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Provide feedback. Follow us on This is the highest number of drug deaths in twenty years, and is similar to the number recorded in the late s, when a steep increase in opioid use, specifically heroin, led to deaths peaking at 1, in Although the number of drug induced deaths is the highest on record, the death rate per capita of 7.
Changes in drug deaths have been significant over this period. In , an individual dying from a drug induced death in Australia was most likely to be a middle aged male, living outside of a capital city who is misusing prescription drugs such as benzodiazepines or oxycodone in a polypharmacy the use of multiple drugs setting. The death was most likely to be an accident.
Physical Activity and the Development of Substance Use Disor : Progress in Preventive Medicine
This profile is quite different from that in , where a person who died from a drug induced death was most likely to be younger early 30s with morphine, heroin or benzodiazepines detected on toxicology at death. There was also a perception among respondents that it caused the most drug deaths when excluding alcohol and tobacco.
While prescription drugs actually cause the highest numbers of drug induced deaths, there has been a rapid increase in the number of methamphetamine deaths, with the death rate in four times that in 1.
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Across the whole population, younger Australians under 35 years of age have lower rates of drug induced death when compared to , while older Australians 45 and over generally have higher rates. This also reflects changes in the types of drugs causing death. Deaths from illicit substances like heroin and methamphetamines tend to occur among younger age groups, while deaths from benzodiazepines and prescription opiates tend to occur among older people.
This article provides further information and analysis on drug induced deaths in Australia in If you are concerned about your own drug use or that of a family member, friend, or colleague, talk to your general practitioner. There are also many organisations which are able to provide help and support. A list of contacts is included at the end of this article. Defining a Drug Induced Death Understanding what constitutes a drug death is complex as mortality from drug use manifests in a multitude of forms. Deaths can be directly attributable to drug abuse such as overdoses, or deaths can occur where a drug is found to be a contributory factor such as a traffic accident where the deceased was found to be under the influence of a substance at time of death.
This article focusses in the main on drug induced deaths. Information on drug related deaths is included towards the end of the article. In Australia, acute drug overdose deaths are referred to a coroner and subject to forensic pathology and toxicology. Autopsy and toxicology reports provide detailed drug information including the identification of specific drugs in the system, approximate levels of drugs in the system and the relatedness of drugs to the death. The Australian Bureau of Statistics accesses this information via the National Coronial Information System and applies codes from the International Classification of Diseases, 10th Revision, to the medical text for tabulation into statistical output.
For the purposes of this report, deaths are output using a modified version of a drug induced death tabulation created by the United States Center for Disease Control and Prevention CDC. The tabulation, which consists of ICD codes can be found here. The CDC drug induced death listing includes overdose deaths of all intents i.
Tobacco has been removed from the tabulation, as the links between smoking and premature mortality, especially in relation to chronic respiratory diseases, is well documented. Excluded from the article are deaths due to drug use in a surgical procedure e.
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Deaths due exclusively to alcohol abuse require specific demographic considerations, and display complications which are distinctive compared to those of drug deaths.. Therefore alcohol related deaths will be explored in future analytical work. Drug Induced Deaths over time Following peak rates of deaths in the late 90s, rates of drug deaths were relatively stable in the early to mids. From there has been a significant increase in rates of drug induced deaths, with a preliminary rate of 7.
The table below shows a 20 year time series of age standardised death rates per , persons. In addition to demonstrating the peak period of drug deaths in and the significant increases in recent years, the table also shows the consistently higher rates of drug induced deaths in males. Over the last two decades, the death rate for males has on average been 1. Although the incline in death rates is more defined in males, both males and females have experienced significant increases over the last five years.
It is therefore expected that rates of drug induced deaths would be higher among males. The high number of heroin related deaths in and corresponding decrease in the early s has been well documented and reported Degenhardt et al. It should be noted that this period also corresponds with the ABS changing classifications from ICD-9 to ICD and the subsequent move to utilising the National Coronial Information System for accessing information relating to a death. However, it is not expected that these administrative changes would have significantly impacted drug death data over this period.
Source s : Drug induced deaths, standardised death rates a b c d e Premature mortality and Drug Induced Deaths Australians currently boast an estimated life expectancy at birth of Looking at a cumulative frequency of deaths for the whole population and comparing that to a cumulative frequency for drug induced deaths, the links of drug misuse to premature mortality are stark. On average, a person who dies from a drug induced death loses Of note, people In addition, many people who died from a drug induced death were living with a chronic health condition.
