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OBJECTIVE: This article describes the patient management processes developed during the Council of Australian Governments (COAG) coordinated care trial and use of health outcome measures to monitor changes in utilisation patterns and patient well-being over time for a subgroup of 398 patients with type 2 diabetes. DESIGN: The Eyre component of the South Australian (SA) HealthPlus coordinated care trial was a matched geographically controlled study in which the outcomes for the intervention group of 1350 patients were compared with those of a similar control group of 500 patients in another rural health region in SA. SETTING: The trial was carried out on Eyre Peninsula in SA across populations in rural communities and in the main centres of Whyalla, Port Lincoln and Ceduna. Care planning was organised through general practitioner practices and services negotiated with allied health services and hospitals to meet patient needs. SUBJECTS: The SA HealthPlus trial included 1350 patients with chronic and complex illness. A subset of this group comprising 398 patients with type 2 diabetes is described in this report. Patients recruited into the three-year trial were care planned using a patient centred care planning model through which patient goals were generated along with medical management goals developed by clinicians and primary health care professionals. Relevant health services were scheduled in line with best practice and care plans were reviewed each year. Patient service utilisation, progress towards achieving health related goals and patient health outcomes were recorded and assessed to determine improvements in health and well-being along with the cost and profile of the services provided. RESULTS: Significant numbers of patients experienced improved health outcomes as a consequence of their involvement in the trial, and utilisation data showed reductions in hospital and medical expenditure for some patients. These results suggest that methods applied in the SA HealthPlus coordinated care trial have led to improvements in health outcomes for patients with diabetes and other chronic illnesses. In addition, the processes associated with the COAG trial motivated significant organisational change in the Regional Health Service as well as providing an opportunity to study the health and well-being outcomes resulting from a major community health intervention. CONCLUSIONS: The importance of the SA HealthPlus trial has been the demonstrated link between a formal research trial and significant developments in the larger health system with the trial not only leading to improvements in clinical outcomes for patients, but also acting as a catalyst for organisational reform. We now need to look beyond the illness focus of health outcome research to develop population based health approaches to improving overall community well-being. [ABSTRACT FROM AUTHOR]

Objective: To analyse the prevalence of neural tube defects in small geographical areas and seek to explain any spatial variations with reference to environmental lead and deprivation.Setting: The Fylde of Lancashire in the north west of England.Design: Cases were ascertained as part of a prospective survey of major congenital malformations in babies born in the Fylde to residents there between 1957 and 1981. A matched case-control analysis used infants with cardiovascular system, alimentary tract, and urinary system malformations as controls. Conditional logistic regression was used to assess the effects of more than 10 micrograms/l lead in drinking water and the Townsend deprivation score.Results: The prevalence of neural tube defects in 1957-73 was higher in Blackpool, Fleetwood, and North Fylde, whereas the three control groups showed no significant spatial variation. In 1957-81 mothers living in electoral wards with either a higher proportion of houses with more than 10 micrograms/l lead in the water or a higher deprivation score had a greater risk of having a baby with a neural tube defect. For spina bifida and cranium bifidum alone, this was also true. For anencephaly, deprivation was less important although the effect of lead was still seen. In some neural tube defects, lead may act independently of other possible factors associated with deprivation. It seemed unlikely that lead levels changed significantly during the survey. The percentage of houses with 10 micrograms/l or more of lead in the water in 1984-5 was similar to that found in Great Britain 10 years previously.Conclusion: There is evidence to suggest that lead is one cause of neural tube defects, especially anencephaly. This could link the known preventive actions of hard water and folic acid. Calcium is a toxicological antagonist of lead. One cause of a deficiency of folic acid is impaired absorption secondary to zinc deficiency, which may be produced or exacerbated by lead. [ABSTRACT FROM AUTHOR]

Objective: To examine the influence of co-occurring conditions on gambling treatment outcomes.Design, Setting and Participants: Prospective cohort study of problem gamblers. Participants were recruited from consecutive referrals to a gambling therapy service in 2008. Inclusion criteria were: (i) assessed as a problem gambler based on a screening interview including DSM-IV criteria for pathological gambling, and (ii) suitable for admission to a treatment program. Cognitive-behavioural therapy was based on graded exposure-to-gambling urge. One-to-one treatment was conducted with 1-hour sessions weekly for up to 12 weeks.Main Outcome Measures: Problem gambling screening and co-occurring conditions including depression, anxiety and alcohol use.Results: Of 127 problem gamblers, 69 were males (54%), mean age was 43.09 years, and 65 (51%) reported a duration of problem gambling greater than 5 years. Median time for participants' enrolment in the study was 8.9 months. Results from mixed effects logistic regression analysis indicated that individuals with higher depression levels had a greater likelihood (13% increase in odds [95% CI, 1%-25%]) of problem gambling during treatment and at follow-up.Conclusion: Addressing depression may be associated with improved treatment outcomes in problem gambling; conversely, treatment of problem gambling improves affective instability. We therefore recommend a dual approach that treats both depression and problem gambling. [ABSTRACT FROM AUTHOR]

Background: According to a World Health Organization (WHO) review of nationally representative surveys from 1993 to 2005, 42% of pregnant women have anemia worldwide. Almost 90% of anemic women reside in Africa or Asia. Most countries have policies and programs for prenatal iron-folic acid supplementation, but coverage remains low and little emphasis is placed on this intervention within efforts to strengthen antenatal care services. The evidence of the public health impact of iron-folic acid supplementation and documentation of the potential for scaling up have not been reviewed recently.Objective: The purpose of this review is to examine the evidence regarding the impact on maternal mortality of iron-folic acid supplementation and the evidence for the effectiveness of this intervention in supplementation trials and large-scale programs.Methods: The impact on mortality is reviewed from observational studies that were analyzed for the Global Burden of Disease Analysis in 2004. Reviews of iron-folic acid supplementation trials were analyzed by other researchers and are summarized. Data on anemia reduction from two large-scale national programs are presented, and factors responsible for high coverage with iron-folic acid supplementation are discussed.Results: Iron-deficiency anemia underlies 115,000 maternal deaths per year. In Asia, anemia is the second highest cause of maternal mortality. Even mild and moderate anemia increase the risk of death in pregnant women. Iron-folic acid supplementation of pregnant women increases hemoglobin by 1.17 g/dL in developed countries and 1.13 g/dL in developing countries. The prevalence of maternal anemia can be reduced by one-third to one-half over a decade if action is taken to launch focused, large-scale programs that are based on lessons learned from countries with successful programs, such as Thailand and Nicaragua.Conclusions: Iron-folic acid supplementation is an under-resourced, affordable intervention with substantial potential for contributing to Millennium Development Goal 5 (maternal mortality reduction) in countries where iron intakes among pregnant women are low and anemia prevalence is high. This can be achieved in the near term, as policies are already in place in most countries and iron-folic acid supplements are already in lists of essential drugs. What is needed is to systematically adopt lessons about how to strengthen demand and supply systems from successful programs. [ABSTRACT FROM AUTHOR]

