as with every other paragraph in your paper.
[Use Subheadings for Each Theme or Topic Addressed]
Subheading 1: Brief, yet clear, description
In these sections, you will critically analyze your chosen question within the context of this particular theme. You can write as many body paragraphs as you need, within page limit, to effectively convey youanalysis.No paragraph shall be longer than approximately half a page.
Subheading 2: Brief, yet clear, description
In these sections, you will critically analyze your chosen question within the context of this particular theme. You can write as many body paragraphs as you need, within page limit, to effectively convey you analysis.No paragraph shall be longer than approximately half a page.
(Above, pages 1-5)
Proposed continuation of paper (page 6)
In this section, you will provide a clear and organized summary of how you propose to continue your paper in your final essay. This section will include any arguments that you plan to proceed with, as well as the sources that you will use to back them up. This, as with the rest of the paper, must be cited using APA.
This paper should be no less than 5 pages, and no more than 6 pages.

Topic: Luxury hospitality management- Research ideas


Course: MA Luxury Hospitality Management
Module: Research methods
Assigment 1: Research Ideas

Introduction Overview of research (100 words)
About CSR, Sustainibility and Smart Luxury

Identification of topic area, definitions and rationale for research (300 words)
Luxury Hospitality
Guest perception
Brand Reputation Management
Upcoming Smart Luxury eg. Red Sea Project in Saudi Arabia

Aim/objectives and RQs (100 words)

Literature 250 words
Journals about: CSR, Sustainability, Smart Luxury, Service Profit Chain, New sustainable projects

Methodology 250
Methodology Method(s)
Questionnaires to hotel’s employees
Hotel guests
Various properties
Various ages
Various educational background
Sampling technique(s)
Sample size(s)

Harvard referencing and bibliography Minimum 10 topic sources

I uploaded work, that I have started myself. The information is copy-pasted, so the need rewriting, but they might be useful. The references are there as well. Please use it,

Topic: Health and social care Values


The good practice guide should include the following elements.
1.title page
2.contents page
4.a mission statement
5.An equalitities and diversity statement
6.Values in practice discussion should be about ETHICS and NORMALISATION.That will be main topic of discussion in this essay

Topic: Do you believe that diagnosis is helpful or do you believe that it is a detriment to individuals who are suffering from psychological problems?


The topic is the diagnosis of mental disorders. Do you believe that diagnosis is helpful or do you think that it is a detriment to individuals who are suffering from psychological problems?

Why? You must argue for a particular perspective, which generally means choosing one side. However, you may qualify your answer.

Thoughtful, brief, clear and concise work. This infers that the paper should “flow” from start to finish and that your main idea should be woven through each paragraph.

Also, Use material from the New Yorker article. Spiegel, A (2005). Annals of medicine. The dictionary of disorder: How one man revolutionized psychiatry. The New Yorker. (3rd January, 2005).

Proportion of patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study


Proportion of patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study


Marta Di Forti, Arianna Marconi, Elena Carra, Sara Fraietta, Antonella Trotta, Matteo Bonomo, Francesca Bianconi, Poonam Gardner-Sood, Jennifer O’Connor, Manuela Russo, Simona A Stilo, Tiago Reis Marques, Valeria Mondelli, Paola Dazzan, Carmine Pariante, Anthony S David, Fiona Gaughran, Zerrin Atakan, Conrad Iyegbe, John Powell, Craig Morgan, Michael Lynskey, Robin M Murray


Background The risk of individuals having adverse effects from drug use (eg, alcohol) generally depends on the frequency of use and potency of the drug used. We aimed to investigate how frequent use of skunk-like (high-potency) cannabis in south London affected the association between cannabis and psychotic disorders.


Methods We applied adjusted logistic regression models to data from patients aged 18–65 years presenting to South London and Maudsley NHS Foundation Trust with first-episode psychosis and population controls recruited from the same area of south London (UK) to estimate the effect of the frequency of use, and type of cannabis used on the risk of psychotic disorders. We then calculated the proportion of new cases of psychosis attributable to different types of cannabis use in south London.


Findings Between May 1, 2005, and May 31, 2011, we obtained data from 410 patients with first-episode psychosis and 370 population controls. The risk of individuals having a psychotic disorder showed a roughly three-times increase in users of skunk-like cannabis compared with those who never used cannabis (adjusted odds ratio [OR] 2·92, 95% CI 1·52–3·45, p=0·001). Use of skunk-like cannabis every day conferred the highest risk of psychotic disorders compared with no use of cannabis (adjusted OR 5·4, 95% CI 2·81–11·31, p=0·002). The population attributable fraction of first-episode psychosis for skunk use for our geographical area was 24% (95% CI 17–31), possibly because of the high prevalence of use of high-potency cannabis (218 [53%] of 410 patients) in our study.


Interpretation The ready availability of high potency cannabis in south London might have resulted in a greater proportion of first onset psychosis cases being attributed to cannabis use than in previous studies.


Funding UK National Institute of Health Research (NIHR) Specialist Biomedical Research Centre for Mental Health, SLaM and the Institute of Psychiatry at King’s College London, Psychiatry Research Trust, Maudsley Charity Research Fund, and th European Community’s Seventh Framework Program grant (agreement No. HEALTH-F2-2009-241909 [Project EU-GEI]).