For example, people 6. Understanding the social and health determinants behind drug misuse and mortality aids in the formulation of effective policy and prevention programs. Composition of Drug Induced Deaths The majority of drug induced deaths in were due to acute accidental overdoses Other types of drug deaths, including addictions and chronic complications of drug abuse as well as homicide and undetermined intent accounted for the remaining 6.
The table below highlights that the composition of drug induced deaths is similar for both males and females. Notably, females have a higher proportion of suicidal drug overdoses On average, for both males and females, accidental drug induced deaths occurred at an earlier age than intentional overdoses. Accidental drug overdoses in had a median age of 42 years for men and 46 years for women. In contrast, suicidal overdoses recorded a median age of death of 51 for men and 52 for women. Proportion of acute drug deaths by sex, a b a Causes of death data for are preliminary and subject to a revisions process.
The graph below shows the ASDRs for males and females from , alongside those of There has been a clear shift from peak rates of drug deaths in younger age groups to middle-aged groups. In , males had the highest rate of death between ages 25 to 29, compared with 35 to 39 years in Females also had the highest rate of death between ages 25 to 29 in This peak rate has shifted in , with women aged between 45 and 49 now recording the highest rate of death.
The shifting age profile of drug induced deaths is an important issue. It is clear that the rate of drug death among younger people has decreased significantly, yet among older age groups, the rate of drug induced is now much higher. This is especially the case among people between the age of 45 and The average age of initiation of drug use has increased from In particular, there has been a large shift in average age of initiation for the misuse of pharmaceutical drugs, increasing from There was also an increase in the proportion of people aged over 35 who used drugs illicitly compared with , with the increase of drug use in year olds being marked as significant.
On the other hand, dyslipidemia has been shown to be significantly associated with olanzapine treatment independently of body mass There are also indications of a direct lipogenic effect of olanzapine caused by increased expression of lipid biosynthesis genes Despite the obvious risks due to metabolic side effects, AP use has not been consistently shown to increase CVD morbidity or mortality in schizophrenia.
Osborn and colleagues 18 concluded that the excess death rates found among mentally ill people could not be explained neither by smoking, social deprivation, nor by the use of AP medication alone, although patients on APs seemed to be at even greater risk than those without.
In a recent meta-analysis of drug trials with placebo controls, AP use was not found to be related to increased mortality in schizophrenia, although the higher general mortality in this patient group was replicated Furthermore, two large Finnish registry studies demonstrated reduced mortality from all causes in people with schizophrenia on long-term treatment with APs 98 , Better somatic care in patients receiving AP medication could be part of the explanation, however, debate continues on the interpretation of these findings and the role of APs in the all-over schizophrenia mortality 41 , , In addition, sudden cardiac death in schizophrenia has in several studies been associated with the use of APs, most probably related to arrhythmias — Not every study confirms this picture; Manu and co-workers found that unexpected deaths in people with schizophrenia most likely was due to coronary events and found no hypermortality related to higher levels of AP-treatment.
Several lines of evidence indicate shared underlying pathobiology between schizophrenia and CVD, beyond the effects accounted for by lifestyle and AP medication. First, this relationship might be due to common genetic factors that contribute to both comorbid medical conditions and mortality in schizophrenia In particular, there seems to be overlapping genes associated with both increased CVD-risk factors and schizophrenia , This might explain recent findings that first-episode psychosis patients not treated with AP medication are more likely to have obesity, insulin-resistance, dyslipidemia, and hypertension compared with age-matched healthy controls 26 , , and the pre-AP era findings mentioned above see Antipsychotic Medication.
Recent molecular studies have indicated that there are abnormalities in the glucose metabolism and insulin signaling pathways in subgroups of unmedicated people with schizophrenia indicating a shared genetic vulnerability between type-2 diabetes and schizophrenia in some cases Third, pathways involving the hypothalamic—pituitary—adrenal axis HPA might be involved. First-episode psychosis patients have increased cortisol levels 28 possibly due to environmental stress and these alterations in the HPA-axis might account for some of the increased CVD mortality Finally, recent studies have implicated the immune system in severe mental disorders such as schizophrenia , , as well as in CVD , and it is possible that the increased CVD-risk associated with schizophrenia is related to inflammatory mechanisms Patients with severe mental disorders report greater difficulty and more barriers in accessing primary health care These patient groups also receive poorer quality of somatic health care services from hospitals.
Thus, there is an increased risk for serious conditions to be undiagnosed or inadequately treated , People with schizophrenia seem to receive less somatic health care also compared to people with other mental disorders 6 , — In schizophrenia, it is shown that treatment and prevention for CVD is suboptimal, and this seems to affect mortality , This is supported by an increased mortality due to other somatic conditions besides CVD In the literature, there are a number of reports of people with schizophrenia who appear to experience little pain despite suffering from painful acute medical conditions, such as myocardial infarction or perforated bowel A meta-analysis of 12 studies on pain perception in schizophrenia indicated reduced pain sensitivity The hypoalgesia was also found in drug-free patients, consistent with clinical observations of reduced sensitivity to pain in schizophrenia reported before the introduction of APs.