Currently, it is unknown whether treatment outcomes derived from randomized controlled trials (RCTs) of cognitive-behavioural therapy (CBT) for problem gamblers still hold when applied to patients seen in routine practice. Thus, data from an RCT of cognitive therapy versus exposure therapy for problem gambling versus patients of a gambling help service were compared. Assessments of problem gambling severity, psychosocial impairment, and alcohol use were undertaken at baseline and post-treatment and evaluated within a counterfactual framework. Findings showed that the contrast between routine CBT for pokies and horse betting had a significant effect, indicative of a 62% lower gambling urge score if routine CBT recipients had all been horse/track betters opposed to gambling with "pokies." However, the majority of contrasts indicated therapeutic outcomes achieved in routine CBT treatments were of equivalent robustness relative to RCT conditions. The present findings infer routine practice treatment outcomes are as efficacious as those generated in RCT contexts., (Copyright © 2017 John Wiley & Sons, Ltd.)

The adrenal has been neglected in endocrine disruption regulatory testing strategy. The adrenal is a vital organ, adrenocortical insufficiency is recognised in life threatening "adrenal crises" and Addison's disease, and the consequences of off-target toxicological inhibition of adrenocortical steroidogenesis is well recognised in clinical medicine, where drugs such as aminoglutethimide and etomidate killed patients via unrecognised inhibition of adrenocortical steroidogenic enzymes (e.g. CYP11B1) along the cortisol and aldosterone pathways. The consequences of adrenocortical dysfunction during early development are also recognised in the congenital salt wasting and adrenogenital syndromes presenting neonatally, yet despite a remit to focus on developmental and reproductive toxicity mechanisms of endocrine disruption by many regulatory agencies (USEPA EDSTAC; REACH) the assessment of adrenocortical function has largely been ignored. Further, every step in the adrenocortical steroidogenic pathway (ACTH receptor, StAR, CYP's 11A1, 17, 21, 11B1, 11B2, and 3-hydroxysteroid dehydrogenase Δ4,5 isomerase) is known to be a potential target with multiple examples of chemicals inhibiting these targets. Many of these chemicals have been detected in human and wildlife tissues. This raises the question of whether exposure to low level environmental chemicals may be affecting adrenocortical function. This review examines the omission of adrenocortical testing in the current regulatory frameworks; the characteristics that make the adrenal cortex particularly vulnerable to toxic insult; chemicals and their toxicological targets within the adrenocortical steroidogenic pathways; the typical manifestations of adrenocortical toxicity (e.g. human iatrogenically induced pharmacotoxicological adrenal insufficiency, manifestations in typical mammalian regulatory general toxicology studies, manifestations in wildlife) and models of adrenocortical functional assessment. The utility of the in vivo ACTH challenge test to prove adrenocortical competency, and the H295R cell line to examine molecular mechanisms of steroidogenic pathway toxicity, are discussed. Finally, because of the central role of the adrenal in the physiologically adaptive stress response, the distinguishing features of stress, compared with adrenocortical toxicity, are discussed with reference to the evidence required to claim that adrenal hypertrophy results from stress rather than adrenocortical enzyme inhibition which is a serious adverse toxicological finding. This article is part of a special issue entitled 'Endocrine disruptors and steroids'., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Problem gambling-specific cognitive therapy (CT) and behavioural (exposure-based) therapy (ET) are two core cognitive-behavioural techniques to treating the disorder, but no studies have directly compared them using a randomised trial., Aims: To evaluate differential efficacy of CT and ET for adult problem gamblers at a South Australian gambling therapy service., Methods: Two-group randomised, parallel design. Primary outcome was rated by participants using the Victorian Gambling Screen (VGS) at baseline, treatment-end, 1, 3, and 6 month follow-up., Findings: Of eighty-seven participants who were randomised and started intervention (CT = 44; ET = 43), 51 (59%) completed intervention (CT = 30; ET = 21). Both groups experienced comparable reductions (improvement) in VGS scores at 12 weeks (mean difference -0.18, 95% CI: -4.48-4.11) and 6 month follow-up (mean difference 1.47, 95% CI: -4.46-7.39)., Conclusions: Cognitive and exposure therapies are both viable and effective treatments for problem gambling. Large-scale trials are needed to compare them individually and combined to enhance retention rates and reduce drop-out., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

To explore the variation of predictors of relapse in treatment and support seeking gamblers. A prospective cohort study with 158 treatment and support seeking problem gamblers in South Australia. Key measures were selected using a consensus process with international experts in problem gambling and related addictions. The outcome measures were Victorian Gambling Screen (VGS) and behaviours related to gambling. Potential predictors were gambling related cognitions and urge, emotional disturbance, social support, sensation seeking traits, and levels of work and social functioning. Mean age of participants was 44 years (SD = 12.92 years) and 85 (54 %) were male. Median time for participants enrollment in the study was 8.38 months (IQR = 2.57 months). Patterns of completed measures for points in time included 116 (73.4 %) with at least a 3 month follow-up. Using generalised mixed-effects regression models we found gambling related urge was significantly associated with relapse in problem gambling as measured by VGS (OR 1.29; 95 % CI 1.12-1.49) and gambling behaviours (OR 1.16; 95 % CI 1.06-1.27). Gambling related cognitions were also significantly associated with VGS (OR 1.06; 95 % CI 1.01-1.12). There is consistent association between urge to gamble and relapse in problem gambling but estimates for other potential predictors may have been attenuated because of methodological limitations. This study also highlighted the challenges presented from a cohort study of treatment and support seeking problem gamblers.