Copyright © Di Forti et al. Open Access article distributed under the terms of CC BY.


Lancet Psychiatry 2015


Published Online February 18, 2015 S2215-0366(14)00117-5


See Online/Comment S2215-0366(14)00130-8


Department of Psychosis


Studies (M Di Forti MD,


A Marconi MD, E Carra MD,


S Fraietta MD, A Trotta MSc,


M Bonomo MSc, F Bianconi MSc, P Gardner-Sood PhD, J O’Connor PhD,


T R Marques PhD, P Dazzan PhD, Prof A S David MD,

F Gaughran MD, Z Atakan MD, C Iyegbe PhD,

Prof R M Murray FRS), Department of Health Services and Public Health (S A Stilo MD, Prof C Morgan PhD), Department of Psychological Medicine (V Mondelli PhD, Prof C Pariante PhD), Department of Neuroscience (Prof J Powell DPhil); Department of Addiction (Prof M Lynskey PhD), Institute of Psychiatry, Kings College London, London, UK; and Department of Psychiatry, Mount Sinai School of




Cannabis is the most popular illicit drug in the world. Uruguay was the first country to legalise its use and several US states have done so or are in the process of doing similar.1 Therefore, any harm caused by cannabis use should be quantified. Prospective epidemiological studies have consistently reported that use of cannabis increases the risk of schizophrenia-like psychosis.2,3 In the UK, the investigators of the 2012 Schizophrenia Commission4 concluded that cannabis use is the most preventable risk factor for psychosis, and research that aims to improve estimation of the drug’s contribution to illness development should be pursued.


The aspects of exposure to cannabis (eg, age at first use, frequency of use, duration of use) that confer the greatest effect on risk of psychosis are unclear. Such information would be valuable for public education and to estimate the proportion of psychosis cases that

could be prevented if harmful patterns of cannabis use were removed from the population. The few studies5,6 that have tried to estimate the effect of cannabis use on the number of new cases of psychosis in specific populations have been limited by the scarcity of accurate information on patterns of cannabis use.

The risk of adverse effects for mental health and cognition posed by cannabis use has been suggested to depend on the potency of the type of cannabis used.7 For example, in a previous study8 of part of the population reported here, we noted that skunk-like types of cannabis, which contain very high concentrations of ∆-9-tetrahydrocannabinol (THC), seemed to have a greater psychotogenic effect than did hash (resin), which is known to contain much less THC.


We analysed detailed data for history of cannabis use, aiming to: compare the patterns and types of cannabis used between patients with first-episode psychosis and a

Medicine, New York, NY, USA (M Russo PhD)


Correspondence to:


Dr Marta Di Forti, Department of Psychosis Studies, Institute of Psychiatry, King’s College, London SE5 8AF, UK  Published online February 18, 2015 1











population control sample; use the data for pattern of cannabis use to develop a cannabis exposure measure that accurately estimates the risk of psychotic disorders; and calculate the proportion of cases of psychosis in our study area attributable to use of cannabis, particularly high-potency cannabis, if we assumed causality.



Study design and participants


As part of the GAP study,8 we did a case-control study at the inpatient units of the South London and Maudsley (SLaM) NHS Foundation Trust. We approached all patients aged 18–65 years who presented with first-episode psychosis. We invited patients to participate if they met the International Classification of Diseases 10 criteria for a diagnosis of non-affective (F20–F29) or affective (F30–F33) psychosis, validated by administration of the Schedules for Clinical Assessment in Neuropsychiatry (SCAN).9 We excluded individuals who met the criteria for organic psychosis (F09). If patients were too unwell to cooperate, we re-contacted them after the start of treatment.


We recruited controls using internet and newspaper advertisements and by distributing leaflets at train stations, shops, and job centres. None of the advertising material mentioned cannabis or illicit drug use. Volunteers were administered the Psychosis Screening Questionnaire10 and were excluded if they met the criteria for a psychotic disorder or if they reported a previous diagnosis of psychotic illness. This study is part of the GAP study, which was granted ethical approval by SLaM and Institute of Psychiatry Local Research Ethics Committee. All case and control individuals included in the study gave written informed consent.




We obtained sociodemographic data using the Medical Research Council Schedule.11 From March, 2006, we took a more detailed history of cannabis use by adding the Cannabis Experience Questionnaire modified version (CEQmv) to the assessment. 8,12 From the CEQmv, we derived information on history of use of tobacco, alcohol, other recreational drugs, and detailed information on cannabis use (age at first use, duration of use, frequency of use, type used).


Measures of cannabis use relevant to the analysis were: lifetime history of cannabis use—ie, had the individual ever used cannabis at any point in their life (no scores 0, yes scores 1); lifetime frequency of cannabis use—ie, the frequency that characterised the individual’s most consistent pattern of use (none scores 0, less than once per week every week scores 1, at weekends scores 2, every day scores 3); and type of cannabis used—ie, the type most used by the subject (none scores 0, low potency [hash-type] scores 1, high potency [skunk-type] scores 2). This variable was grouped in accordance with the characteristics of the cannabis samples seized by the Metropolitan Police in London, as reported by Potter and colleagues13 and the


See Online for appendix   Home  Office  study  (appendix).14   Finally,  we  used  a








seven-item composite cannabis exposure measure derived from the lifetime frequency of use and the most used type (none scores 0, hash less than once per week every week scores 1, hash at weekends scores 2, hash every day scores 3, skunk less than once per week scores 4, skunk at weekends scores 5, skunk every day scores 6) to investigate which patterns of use conferred the greatest risk.