Pain insensitivity is also found in the healthy relatives of patients with schizophrenia, suggesting a genetic component There is a concern that lack of physical pain sensitivity may result in potentially serious medical conditions passing undiagnosed in schizophrenia There is some evidence that the insula, a cortical structure with extensive connections to different parts of the cortex and the limbic system, is affected in schizophrenia. Apart from patient-related barriers, inadequately organized somatic care in the mental health services and an existing culture with little focus on somatic health issues in psychiatric or mental health clinics may be an important part of the explanation , Reducing smoking-related mortality will require the delivery of effective anti-smoking strategies.
Smoking cessation may have considerable impact on CVD death risk, while just a reduction in smoking does not seem to have the same effect , Both pharmacological and psychosocial interventions for smoking cessation have been found to be useful in helping people with schizophrenia quit smoking, but the evidence for a lasting effects is poor Concerns that individuals with severe mental illness might suffer negative mental consequences when quitting smoking seem to have little scientific support , In a Cochrane review of 21 trials , pharmacological treatment with bupropion, a dopamine agonist, was found to increase smoking abstinence rates in smokers with schizophrenia.
Another pharmacological agent, varenicline, a nicotinic receptor partial agonist, could also facilitate smoking cessation, but with possible psychiatric adverse effects. Psychological interventions such as contingent reinforcement might also help people with schizophrenia to quit or reduce smoking in the short-term. At the present time, there are indications that individuals with schizophrenia can stop smoking with appropriate help, although, convincing evidence that such interventions have a long-term benefit is lacking.vibelecdentchea.tk
Health matters: preventing drug misuse deaths
Patients with schizophrenia have low levels of physical activity Increased physical exercise has beneficial effect on several CVD-risk factors such as body weight and blood lipid concentrations and may reduce mortality Improvement in physical fitness seems possible in schizophrenia , and improved physical fitness seems likely to reduce the elevated mortality in this patient group A Cochrane database review concludes that exercise programs are feasible and may improve mental well-being and overall outcome among patients with schizophrenia , as well as in mental illness in general Positive results of promoting physical exercise in people with schizophrenia in outpatient and day care settings have also been reported — The association between high cardiorespiratory fitness specifically max oxygen uptake — VO max and low risk of CVD independently of weight reduction is established in healthy men and women Studies have shown that people with schizophrenia have reduced peak oxygen uptake, but are capable of participating in physical exercise programs, which improve their peak oxygen uptake , The effect of the improvement seems to be comparable with effects of physical training in healthy controls and patients with CVD Obesity is a condition mainly caused by a relative excess intake of calories versus energy expenditure.
A focus on these parameters diet and activity is therefore a natural starting point for prevention and treatment. Effective weight management may best be reached by the implementation of several measures in an integrated fashion. As there is a complex interplay between the factors responsible for obesity and the other components of the MetS e.
Diet modifications may hold some of the same benefits as physical activity for reducing CVD-risk Specific diets e. Studies have shown that weight reduction is possible when applying specific intervention programs for individuals with psychotic disorders , The combined effect of behavioral intervention, nutritional information, and physical exercise was investigated in a study of people with schizophrenia and body mass index BMI exceeding The 3-month intervention program showed significant reduction in weight and BMI, which lasted 12 months Intriguingly, weight reduction was gradual, with increasing weight loss as the program progressed, in contrast to weight reductions patterns in diet programs in healthy individuals, where there is often a larger reduction of weight early on.
People with schizophrenia treated with atypical APs participated in a 1-year multimodal weight control program, comprising nutrition, exercise, and behavioral interventions. Clinically significant reductions in weight and other risk factors for poor somatic health, including hemoglobin A1c were found in the patients who participated in the program. In contrast, patients who did not receive the weight control intervention continued to gain weight A Cochrane review investigating the effects of 23 randomized controlled trials found that modest weight reduction can be obtained in people with schizophrenia with selective pharmacological and psychological interventions both on diet and activity levels For established obesity or MetS, pharmacological and surgical treatment may be needed and constitute important adjunctive measures.
Finding safe and effective pharmacological interventions is difficult. Several drugs have been tested for weight reduction. There is evidence for some efficacy for different classes of drugs currently on the market such as, e. Amphetamine-like appetite suppressants e. Sibutramin was withdrawn from the European markets in because of cardiovascular side effects.