A framework for understanding the complexity of cancer development was established by Hanahan and Weinberg in their definition of the hallmarks of cancer. In this review, we consider the evidence that parabens can enable development in human breast epithelial cells of four of six of the basic hallmarks, one of two of the emerging hallmarks and one of two of the enabling characteristics. In Hallmark 1, parabens have been measured as present in 99% of human breast tissue samples, possess oestrogenic activity and can stimulate sustained proliferation of human breast cancer cells at concentrations measurable in the breast. In Hallmark 2, parabens can inhibit the suppression of breast cancer cell growth by hydroxytamoxifen, and through binding to the oestrogen-related receptor gamma may prevent its deactivation by growth inhibitors. In Hallmark 3, in the 10 nm-1 μm range, parabens give a dose-dependent evasion of apoptosis in high-risk donor breast epithelial cells. In Hallmark 4, long-term exposure (>20 weeks) to parabens leads to increased migratory and invasive activity in human breast cancer cells, properties that are linked to the metastatic process. As an emerging hallmark methylparaben has been shown in human breast epithelial cells to increase mTOR, a key regulator of energy metabolism. As an enabling characteristic parabens can cause DNA damage at high concentrations in the short term but more work is needed to investigate long-term, low-dose mixtures. The ability of parabens to enable multiple cancer hallmarks in human breast epithelial cells provides grounds for regulatory review of the implications of the presence of parabens in human breast tissue., (Copyright © 2014 John Wiley & Sons, Ltd.)

Background: Problem gambling is a serious public health concern at an international level where population prevalence rates average 2% or more and occurs more frequently in younger populations. The most empirically established treatments until now are combinations of cognitive and behavioural techniques labelled cognitive behaviour therapy (CBT). However, there is a paucity of high quality evidence for the comparative efficacy of core CBT interventions in treating problem gamblers. This study aims to isolate and compare cognitive and behavioural (exposure-based) techniques to determine their relative efficacy., Methods: A sample of 130 treatment-seeking problem gamblers will be allocated to either cognitive or exposure therapy in a two-group randomised, parallel design. Repeated measures will be conducted at baseline, mid and end of treatment (12 sessions intervention period), and at 3, 6 and 12 months (maintenance effects). The primary outcome measure is improvement in problem gambling severity symptoms using the Victorian Gambling Screen (VGS) harm to self-subscale. VGS measures gambling severity on an extensive continuum, thereby enhancing sensitivity to change within and between individuals over time., Discussion: This article describes the research methods, treatments and outcome measures used to evaluate gambling behaviours, problems caused by gambling and mechanisms of change. This study will be the first randomised, parallel trial to compare cognitive and exposure therapies in this population., Ethics and Dissemination: The study was approved by the Southern Adelaide Health Service/Flinders University Human Research Ethics Committee. Study findings will be disseminated through peer-reviewed publications and conference presentations., Trial Registration: Australian New Zealand Clinical Trials Registry: ACTRN 12610000828022.

Background: Concern over micronutrient inadequacies in Uganda has prompted the introduction of mass fortification., Objective: To use food intake to determine nutrient inadequacies in children aged 24 to 59 months and nonpregnant women of reproductive age, and to model the adequacy of mass fortification., Methods: Data were collected by the 24-hour recall method in three regions. Usual nutrient intakes were calculated by adjusting actual intake distribution for the intraindividual variance. The impact of fortification on intake adequacy was simulated., Results: The nutrients with the highest prevalence of inadequate intake across regions were vitamin A (30% to 99%), vitamin B12 (32% to 100%), iron (55% to 89%), zinc (18% to 82%), and calcium (84% to 100%). According to simulations, fortification of vegetable oil and sugar with vitamin A would reduce the prevalence of vitamin A inadequacy in the Western and Northern regions; in Kampala it would eliminate vitamin A inadequacy but would cause 2% to 48% of children to exceed the Tolerable Upper Intake Level (UL). The proposed fortification of wheat flour would reduce the prevalence of inadequate intakes of thiamine, riboflavin, folate, and niacin in Kampala, but would have little impact in the other two regions due to low flour consumption., Conclusions: Micronutrient fortification of vegetable oil and sugar in all regions and of wheat flour in Kampala would reduce the prevalence of micronutrient inadequacies. However, the wheat flour formulation should be modified to better meet requirements, and the vitamin A content in sugar should be reduced to minimize the risk of high intakes. Maize flour may be suitable for targeted fortification, but prior consolidation of the industry would be required for maize flour to become a good vehicle for mass fortification.

Objectives: This paper describes the longitudinal component of a larger mixed methods study into the processes and outcomes of chronic condition management and self-management strategies implemented in three Aboriginal communities in South Australia. The study was designed to document the connection between the application of structured systems of care for Aboriginal people and their longer-term health status., Methods: The study concentrated on three diverse Aboriginal communities in South Australia; the Port Lincoln Aboriginal Health Service, the Riverland community, and Nunkuwarrin Yunti Aboriginal Health Service in the Adelaide metropolitan area. Repeated-measure clinical data were collected for individual participants using a range of clinical indicators for diabetes (type 1 and 2) and related chronic conditions. Clinical data were analysed using random effects modelling techniques with changes in key clinical indicators being modelled at both the individual and group levels., Results: Where care planning has been in place longer than in other sites overall improvements were noted in BMI, cholesterol (high density and low density lipids) and HbA1c. These results indicate that for Aboriginal patients with complex chronic conditions, participation in and adherence to structured care planning and self-management strategies can contribute to improved overall health status and health outcomes., Conclusions: The outcomes reported here represent an initial and important step in quantifying the health benefits that can accrue for Aboriginal people living with complex chronic conditions such as diabetes, heart disease and respiratory disease. The study highlights the benefits of developing long-term working relationships with Aboriginal communities as a basis for conducting effective collaborative health research programs. WHAT IS KNOWN ABOUT THE TOPIC? Chronic condition management and self-management programs have been available to Aboriginal people in a range of forms for some time. We know that some groups of patients are keen to engage with care planning and self-management protocols and we have anecdotal evidence of this engagement leading to improved quality of life and health outcomes for Aboriginal people. WHAT DOES THIS PAPER ADD? This paper provides early evidence of sustained improvement over time for a cohort of Aboriginal people who are learning to deal with a range of chronic illnesses through accessing structured systems of support and care. WHAT ARE THE IMPLICATIONS FOR PRACTITIONERS? This longitudinal evidence of improved outcomes for Aboriginal people is encouraging and should lead on to more definitive studies of outcomes accruing for people engaged in structured systems of care. Not only does this finding have implications for the overall management of chronic illness in Aboriginal communities, but it points the way to how health services might best invest their resources and efforts to improve the health status of people with chronic conditions and, in the process, close the gap between the life expectancy of Aboriginal people and that of other community groups in Australia.