Statistical analysis


We analysed data using Stata 13. We used χ² tests and t tests (or Mann-Whitney U tests) to test for associations between potential confounding variables and between presence of psychotic disorder and exposure to cannabis use. We also used these tests to establish whether missing data for the cannabis use exposure were associated with case-control status and therefore likely to bias the results.


We used logistic regression to analyse whether individual indicators of cannabis use (lifetime use, age at first use, duration and frequency of use, and most used type of cannabis) improved estimation of the likelihood of psychotic disorders (ie, case status), in comparisons of cannabis users with non-users.

We used the punafcc command in Stata 13 to estimate the population attributable fraction (PAF), with confidence intervals, for each cannabis use variable. The PAF measures the population effect of an exposure by providing an estimate of the proportion of disorder that would be prevented if the exposure were removed. However, causality does not have to be proven before the PAF can be estimated, and this causation is not usually established when PAFs are estimated (indeed no single study could ever prove causation). Because the same proportion of disorder attributable to a specific risk factor can also be attributable to other factors with which the specific risk factor might interact, PAFs for multiple risk factors can add up to more than 100%. Furthermore, the PAF depends on both the prevalence of exposure (ie, measures of cannabis use) in cases and the odds ratio (OR) for the exposure, such that a risk factor with a modest OR can have a major population effect if the factor is common.


Role of the funding source


All funders contributed to data collection by providing the salaries of the research workers collecting the data. The funders of the study had no role in study design, data analysis, data interpretation, or writing of the report. All authors had full access to all the data in the study and had final responsibility for the decision to submit for publication.




Between May 1, 2005, and May 31, 2011, we approached 606 patients with first-episode psychosis. Of these 606 patients, 145 (24%) refused to participate. Thus, we recruited 461 patients with first-episode psychosis. Patients who refused to participate were more likely to be men (p<0·004) and of Black Caribbean and Black African ethnic



2                                                                           Published online February 18, 2015











First-episode Control p value
psychosis group
group (n=370)
Age, years 27·1 (8·7) 30·0 (9·0) 0·0001
Gender ·· ·· 0·004
Male 271 (66%) 209 (56%) ··
Female 139 (34%) 161 (44%) ··
Ethnic origin ·· ·· 0·0001
White 132 (32%) 212 (57%) ··
Black Caribbean 136 (33%) 73 (20%) ··
Black African 98 (24%) 38 (10%) ··
Asian/other 44 (11%) 47 (13%) ··
Education ·· ·· 0·0003
No qualification 60 (15%) 8 (2%) ··
GCSEs 116 (28%) 31 (8%) ··
A levels or vocational training 153 (37%) 151 (41%) ··
University 81 (20%) 180 (49%) ··
Ever employed ·· ·· 0·001
Yes 361 (88%) 353 (95%) ··
No 46 (11%) 15 (4%) ··
No details 3 (1%) 2 (1%) ··


Data are mean (SD) or n (%) unless stated otherwise.


Table 1: Population sociodemographics


origin (p=0·001) than were those who consented. Therefore, in all the analyses, we tested for the potential confounding effects of ethnic origin and gender. During









First-episode Control p value
psychosis group
group (n=370)
Total population
Lifetime history of cannabis use ·· ·· 0·277
Yes 275 (67%) 232 (63%) ··
No (never used) 135 (33%) 138 (37%) ··
Frequency of use ·· ·· <0·0001
Less than once per week 68 (17%) 128 (35%) ··
At weekends 84 (20%) 63 (17%) ··
Every day 123 (30%) 41 (11%) ··
Most used type of cannabis ·· ·· <0·0001
Never used 135 (33%) 138 (37%) ··
Hash-like 57 (14%) 162 (44%) ··
Skunk-like 218 (53%) 70 (19%) ··
Cannabis users
Duration of use (years) 9·7 (7·4) 9·1 (7·8) 0·635
No details 3 1 ··
Age at first cannabis use (years) 16·1 (4·2) 16·6 (3·2) 0·146
No details 3 1 ··
Age at first use ≤15 years ·· ·· 0·028
No 172 (63%) 178 (77%) ··
Yes 100 (36%) 53 (23%) ··
No details 3 1 ··


Data are n (%) or mean (SD) unless stated otherwise.


Table 2: Cannabis use

the same period and from the geographical area served by the clinical units, we recruited 389 control individuals, aged 18–65 years, who were similar to the local population in terms of ethnic origin, education, and employment status (table 1). The later addition of CEQmv meant that there were data missing on detailed patterns of cannabis use for those participants recruited early in the project. The data we present here are therefore based on 410 (89%) of 461 patients with first-episode psychosis and 370 (95%) of 389 controls for whom we had data for cannabis use.