Carcinogenic properties of ulipristal acetate (UPA), a selective progesterone receptor modulator developed for the treatment of benign gynecological conditions such as uterine fibroids, were assessed in a 26-week carcinogenicity study in transgenic TgRasH2 mice and a 104-week study in Sprague Dawley rats. Dose levels used in the mouse study were 15, 45, or 130 mg/kg/day and for the ratstudy the doses used were 1, 3, or 10 mg/kg/day. Vehicle and water controls were part of both studies and a positive control, N-Nitroso-N-methylurea intraperitoneally, was included in the transgenic mouse assay. Survival at all dose levels was similar to vehicle controls in both sexes of both species and there was no evidence of any UPA-induced carcinogenicity in either species. Rats receiving UPA had decreased incidences of fibroadenomas and adenocarcinomas in the mammary gland in all treated groups. UPA exposure [AUC(0-24h)] at the highest dose in rats was 67 times human therapeutic exposure at 10 mg/day. In mice, no tumor of any type increased at UPA exposures up to 313 times of therapeutic exposure. UPA-related findings in mice were limited to organ weight changes in the liver, pituitary, thyroid/parathyroid glands, and epididymis as well as minimal panlobular hepatocellular hypertrophy in male and female mice receiving 130 mg/kg/day. Rats had UPA-related non-neoplastic findings in the reproductive system (mammary gland, ovary, uterus, vagina, seminal vesicle, prostate), endocrine system (adrenal, pituitary), thymus, muscle, liver, pancreas and lungs most of which are considered to be due to exaggerated pharmacological action of the compound.

The commonly held assumption that rodent mammary tumors resulting from elevated prolactin are species-specific, or not biologically relevant to humans, is incorrect. Substantial epidemiological, clinical, and biological evidence now exists confirming the role of prolactin in human breast cancer. This evidence is evaluated and the argument presented that the tumorigenic risk from prolactin is therefore not species-specific to rodents but directly applies to humans. Further, as the mechanisms of prolactin-induced mammary tumor promotion and development appear analogous between rodents and humans, mammary tumorigenic findings in rodent carcinogenicity bioassays are both predictive and biologically relevant to the human response. Toxicologists and regulators need to consider this in carcinogenicity risk assessments., (Copyright © 2011 John Wiley & Sons, Ltd.)

The primary cause of adrenocortical hypertrophy is increased adrenocorticotrophic hormone (ACTH) stimulation. In toxicology studies, such a condition can arise as a result of the stress response, but it may also occur due to deficient glucocorticoid feedback regulation of ACTH due to toxicity to the adrenal cortex. This latter condition is defined as adrenocortical insufficiency and represents a serious adverse toxic effect on the function of the adrenal cortex. Adrenocortical hypertrophy may occur in the absence of other adrenocortical lesions such that a toxicopathological mechanism is not obvious, for example by pharmacological inhibition of steroidogenesis at the biochemical level. This review discusses the different aetiological factors and mechanisms producing adrenocortical hypertrophy. The need for further evidence in ascribing findings to stress is discussed, as is a protocol for establishing differential diagnoses between stress-induced and toxicity-induced adrenocortical hypertrophy, which is useful in cases where there are no other histopathological lesions in the adrenal cortex. It is concluded that all cases of adrenocortical hypertrophy require further investigation or evidence to ascribe such findings to either stress or adrenocortical inhibition/insufficiency, and that all cases of adrenocortical insufficiency (whether due to a histopathological lesion or reversible pharmacological enzyme inhibition) represent a serious adverse effect that must be properly considered in toxicological risk assessment., (Copyright © 2010 John Wiley & Sons, Ltd.)

History tells us of the overwhelming destructive influence of exotic culture, politics and knowledge forms upon the worldview and wellbeing of Indigenous Australians. The power of dominant culture to oppress, control and dominate traditional Indigenous ways of knowing and being has been identified as a being a crucial influence on the health status, future hopes and aspirations of Indigenous Australians. Fundamental to this assertion is that the alienating effect of the belief in and application of the scientific method in relation to learning and knowing is a phenomenon that is incompatible with the law and cultural ways of traditional Indigenous people. The establishment of the Centre of Clinical Research Excellence (CCRE) is predicated upon and responds to a deep need in our community today to synthesise the ideological and epistemological premises of an increasing range of cultures and world views. It recognises that clinical research, for example, is important to the health of Aboriginal and Torres Strait Islander peoples, but also that the way such research is designed and carried out is also crucial to its potential to effect change in and improve the state of Indigenous health in Australia. This paper examines knowledge principles and processes associated with research in Indigenous communities, explores emerging research trends in science and proposes an epistemological framework for synthesis of traditional approaches with those of the scientific paradigm.