The patients with first-episode psychosis consisted of more men and were younger than the control group (table 1). As noted previously,15 patients with first-episode psychosis were also more likely to be of Black ethnic origin (Caribbean or African) compared with controls, and less likely to have completed a high level of education than were controls (table 1).


A larger proportion of patients with first-episode psychosis (184 [45%] of 410 individuals) reported having smoked 100 tobacco cigarettes or more than did controls (60 [16%] of 370 individuals; p<0·0001), but the groups did not differ in lifetime history of other substance use (p=0·615), or alcohol units consumed per week (p=0·083). Patients with first-episode psychosis were no more likely than were controls to report a lifetime history of ever having used cannabis, but were more likely to use cannabis every day and to mostly use high-potency

(skunk-like) cannabis (table 2). A small proportion of cannabis users (3 [0·6%] of 507 individuals) reported having used cannabis more than four days a week and they were included in the every day category.

Among cannabis users, the mean duration of use did not differ between patients with first-episode psychosis and controls (table 2). On average, both groups started using cannabis in their mid-teens, although distribution of the age at first cannabis use seemed to be skewed (mean 16·1 years, SD 4·2, median 16 years in the patients with first-episode psychosis vs mean 16·6 years, SD 3·2, median 17 years in the control group; Z=2·88; p=0·146). Patients with first-episode psychosis were more likely to start using cannabis at age 15 years or younger than were controls.


When we combined data on frequency of cannabis use and most used type into a single variable, the composite cannabis exposure measure, controls were more likely to be occasional users of low-potency cannabis (hash), and patients with first-episode psychosis were more likely to be daily users of high-potency cannabis (skunk; figure 1; p<0·0001).


A logistic regression, adjusted for age, gender, ethnic origin, number of cigarettes smoked, alcohol units and lifetime use of other illicit drugs, education, and employment history, showed that individuals who had ever used cannabis were not at increased risk of psychotic disorder compared with those who had never used


For more on demographic composition of the local population see www.statistics.  Published online February 18, 2015 3











Patients with first-episode psychosis (n=410)

Controls (n=370)


Skunk every day 25% (n=103)
9% (n=32) 17% (n=70)
Skunk at weekends
use 10% (n=37)
Skunk less than once per week 11% (n=46)
cannabis 10% (n=37)
5% (n=22)
Hash every day
of 7% (n=27)
Pattern Hash at weekends 4% (n=14)
10% (n=35)
5% (n=20)
Hash less than once per week 18% (n=65)
33% (n=135)
Never used cannabis
37% (n=137)
0 10 20 30 40
Proportion of individuals (%)


Figure 1: Patterns of cannabis use between patients with first-episode psychosis and population controls


Odds ratio* (95% CI) p value
Age at first use, years
Never used 1 ··
≥15 years 0·68 (0·34–1·37) 0·292
<15 years 1·55 (1·00–1·39) 0·048
Frequency of use
Never used 1 ··
Less than once per week 0·58 (0·25–1·32) 0·198
Weekends 1·04 (0·41–1·62) 0·929
Every day 3·04 (1·91–7·76) 0·020
Most used type
Never used 1 ··
Hash-like 0·83 (0·52–1·77) 0·903
Skunk-like 2·91 (1·52–3·60) 0·001


*Adjusted for age, gender, ethnic origin, number of cigarettes, alcohol units, other drugs used, education, and employment status.


Table 3: Risk for first-episode psychosis for each measure of cannabis exposure


cannabis (n=775 [data for employment history was missing for five participants, OR 0·93, 95% CI 0·67–1·52, p=0·569). Individuals who started using cannabis at ages younger than 15 years had modestly, but significantly, increased risk of psychotic disorders compared with those who never used cannabis (table 3). People who used cannabis or skunk every day were both roughly three times more likely to have a diagnosis of a psychotic disorder than were those who never used cannabis (table 3).


We used logistic regression (n=775) to test whether the composite cannabis exposure measure predicted risk of psychotic disorder more accurately than the individual markers, frequency of cannabis use and most used type of cannabis, alone. Individuals who mostly used low-potency (hash-like) cannabis occasionally (p=0·493), at weekends (p=0·102), or daily (p=0·626) had no increased likelihood of psychotic disorders compared with those who never used cannabis (figure 2).








Compared with those who never used cannabis, individuals who mostly used skunk-like cannabis were nearly twice as likely to be diagnosed with a psychotic disorder if they used it less than once per week (p=0·020), almost three times as likely if they used it at weekends (p=0·008), and more than five times as likely if they were daily users (p=0·001; figure 2).


Based on the estimated adjusted OR for daily cannabis use (3·04, 95% CI 1·91–7·76), we calculated that, if we assumed causality, 19·3% (13·1–27·0) of psychotic disorders in the study population were attributable to exposure to daily cannabis use. The PAF of psychotic disorders in the study population that were attributable to high potency cannabis use was 24·0% (17·4–30·6) and the PAF for the two exposures combined, skunk use every day, was 16·0% (14·0–20·3; table 4). If causality is assumed, this finding suggests that skunk alone was responsible for the largest proportion of new cases (24%) of psychotic disorder in the study population, an effect driven by its high prevalence among patients with first-episode psychosis who used cannabis (218 [53%] of 410 patients).