This toxicology update reviews research over the past four years since publication in 2004 of the first measurement of intact esters of p-hydroxybenzoic acid (parabens) in human breast cancer tissues, and the suggestion that their presence in the human body might originate from topical application of bodycare cosmetics. The presence of intact paraben esters in human body tissues has now been confirmed by independent measurements in human urine, and the ability of parabens to penetrate human skin intact without breakdown by esterases and to be absorbed systemically has been demonstrated through studies not only in vitro but also in vivo using healthy human subjects. Using a wide variety of assay systems in vitro and in vivo, the oestrogen agonist properties of parabens together with their common metabolite (p-hydroxybenzoic acid) have been extensively documented, and, in addition, the parabens have now also been shown to possess androgen antagonist activity, to act as inhibitors of sulfotransferase enzymes and to possess genotoxic activity. With the continued use of parabens in the majority of bodycare cosmetics, there is a need to carry out detailed evaluation of the potential for parabens, together with other oestrogenic and genotoxic co-formulants of bodycare cosmetics, to increase female breast cancer incidence, to interfere with male reproductive functions and to influence development of malignant melanoma which has also recently been shown to be influenced by oestrogenic stimulation., (2008 John Wiley & Sons, Ltd)

The Sharing Health Care SA chronic disease self-management (CDSM) project in rural South Australia was designed to assist patients with chronic and complex conditions (diabetes, cardiovascular disease and arthritis) to learn how to participate more effectively in the management of their condition and to improve their self-management skills. Participants with chronic and complex conditions were recruited into the Sharing Health Care SA program and offered a range of education and support options (including a 6-week peer-led chronic disease self-management program) as part of the Enhanced Primary Care care planning process. Patient self-reported data were collected at baseline and subsequent 6-month intervals using the Partners in Health (PIH) scale to assess self-management skill and ability for 175 patients across four data collection points. Health providers also scored patient knowledge and self-management skills using the same scale over the same intervals. Patients also completed a modified Stanford 2000 Health Survey for the same time intervals to assess service utilisation and health-related lifestyle factors. Results show that both mean patient self-reported PIH scores and mean health provider PIH scores for patients improved significantly over time, indicating that patients demonstrated improved understanding of their condition and improved their ability to manage and deal with their symptoms. These results suggest that involvement in peer-led self-management education programs has a positive effect on patient self-management skill, confidence and health-related behaviour.

Drugs and chemicals shown to induce mammary carcinogenesis in the rat/rodent via prolactin excess have traditionally been argued to pose little or no risk to humans in a regulatory toxicology context. The basis for this assumption is reviewed and placed into context with new evidence in humans that prolactin may be a tumour promoter in the breast and prostate. This evidence includes epidemiology, patient studies involving endocrine evaluation and molecular biology in human cells. It is concluded that hyperprolactinaemia is associated with an increase in breast cancer risk in both post and premenopausal women, that rat carcinogenicity studies are predictive of the human response, and that in a regulatory toxicology context prolactin-induced mammary tumours from nongenotoxic drugs and chemicals are an adverse effect that should not be ignored. More evidence is required concerning prostate cancer risk but molecular biology indicates that prolactin also induces prostate cell proliferation and inhibits apoptosis, which are similar to the responses observed in breast cancer cells.

A group of international experts in psychiatry, medicine, toxicology and pharmacy assembled to undertake a critical examination of the currently available clinical guidance on hyperprolactinaemia. This paper summarises the group's collective views and provides a summary of the recommendations agreed by the consensus group to assist clinicians in the recognition, clinical assessment, investigation and management of elevated plasma prolactin levels in patients being treated for severe mental illness. It also deals with the special problems of particular populations, gives advice about information that should be provided to patients, and suggests a strategy for routine monitoring of prolactin. The recommendations are based upon the evidence contained in the supplement 'Hyperprolactinaemia in schizophrenia and bipolar disorder: Clinical Implications' (2008). The guidance contained in this article is not intended to replace national guidance (such as that of the National Institute of Clinical Excellence), however, it does provide additional detail that is unlikely to be covered in existing guidelines, and focuses on areas of uncertainty and disagreement. We hope it will add to the debate about this topic.

The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing. There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment. Consequently, a strategy is proposed to evaluate adrenocortical toxicity. Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern. The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted. The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression. The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression. Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described. Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems. In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models. The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans. Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals. The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied.

Historically, hyperprolactinaemia has been considered of low toxicological relevance when detected in toxicity studies, and even mammary carcinogenesis induced in the rat by prolactin excess has been considered of no relevance to humans. However, recent findings from human epidemiology and molecular biology suggests that prolactin is a risk factor for human breast cancer, and probably prostate cancer. Therefore, this new evidence should be considered in the various decisions to develop and license a new drug or chemical if the compound causes hyperprolactinaemia. This emerging evidence suggests that prolactin can also be produced locally from human breast cancer cells, and that, regardless of source (ie, pituitary or autocrine/paracrine production from cancer cells), prolactin is mitogenic, stimulates proliferation and suppresses apoptosis in breast and prostate cancer cells. This review outlines the evidence that hyperprolactinaemia should be considered a toxicological adverse effect and concludes that prolactin-induced rodent mammary carcinogenesis is relevant to humans and is not species-specific. The effects of prolactin on the prostate gland are also discussed; hyperprolactinaemia may be an additional risk factor for prostate cancer and this also requires consideration in toxicological risk assessments. The implications of increased prolactin secretion as an adverse effect for regulatory toxicology of drugs and chemicals, and in high risk patients receiving therapeutic drugs with hyperprolactinaemic side effects, is discussed. Alteration of prolactin level is also a novel mechanism that requires consideration in endocrine disruption research, since both endogenous oestrogens and also xenoestrogens stimulate prolactin secretion or affect prolactin receptors.

Regulation of endocrine-disrupting chemicals is reviewed in terms of hazard assessment (regulatory toxicology) and risk assessment. The current range of regulatory general toxicology protocols can detect endocrine toxicity, but specific endocrine toxicology tests are required to confirm mechanisms (e.g. oestrogenic, anti-androgenic). Strategies for validating new endocrine toxicology protocols and approaches to data assessment are discussed, and deficiencies in regulatory toxicology testing (e.g. lack of adrenocortical function assessment) identified. Recent evidence of a role of prolactin in human breast cancer also highlights deficiencies in regulatory evaluation. Actual human exposure to chemicals and the high-exposure example of chemicals in body-care cosmetics is reviewed with reference to evidence that common ingredients (e.g. parabens, cyclosiloxanes) are oestrogenic. The hypothesis and epidemiology concerning chemical exposure from body-care cosmetics (moisturizers, lotions, sun screens, deodorants) and breast cancer in women is reviewed, applying Bradford-Hill criteria for association and causality, and research requirements are identified.