The results of our study support our previous conclusions from analysis of part of the sample;8 use of high-potency cannabis (skunk) confers an increased risk of psychosis compared with traditional low-potency cannabis (hash). Additionally, because of the increased sample size in the present study, we were able to combine information on frequency of use and type of cannabis used into a single measure. This combined measure suggested that the strongest predictor of case-control status (ie, predictor of whether a random individual would be case or control) was daily-skunk use. Figure 2, which shows the adjusted ORs for psychotic disorders for each of the composite cannabis exposure measure groups, shows how the ORs for skunk users increase with the frequency of use.


Samples of skunk seized in the London area in 2005,13 2008,14 and more recently, as reported by Freeman and colleagues,16 contained more THC than did samples of hash, and virtually no cannabidiol. Use of cannabis with a high concentration of THC might have a more detrimental effect on mental health than use of a weaker form. Indeed, in line with epidemiological evidence,2,3 the results of experimental studies17,18 that investigated the acute effects of intravenous administration of THC in non-psychotic volunteers showed that the resulting psychotic symptoms were dependent on the dose. Furthermore, the scarcity of cannabidiol in skunk-like cannabis might also be relevant because evidence suggests that cannabidiol ameliorates the psychotogenic effect of THC and might even have antipsychotic properties.19,20 The presence of cannabidiol might explain our results, which showed that hash users do not have any increase in risk of psychotic disorders compared with non-users, irrespective of their frequency of use. Morgan and colleagues21 previously reported that, in healthy volunteers who smoked cannabis, individuals with



4                                                                           Published online February 18, 2015











hair traces of THC and cannabidiol had fewer schizophrenia-like symptoms than those with hair traces of THC only.

In our results, a combined measure of exposure to cannabis, daily use of high-potency cannabis, predicted a greater risk of psychotic disorders than did the single measures of either frequency or potency. However, a simple yes-or-no question of whether people use skunk might be more useful to identify those at increased risk to develop psychosis because of their cannabis use. In view of the high prevalence of skunk use in our study population, if a causal role for cannabis is assumed, skunk use alone was responsible for 24% of those adults presenting with first-episode psychosis to the psychiatric services in south London.


South London has one of the highest recorded incidence rates of psychosis in the UK.22 Boydell and colleagues23 showed that the incidence of schizophrenia had doubled since 1965,24 and that one possible contribution to this was the increase in cannabis use among individuals who developed schizophrenia. In the present study, we identified an increased estimate for the PAF accounted for by cannabis (24%) compared with previous studies, which reported PAFs of 6·2% in Germany,25 8% in New Zealand,26 and 13·3% in Holland.5 This finding could be caused by, not only the greater use of cannabis, but also the greater use of high-potency (skunk-like) cannabis in south London than in these other countries in earlier periods.27


Hickman and colleagues6 suggested that the number of people who need to be treated to stop their cannabis use to prevent one case of schizophrenia is large, but would become substantially lower if more was understood about which individuals are at greatest risk because of their pattern of use or their susceptibility to psychosis.6 In relation to susceptibility to schizophrenia, Henquet and colleagues25 calculated that the PAF for individuals in the general population with a predisposition for psychosis at baseline was more than double (14·2%) that of the total population (6·2%). Our data suggest that the potency of the cannabis used also needs to be taken into account in calculations of the PAF.


The strategy we used for control recruitment, based on a variety of advertising strategies rather than on random selection, might have biased the findings. However, the final sample of controls was similar, according to the last UK census data, to the population from which the cases were drawn. Moreover, rather than this approach undersampling individuals who used cannabis, the proportion of controls with a history of cannabis use (63%) was more than the national average (40%) for similar age groups,28 showing the high prevalence of cannabis use in south London. Furthermore, if we had oversampled individuals who used cannabis, this oversampling would have caused underestimation of the effects of cannabis use on risk of psychotic disorders.


A theoretical explanation of why skunk might have been preferred by patients with first-episode psychosis is that, when they began to experience their illness prodrome, these









12 5·40*
(OR) 10 2·70*
psychosis 6
of 3 1·90
Risk 0·49 0·91
1 1 0·62
cannabis once week weekends y than week weekends y
than every da less every da
used less per Hash per Skunk
Never Hash Hash at Skunk    once Skunk at
Pattern of cannabis use


Figure 2: Probability of individuals having a psychotic disorder by pattern of cannabis use


OR adjusted for age, gender, ethnic origin, education, employment status, and tobacco use. OR=odds ratio. *p<0·05.


Odds ratio* Prevalence of exposure Population
(95% CI) in patients with first- attributable fraction
episode psychosis (95% CI)
Daily cannabis use 3·04 (1·91–7·76) 123/410 (30%) 19·3% (13·1–27·0)
Skunk use 2·91 (1·52–3·60) 218/410 (53%) 24·0% (17·4–30·6)
Skunk use every day 5·40 (2·80–11·30) 103/410 (25%) 16·0% (14·0–20·3)


*Adjusted for age, gender, ethnic origin, number of cigarettes, alcohol units, other drugs used, level of education, and employment status.


Table 4: Population attributable fraction for daily use of cannabis, skunk use, and skunk use every day


individuals might have sought increased concentrations of THC to self-medicate. However, experimental studies show that THC induces psychotic symptoms, while cannabidiol ameliorates them and reduces anxiety.16–19 That people who already have prodromal symptoms would choose a type of cannabis that is high in THC and has little cannabidiol (such as skunk), which might exacerbate their symptoms, rather than a cannabidiol-containing type (such as hash), would seem counterintuitive.


A possible limitation of our study is the absence of data on number of joints or grams used per day. However, because we collected information about use over a period of years and not about present use, the reliability of such detailed information would probably have been confounded by recall bias to a greater extent than was the general description of pattern of use that we obtained. The fact that we were able to collect detailed information on other environmental factors and control for their potential confounding effects is a key strength of our study.


Our findings show the importance of raising public awareness of the risk associated with use of high-potency cannabis (panel), especially when such varieties of cannabis are becoming more available.29 The worldwide  Published online February 18, 2015 5











Panel: Research in context


Systematic review


We searched PubMed for studies that estimated the effect of cannabis use on the number of new cases of psychosis arising in specific populations, using both the terms “population attributable fraction”, and “number needed to treat”. We also searched for studies that investigated the association between the “high potency and/or skunk” type of cannabis and psychosis. We included all studies available on PubMed until Sept 31, 2014. We identified three studies,7,8.16 all of which met our inclusion criteria.




The association between cannabis use and increased risk of developing schizophrenia-like psychosis has been consistently reported by prospective epidemiological studies.2,3 Our previous study was the first to show that use of high-potency (skunk-like) cannabis carries the highest risk for psychotic disorders.8 In the present larger sample analysis, we replicated our previous report and showed that the highest probability to suffer a psychotic disorder is in those who are daily users of high potency cannabis. Indeed, skunk use appears to contribute to 24% of cases of first episode psychosis in south London. Our findings show the importance of raising awareness among young people of the risks associated with the use of high-potency cannabis. The need for such public education is emphasised by the worldwide trend of liberalisation of the legal constraints on cannabis and the fact that high potency varieties are becoming much more widely available. Finally, in both primary care and mental health services, a simple yes-or-no question of whether people use skunk might be more useful to identify those at increased risk to develop psychosis because of their cannabis use.


trend of liberalisation of the legal constraints on the use of cannabis further emphasises the urgent need to develop public education to inform young people about the risks of high-potency cannabis.




In collaboration with the Genetics and Psychosis Study (VM, TRM, SAS, MR, AM, JO’C, CI, PD, CP) and the PUMP study (FG, ZA, PG-S) teams, MDF, AT, and SAS collected the data and MDF prepared the data for the analysis. MDF did the data analysis with CM. MB and FB contributed to the data entry. ML and RMM supervised MDF in the interpretation of the results. EC and SF contributed to the literature review and to the selection of the references. ASD and JP reviewed the manuscript and contributed to its final draft. All authors had full access to all data (including statistical reports and tables) in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.


Declaration of interests


RMM reports honoraria from Otsuka, Lundbeck, and Janssen, which he received for lecturing on the report of the Schizophrenia Commission. All other authors declare no competing interests.




The study was funded by the UK National Institute of Health Research (NIHR) Specialist Biomedical Research Centre for Mental Health, the South London and Maudsley (SLaM) NHS Foundation, the Institute of Psychiatry of King’s College London, the Psychiatry Research Trust, Maudsley Charity Research Fund, and the European Community’s Seventh Framework Programme (grant agreement No. HEALTH-F2-2009-241909 [project EU-GEI]). The study was supported by the Genetics and Psychosis (GAP) and Physical Health and Substance Use Measures in First Onset Psychosis (PUMP) study teams of the Institute of Psychiatry, King’s College London, and SLaM.



  • Coombes R. Cannabis regulation: high time for change? BMJ 2014;

348: g3382.


  • Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and

risk of psychotic or affective    mental health outcomes: a systematic

review. Lancet 2007; 370: 319–28.


  • Casadio P, Fernandes C, Murray RM, Di Forti M. Cannabis use in young people: the risk for schizophrenia. Neurosci Biobehav 2011; 35: 1779–87.








  • Schizophrenia Commission. The abandoned illness: a report by the

Schizophrenia Commission. London: Rethink Mental Illness, 2012.


  • van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study.

Am J Epidemiol 2002; 156: 319–27.


  • Hickman M, Vickerman P, Macleod J, et al. If cannabis caused schizophrenia—how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations. Addiction 2009; 104: 1856–61.


  • Smith N. High potency cannabis: the forgotten variable. Addiction

2005; 100: 1558–60.


  • Di Forti M, Morgan C, Dazzan P, et al. High-potency cannabis and the risk of psychosis. Br J Psychiatry 2009; 195: 488–91.


  • Schedules for clinical assessment in neuropsychiatry (SCAN). Geneva: World Health Organization, 1992.


  • Bebbington P, Nayani T. The psychosis screening questionnaire.

Int J Methods Psychiatry Res 1995; 5: 11–19.


  • Mallett R, Leff J, Bhugra D, Pang D, Zhao JH. Social environment, ethnicity and schizophrenia. A case-control study.

Soc Psychiatry Psychiatr Epidemiol 2002; 37: 329–35.