Prolactin-induced mammary carcinogenesis in rodents, particularly rats, is often stated to be of low toxicological relevance to humans. This opinion appears to have developed from a number of lines of cited evidence. Firstly, there had been long experience of use of dopamine antagonists (that increase prolactin) in human medicine and no evidence of an increase in breast cancer incidence or risk had been reported. Secondly, dopamine agonists (that lower prolactin) had been shown to have no effect in human breast cancer treatment. Thirdly, the actions of prolactin were considered different between rodents and humans. However, recent evidence now suggests that prolactin has a major role in human breast cancer, and the similarity of mechanism with the rodent suggests that prolactin-mediated mammary carcinogenesis in rodents could be of much higher toxicological relevance to humans than previously thought. Large epidemiology studies have upgraded a limited database and shown that dopamine antagonists (both antipsychotics and anti-emetics) increase breast cancer risk, that hyperprolactinaemia is consistently associated with human breast cancer growth, development and poor prognosis, and that prolactin is indeed a mitogen in human breast cancer cells that suppresses apoptosis and upregulates BRCA1. It is now clear that initial studies giving dopamine agonists to breast cancer patients had no effect because breast cancer cells also produced prolactin independently of the pituitary, which remained uncontrolled and unrecognized in early clinical studies. The evidence for the role of prolactin in human breast cancer is now strong and consistent, and is discussed and related to the risk assessment of drugs and chemicals. The conclusion is that it is invalid to suggest that prolactin-induced mammary carcinogenesis in rodents is of low relevance to humans because prolactin can induce an adverse response in the mammary tissue of both rodents and humans alike. Drugs and chemicals causing rodent prolactin-induced mammary carcinogenesis may therefore pose a risk to humans via the same mechanism if exposures also increase prolactin secretion in humans., (Copyright 2005 John Wiley & Sons, Ltd)

Vitamin and mineral deficiencies adversely affect a third of the world's people. Consequently, a series of global goals and a serious amount of donor and national resources have been directed at such micronutrient deficiencies. Drawing on the extensive experience of the authors in a variety of institutional settings, the article used a computer search of the published scientific literature of the topic, supplemented by reports and published and unpublished work from the various agencies. In examining the effect of sex on the economic and social costs of micronutrient deficiencies, the paper found that: (1) micronutrient deficiencies affect global health outcomes; (2) micronutrient deficiencies incur substantial economic costs; (3) health and nutrition outcomes are affected by sex; (4) micronutrient deficiencies are affected by sex, but this is often culturally specific; and finally, (5) the social and economic costs of micronutrient deficiencies, with particular reference to women and female adolescents and children, are likely to be considerable but are not well quantified. Given the potential impact on reducing infant and child mortality, reducing maternal mortality, and enhancing neuro-intellectual development and growth, the right of women and children to adequate food and nutrition should more explicitly reflect their special requirements in terms of micronutrients. The positive impact of alleviating micronutrient malnutrition on physical activity, education and productivity, and hence on national economies suggests that there is also an urgent need for increased effort to demonstrate the cost of these deficiencies, as well as the benefits of addressing them, especially compared with other health and nutrition interventions.

In the decade that has elapsed since the suggestion that exposure of the foetal/developing male to environmental oestrogens could be the cause of subsequent reproductive and developmental effects in men, there has been little definitive research to provide conclusions to the hypothesis. Issues of exposure and low potency of environmental oestrogens may have reduced concerns. However, the hypothesis that chemicals applied in body care cosmetics (including moisturizers, creams, sprays or lotions applied to axilla or chest or breast areas) may be affecting breast cancer incidence in women presents a different case scenario, not least in the consideration of the exposure issues. The specific cosmetic type is not relevant but the chemical ingredients in the formulations and the application to the skin is important. The most common group of body care cosmetic formulation excipients, namely p-hydroxybenzoic acid esters or parabens, have been shown recently to be oestrogenic in vitro and in vivo and now have been detected in human breast tumour tissue, indicating absorption (route and causal associations have yet to be confirmed). The hypothesis for a link between oestrogenic ingredients in underarm and body care cosmetics and breast cancer is forwarded and reviewed here in terms of: data on exposure to body care cosmetics and parabens, including dermal absorption; paraben oestrogenicity; the role of oestrogen in breast cancer; detection of parabens in breast tumours; recent epidemiology studies of underarm cosmetics use and breast cancer; the toxicology database; the current regulatory status of parabens and regulatory toxicology data uncertainties. Notwithstanding the major public health issue of the causes of the rising incidence of breast cancer in women, this call for further research may provide the first evidence that environmental factors may be adversely affecting human health by endocrine disruption, because exposure to oestrogenic chemicals through application of body care products (unlike diffuse environmental chemical exposures) should be amenable to evaluation, quantification and control. The exposure issues are clear and the exposed population is large, and these factors should provide the necessary impetus to investigate this potential issue of public health., (Copyright 2004 John Wiley & Sons, Ltd.)

Background: S-adenosylmethionine (SAMe) is a dietary supplement used in the management of osteoarthritis (OA) symptoms. Studies evaluating SAMe in the management of OA have been limited to Non Steroidal Anti-inflammatory Drugs (NSAIDs) for comparison. The present study compares the effectiveness of SAMe to a cyclooxygenase-2 (COX-2) inhibitor (celecoxib) for pain control, functional improvement and to decrease side effects in people with osteoarthritis of the knee., Methods: A randomized double-blind cross-over study, comparing SAMe (1200 mg) with celecoxib (Celebrex 200 mg) for 16 weeks to reduce pain associated with OA of the knee. Sixty-one adults diagnosed with OA of the knee were enrolled and 56 completed the study. Subjects were tested for pain, functional health, mood status, isometric joint function tests, and side effects., Results: On the first month of Phase 1, celecoxib showed significantly more reduction in pain than SAMe (p = 0.024). By the second month of Phase 1, there was no significant difference between both groups (p < 0.01). The duration of treatment and the interaction of duration with type of treatment were statistically significant (ps < or = 0.029). On most functional health measures both groups showed a notable improvement from baseline, however no significant difference between SAMe and celecoxib was observed. Isometric joint function tests appeared to be steadily improving over the entire study period regardless of treatment., Conclusion: SAMe has a slower onset of action but is as effective as celecoxib in the management of symptoms of knee osteoarthritis. Longer studies are needed to evaluate the long-term effectiveness of SAMe and the optimal dose to be used.