  • Di Forti M, Iyegbe C, Sallis H, et al. Confirmation that the AKT1 (rs2494732) genotype influences the risk of psychosis in cannabis users. Biol Psychiatry 2012; 72: 811–16.


  • Potter DJ, Clark P, Brown MB. Potency of delta 9-THC and other cannabinoids in cannabis in England in 2005: implications for psychoactivity and pharmacology. J Forensic Sci 2008; 53: 90–94.


  • Hardwick S, King L. Home Office cannabis potency study 2008. London: Home Office Scientific Development Branch, 2008.


  • Morgan C, Kirkbride J, Hutchinson G, et al. Cumulative social disadvantage, ethnicity and first-episode psychosis: a case-control study. Psychol Med 2008; 38: 1701–15.


  • Freeman TP, Morgan CJ, Hindocha C, Schafer G, Das RK, Curran HV. Just say ‘know’: how do cannabinoid concentrations influence users’ estimates of cannabis potency and the amount they roll in joints? Addiction 2014; 109: 1686–94.


  • Murray RM, Morrison PD, Henquet C, Di Forti M. Cannabis, the mind and society: the hash realities. Nat Rev Neurosci 2007; 8: 885–95.
  • D’Souza DC, Perry E, MacDougall L, et al. The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis. Neuropsychopharmacology 2004; 29: 1558–72.


  • Englund A, Morrison PD, Nottage J, et al. Cannabidiol inhibits THC-elicited paranoid symptoms and hippocampal-dependent memory impairment. J Psychopharmacol 2013; 27: 19–27.


  • Leweke F, Piomelli D, Pahlisch F, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry 2012; 2:


  • Morgan CJ, Curran HV. Effects of cannabidiol on schizophrenia-like symptoms in people who use cannabis. Br J Psychiatry 2008;
    • 306–07.


  • Kirkbride JB, Fearon P, Morgan C, et al. Heterogeneity in incidence rates of schizophrenia and other psychotic syndromes: findings from the 3-center AeSOP study. Arch Gen Psychiatry 2006; 63: 250–58.


  • Boydell J, van Os J, Lambri M, et al. Incidence of schizophrenia in south-east London between 1965 and 1997. Br J Psychiatry 2003;
    • 45–49.


  • Boydell J, van Os J, Caspi A, et al. Trends in cannabis use prior to first presentation with schizophrenia, in South-East London between 1965 and 1999. Psychol Med 2006; 36: 1441–46.


  • Henquet C, Krabbendam L, Spauwen J, et al. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ 2005; 330:


  • Arseneault L, Cannon M, Witton J, Murray RM. Causal association between cannabis and psychosis: examination of the evidence.

Br J Psychiatry 2004; 184: 110–17.


  • World Drug Report 2009. Vienna: United Nations Office on Drugs and Crime, 2009.


  • Home Office, Research, Development and Statistics Directorate, BMRB. British crime survey, 2007–2008. London: Home Office, 2008.
  • Cascini F, Aiello C, Di Tanna G. Increasing delta-9-tetrahydrocannabinol (Δ-9-THC) content in herbal cannabis over time: systematic review and meta-analysis. Curr Drug Abuse Rev 2012; 5: 32–40.



6                                                                           Published online February 18, 2015

Topic: Dashboard Benchmark Evaluation


the paper is on a review of a performance dashboard for a health care organization written in a report. choosing OPTION 1 from the assignment instructions. (provided the simulation dashboard transcript to refer from). structure the report per instructions so a colleague or supervisor can refer to it with ease.

The hospital in the simulation is located in Minnesota so state, local and federal benchmarks to compare can be searched online. I provided detailed assignment instructions with competencies that need to be met at either proficient or distinguished per scoring guide provided.

I provided references if any other references are used they need to be peer-reviewed and less than 5 years old. Instructions don’t specify how long the report needs to be I put 4 pages if additional needed let me know. any questions please message me, thanks

Topic: Borderline Personality Disorder

Write 2 pages paper excluding the title page and the reference page in APA format supported by at least 3 current, credible scholarly sources for each paper. Credible sources include scholarly peer-reviewed journal articles, evidence-based resources, and professional (org), educational (.edu), and government websites (.gov).

Commercial websites (.com) are not considered credible sources. Also referencescant be older than 5 years old. Sample SOAP note paper attached for guidance. Please don’t plagiarism or reworded the paper, the paper will be run through SafeAssign software for plagiarism.


Please note: This paper require a title page, introduction, body of the paper, conclusion, and reference page.

  • The introductionshould provide an overview of the topic, the purpose of the paper, and topics that will be addressed.
  • The bodyof the paper needs to address all required topics.
  • The conclusionought to provide closure for the reader, synthesize the content, and tie everything together to help clarify the main points of the paper.
  • The reference pageshould include all references cited in the assignment in correct APA format.
  • An abstract is not required. The use of direct quotes is discouraged and should only be used when the source material uses language that is particularly striking or notable.




Title: Therapy for Clients With Personality Disorders


Borderline Personality Disorder




Write a description of the personality disorder you selected (Borderline Personality Disorder). Explain a therapeutic approach (including psychotropic medications if appropriate) you might use to treat a client presenting with this disorder, including how you would share your diagnosis of this disorder to the client in order to avoid damaging the therapeutic relationship. Support your approach with evidence-based literature.