We evaluated the effects of various food groups and micronutrients in the diet on survival among women who originally participated in a population-based case-control study of ovarian cancer conducted across 3 Australian states between 1990 and 1993. This analysis included 609 women with invasive epithelial ovarian cancer, primarily because there was negligible mortality in women with borderline tumors. The women's usual diet was assessed using a validated food frequency questionnaire. Deaths in the cohort were identified using state-based cancer registries and the Australian National Death Index (NDI). Crude 5-year survival probabilities were estimated using the Kaplan-Meier technique, and adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were obtained from Cox regression models. After adjusting for important confounding factors, a survival advantage was observed for those who reported higher intake of vegetables in general (HR = 0.75, 95% CI = 0.57-0.99, p-value trend 0.01 for the highest third, compared to the lowest third), and cruciferous vegetables in particular (HR = 0.75, 95% CI = 0.57-0.98, p-value trend 0.03), and among women in the upper third of intake of vitamin E (HR = 0.76, 95% CI = 0.58-1.01, p-value trend 0.04). Inverse associations were also seen with protein (p-value trend 0.09), red meat (p-value trend 0.06) and white meat (p-value trend 0.07), and modest positive trends (maximum 30% excess) with lactose (p-value trend 0.04), calcium and dairy products. Although much remains to be learned about the influence of nutritional factors after a diagnosis of ovarian cancer, our study suggests the possibility that a diet high in vegetable intake may help improve survival., (Copyright 2003 Wiley-Liss, Inc.)

Current testing strategies to assess the endocrine disrupting properties of chemicals have omitted examination of the adrenal gland and do not adequately cover the process of steroidogenesis. Steroidogenesis is critical for adrenocortical function as well as that of the testes and ovaries, and presents multiple molecular targets for toxicity, ranging from general effects on all steroidogenic tissues (e.g. via StAR protein or CYP11A1 cholesterol side-chain cleavage) through to specific targets affecting only adrenocortical function (e.g. CYP11beta/18 and glucocorticoid synthesis). Numerous chemicals of environmental relevance are now being shown to affect adrenocortical function both in vivo in aquatic species and in vitro in human cell lines, and given the vital role of the adrenal gland to human health and development, there is a strong case for including dedicated assessment techniques in screening batteries for endocrine-disrupting chemicals, not least to assist in general data interpretation (e.g. whether adrenal hypertrophy is due to stress or to a more sinister adrenocortical insufficiency). Cell lines such as H295R (derived from a human adrenocortical adenocarcinoma) currently exist that will allow assessment of cortisol production and most of the major enzymes and functional proteins in the steroidogenic pathway (e.g. StAR; CYP11A1/scc; CYP11beta/18; CYP17; CYP19; CYP21; 3beta-hydroxysteroid dehydrogenase). Adequate assessment of adrenocortical function, as with any component of the integrated endocrine system, probably also will require the development of specific in vivo methodology to include effects on hypothalamo-pituitary function. Finally, although there is currently no direct evidence that environmental exposure to endocrine-disrupting (oestrogenic) chemicals has actually caused adverse human health effects, lessons have been learned on their potential from the diethylstilboestrol case. Similar evidence exists from aminoglutethimide and etomidate on the lethal impact of unpredicted chemically induced adrenal insufficiency in sensitive human subgroups, and it would seem prudent to incorporate relevant tests for adrenal function and steroidogenesis into current regulatory validation programmes.

Objective: To provide information on the potential contribution to vitamin A nutrition in infants of strategies for improving maternal vitamin A status and increasing the consumption of breast milk., Methods: The contribution of breastfeeding to the vitamin A nutrition of children in eight age groups between 0 and 24 months was simulated under four sets of conditions involving two levels of breast milk consumption with or without maternal vitamin A supplementation., Findings: During the first 6 months, optimal breastfeeding on its own (compared with withholding colostrum and then partially breastfeeding after the first week) was as effective as postpartum maternal supplementation alone, retinol intakes being increased by 59 micrograms per day and 68 micrograms per day, respectively. Combined in synergy, these strategies increase retinol intake by 144 micrograms per day, or 36% of the recommended intake. After 6 months, partial breastfeeding continued to provide a significant proportion of the recommended intakes: 42% from 6-12 months and 61% during the second year., Conclusion: Maternal supplementation with a high dose of vitamin A at the time of delivery and the promotion of optimal breastfeeding practices are highly effective strategies for improving vitamin A nutrition in infants and should be strengthened as key components of comprehensive child survival programmes.

There has been a substantial proliferation in the number of studies reporting endocrine effects as an endpoint. The vast majority have focused on oestrogenicity in vitro but, with recent recommendations by the USEPA Endocrine Disrupter Screening and Testing Advisory Committee, tests are now being developed for (anti)-androgenicity and effects on the thyroid, largely because of the potential for altering reproduction or development via these mechanisms. Despite being a vital organ and involved in reproduction and development, there is currently no provision for assessing adrenocortical function. Similarly, the entire process of steroidogenesis poses multiple molecular targets for toxic disruption that are not included in current test strategies and at present there is no clear position on the significance of the data being generated. This review provides a framework for approaching endocrine data: that all the glands, tissues, receptors, transporter proteins and enzymes that comprise the endocrine system are targets for toxicity. They should be considered in much the same way as other target organs, with appropriate provision for the special cases of carcinogenesis and teratogenesis, and a pragmatic weight of evidence approach should be adopted considering all available data and recognizing its limitations. In this approach, structure-activity relationships and in vitro and targeted in vivo screens provide useful data but repeat-dose regulatory studies with defined endpoints provide the most powerful tools for hazard assessment. Pragmatic consideration should be given to exposure issues (which may highlight the practical irrelevance, for example, of very low potency oestrogens) and subsequently whether endocrine disruption is the critical or most sensitive endpoint for a compound. Finally, endocrine disruption may be considered a mechanism and, as with other toxic endpoints, knowledge of effect and no-observable-effect levels and reversibility is as important as identifying the target tissue or any inherent hormone-like property., (Copyright 2002 John Wiley & Sons, Ltd.)