Chronic obstructive pulmonary disease is also known as chronic obstructive lung disease and chronic obstructive airway disease, among others. It is a type of obstructive lung disease characterized by chronically poor airflow. It typically worsens over time. The main symptoms include shortness of breath, cough, and sputum production. Most people with chronic bronchitis have COPD.

Tobacco smoking is the most common cause of COPD, with a number of other factors such as air pollution and genetics playing a smaller role.  In the developing world, one of the common sources of air pollution is from poorly vented cooking and heating fires. Long-term exposure to these irritant causes an inflammatory response in the lungs resulting in narrowing of the small airways and the breakdown of lung tissue known as emphysema.

COPD can be prevented by reducing exposure to the known causes. This includes efforts to decrease rates of smoking and to improve indoor and outdoor air quality. COPD treatments include; quitting smoking, vaccinations, rehabilitation, and often inhaled bronchodilators and steroids. Some people may benefit from long-term oxygen therapy or lung transplantation.

In those who have periods of acute worsening, increased use of medicines and hospitalization may be needed. Worldwide, COPD affects 329 million people or nearly 5% of the population. In 2012, it ranked as the third-leading cause of death, killing over 3 million people. The number of deaths is projected to increase due to higher smoking rates and an aging population in many countries.

History of autism essay

Autism spectrum disorder

Autism is a general term for a group of complex disorders of brain development. These disorders are characterized by difficulties in social interaction, both verbal and non verbal communication and repetitive behaviors.

It has its roots in very early brain development. Obvious signs of autism appear between the ages of 2 and 3. Early diagnosis is very important since intervention through therapy can improve the outcome.

According to statistics, 1 in 68 American children suffer from autism, a ten-fold increase in prevalence in 40 years. This increase is accredited to widespread awareness and improved diagnosis.

Studies also show that autism is four to five times more common among boys than girls. An estimated 1 out of 42 boys and 1 in 189 girls are diagnosed with autism in the United States. Big difference right?

Autism affects over 2 million individuals in the U.S. and tens of millions worldwide. Only recently, scientists discovered that there is no one cause of autism. Rare gene changes and mutations are associated with autism. Most cases of autism, however, appear to be caused by a combination of risk genes and environmental factors surrounding brain growth.

Some genetic causes include; advanced parental age of both parents, maternal illness during pregnancy, difficulties during birth especially those that deprive the baby of oxygen. A growing body of research suggests that women can reduce risk of having a child with autism by taking prenatal vitamins containing folic acid before and after conception.

Each individual with autism is unique, have exceptional abilities in visual skills, music, art and academic skills. Others have disability and cannot live independently. Families can attest to the fact that raising an autistic child needs lots of care but in the end, love counts more than anything. It is not the end of the world.

How to prevent Insomnia essay

Causes and effects of INSOMNIA

It is a sleep disorder that is characterized by difficulty falling asleep and or staying asleep. Other symptoms may be waking up often during the night, having trouble falling back asleep, waking up too early in the morning or feeling too tired upon waking up. These may sound normal to many since many people count sheep or even beats to a certain song so as to lull themselves to sleep.

There are two types of insomnia:

(a) Primary; which is a type of insomnia that is not associated with any other health condition and

(b) Secondary; this type of insomnia is associated with other health conditions such as asthma. The determination of a type of insomnia also depends on the amount of time it lasts. Short term insomnia is also known as acute insomnia and is not as serious as chronic insomnia which lasts long.

Causes of insomnia may vary from one individual to another but have roots based on the psychological state of a human being. Such causes include: emotional/ physical discomfort; probably due to one’s surroundings or what one is currently going through in his/her life, environmental factors when one is asleep e.g. light or noise may definitely affect one’s sleep since the brain is alert, medications for example those used in the treatment of allergies or colds and interferences in normal sleep schedule such as change from night shift to a day shift or jet lag after travel by airplane.

Chronic insomnia has its own list of causes: –

  • Depression
  • Chronic stress
  • Pain/discomfort at night

30% to 50% of the general population has insomnia with 10% suffering from chronic insomnia. Simple treatments for insomnia vary from proper sleeping habits to maintaining a sleeping schedule. There are also methods such as self-hypnosis which helps the mind to relax.

Taking the right meals right before you sleep and avoiding consumption of fluids as well as nicotine and caffeine before going to bed promotes good sleep. Those who have free time during the day should limit the time they spend during naps. Naps should last a maximum of 15 minutes during the day, experts say.

There are also available insomnia medications for example Ramelteon (Rozerem) which promotes the onset of sleep. This is a prescription drug which individuals should ensure to get from their doctors. However there are over the counter drugs available in pharmacies for example diphenhyndramine (Benandryl) that induces drowsiness but does not improve sleep and should not be used to treat chronic insomnia. This drug is an antihistamine with sedative properties.

Studies have shown that insomnia is a common disorder in many people in the US and UK and therefore individuals should get checked out if and when symptoms present themselves. Sleep being very important, we cannot afford to have a sleepless nation if we want good quality of work and service.