Objective: : To determine the impact of contaminant iron and geophagy on iron intake and status of persons living in developing countries., Design: : Literature for review was identified by searching Medline and Agricola, from appropriate other texts and from three reports from the Opportunities for Micronutrient Interventions (OMNI) Project of USAID., Setting: : The dietary intake of iron by people living in developing countries is generally high but iron deficiency remains prevalent. This apparent paradox is because the iron being consumed is predominantly in the non-haem form, which is poorly absorbed. Some of this non-haem iron is from contamination of food with iron from soil, dust and water; iron leaching into food during storage and cooking; contamination during food processing such as milling; and the practice of geophagy., Results: : Although the contribution of contaminant iron to overall iron intake is well documented, its absorption and thus its impact on iron status is not. To be available for absorption, contaminant iron must join the common non-haem pool, i.e. be exchangeable. The absorption of exchangeable contaminant iron is subject to the same interactions with other constituents in the diet as the non-haem iron that is intrinsic to food. The limited available evidence suggests wide variation in exchangeability. In situations where a significant fraction of the contaminating iron joins the pool, the impact on iron status could be substantial. Without a simple method for predicting exchangeability, the impact of contaminant iron on iron status in any particular situation is uncertain., Conclusions: : Interventions known to increase the absorption of iron intrinsic to foods will also increase absorption of any contaminant iron that has joined the common pool. Any positive effect of geophagy resulting from an increased intake of iron is highly unlikely, due to inhibiting constituents contained in soils and clays. The efficacy of approaches designed to increase the intake of contaminant iron remains encouraging but uncertain. An approach using multiple interventions will continue to be essential to reduce iron deficiency anaemia.

Objectives: It has been suggested that increased exposure to galactose, due to high consumption of dairy foods or reduced galactose metabolism, is associated with the development of ovarian cancer. We have investigated this in a large case-control study conducted in three Australian states between 1990 and 1993., Methods: Approximately 800 histologically-confirmed cases, 800 community controls and 300 controls recruited through breast-screening clinics completed dietary questionnaires. Approximately 100 cases and all breast-screening controls also provided a blood sample for analysis of galactose-1-phosphate-uridyltransferase (GALT)., Results: Ovarian cancer risk was positively associated with increasing consumption of whole milk and other full-fat dairy foods, but was not associated with consumption of low-fat dairy foods and was inversely related to consumption of skimmed milk. There was no association between ovarian cancer and GALT except among women with abnormally low GALT who had a non-significant 2.5-fold increased risk of ovarian cancer., Conclusions: These data do not support the hypothesis that galactose plays a major role in the development of ovarian cancer and suggest that reported associations between milk consumption and ovarian cancer are due to the fat content of milk and not to lactose or galactose. An increased risk of ovarian cancer in women with abnormally low levels of GALT cannot, however, be ruled out.

Unlabelled: Programs of widely ranging size were conducted successfully in seven localities and thus the program was considered an operational success. The reductions in weight, blood pressure, and waist and hip measurements observed at the 3-month follow-up compared well with reports of other community-based programs. Almost all participants evaluated the program highly and reported positive changes in behaviors related to food and exercise. Qualitative data indicate that the coordinators developed a sense of ownership of the program--which will be vital to its sustainability. Rapport between coordinators and participants was more easily established in smaller programs than in larger ones and was an important underlying determinant of retention rates., Significance: The Lighten Up program integrates environmental and individual strategies to facilitate changes towards a positive, lifestyle approach to long-term weight management. The program aims to establish sustainable social support networks with effective links to health services. This study has demonstrated that, with appropriate training and resources, existing public sector, primary health care personnel with no previous experience in health promotion can implement the program successfully in several communities concurrently. In the Australian context, this program can play an important role as one strategy in a range of interventions required to address the issue of obesity. The stepped-care model described by Brownell proposes that program options of varying intensity, and thus cost, be available to meet the variety of needs of overweight people who wish to lose weight. The Lighten Up program was close to the midpoint of that range in that it combined population strategies with one-on-one contact with health care personnel., Limitations: Participants in the study were self-selected people who had acted quickly to enroll in the program, and it is therefore likely that the sample was overrepresented with early adopters who may have been more successful than others would have been. We cannot tell from this developmental study whether or not the program will appeal to population groups known to be at high risk for obesity. This is an important question that needs to be addressed in future research. No control group was included in the design and thus we cannot be sure the benefits experienced by the participants resulted from the program. However, process evaluation data indicate that nothing that might explain the findings, other than the program, occurred in the communities during the time of the study. Further important issues to be evaluated include: the long-term maintenance of weight loss; whether or not the program will reach targeted populations, particularly groups of low socioeconomic status; and the extent to which the public health staff will maintain enthusiasm for the training and the programs.

This study assesses the validity and reproducibility of a 145-item self-administered food frequency questionnaire (FFQ) in a representative older population aged 63 to 80. Semi-quantitative FFQs were completed by 89% of 3,654 residents attending a community-based eye study in Sydney, Australia. The FFQ's validity was assessed against three, four-day weighed food records (WFRs) completed four months apart by 79 people. A further 152 subjects completed a repeat FFQ about a year after the baseline FFQ, of whom 131 completed a second repeat FFQ about six weeks later. Both short and long-term reproducibility of the FFQ were assessed using data from these subjects. Comparison of the FFQ with the average of the three, four-day weighed food records resulted in energy-adjusted Spearman correlations above 0.5 for most of the nutrients. The proportion of subjects correctly classified to within one quintile category for each nutrient intake ranged from 57% for zinc to 82% for vitamin C. with most nutrients correctly classified within one quintile for about 70% of subjects. Quadratic weighted kappas were reasonable, between 0.3 and 0.5 for most nutrients. The FFQ was highly reproducible in the short term, with correlations for most nutrients about 0.70 to 0.80 and acceptably reproducible in the longer term, with correlations mostly 0.60 to 0.70. The results verify that it is possible to use relatively simple, but comprehensive, self-administered FFQs to study nutrient exposures in large-scale epidemiological studies of the elderly and to expect reasonably high FFQ response rates.

Objective: Examine the validity of self-reported use of reduced fat and reduced salt foods., Design: Compare data collected in a food frequency questionnaire with supermarket sales data and food supply data., Setting: Rural Australia., Subjects: Four hundred and fifty-three respondents from an original sample of 1616 randomly-selected residents., Interventions: Community health campaign to reduce cardiovascular disease., Results: Reported use of reduced fat and reduced salt foods was greater than store sales and milk deliveries of these products., Conclusions: External data did not support the validity of self-reported use of these products.