Population Strategies For Prevention Research Articles

SARS-CoV-2: influence of phosphate and magnesium, moderated by vitamin D, on energy (ATP) metabolism and on severity of COVID-19.

The use of vitamin D to reduce the severity of COVID-19 complications is receiving considerable attention, backed by encouraging data. Its purported mode of action is as an immune modulator. Vitamin D, however, also affects the metabolism of phosphate and Mg, which may well play a critical role in SARS-CoV-2 pathogenesis. SARS-CoV-2 may induce a cytokine storm that drains ATP whose regeneration requires phosphate and Mg. These minerals, however, are often deficient in conditions that predispose people to severe COVID-19, including older age (especially males), diabetes, obesity, and usage of diuretics. Symptoms observed in severe COVID-19 also fit well with those seen in classical hypophosphatemia and hypomagnesemia, such as thrombocytopenia, coagulopathy, dysfunction of liver and kidneys, neurologic disturbances, immunodeficiency, failure of heart and lungs, delayed weaning from a respirator, cardiac arrhythmia, seizures, and, finally, multiorgan failure. Deficiencies of phosphate and Mg can be amplified by kidney problems commonly observed in patients with COVID-19 resulting in their wastage into urine. Available data show that phosphate and Mg are deficient in COVID-19, with phosphate showing a remarkable correlation with its severity. In one experiment, patients with COVID-19 were supplemented with a cocktail of vitamin D3, Mg, and vitamin B12, with very encouraging results. We, thus, argue that patients with COVID-19 should be monitored and treated for phosphate and Mg deficiencies, ideally already in the early phases of infection. Supplementation of phosphate and Mg combined with vitamin D could also be implemented as a preventative strategy in populations at risk.

A study protocol for a predictive algorithm to assess population-based premature mortality risk: Premature Mortality Population Risk Tool (PreMPoRT)

BackgroundPremature mortality is an important population health indicator used to assess health system functioning and to identify areas in need of health system intervention. Predicting the future incidence of premature mortality in the population can facilitate initiatives that promote equitable health policies and effective delivery of public health services. This study protocol proposes the development and validation of the Premature Mortality Risk Prediction Tool (PreMPoRT) that will predict the incidence of premature mortality using large population-based community health surveys and multivariable modeling approaches.MethodsPreMPoRT will be developed and validated using various training, validation, and test data sets generated from the six cycles of the Canadian Community Health Survey (CCHS) linked to the Canadian Vital Statistics Database from 2000 to 2017. Population-level risk factor information on demographic characteristics, health behaviors, area level measures, and other health-related factors will be used to develop PreMPoRT and to predict the incidence of premature mortality, defined as death prior to age 75, over a 5-year period. Sex-specific Weibull accelerated failure time models will be developed using a Canadian provincial derivation cohort consisting of approximately 500,000 individuals, with approximately equal proportion of males and females, and about 12,000 events of premature mortality. External validation will be performed using separate linked files (CCHS cycles 2007–2008, 2009–2010, and 2011–2012) from the development cohort (CCHS cycles 2000–2001, 2003–2004, and 2005–2006) to check the robustness of the prediction model. Measures of overall predictive performance (e.g., Nagelkerke’s R2), calibration (e.g., calibration plots), and discrimination (e.g., Harrell’s concordance statistic) will be assessed, including calibration within defined subgroups of importance to knowledge users and policymakers.DiscussionUsing routinely collected risk factor information, we anticipate that PreMPoRT will produce population-based estimates of premature mortality and will be used to inform population strategies for prevention.

Behavioral Sleep Interventions in the First Six Months of Life Do not Improve Outcomes for Mothers or Infants

The United Kingdom's National Institute for Health Research has recently invited proposals for the design of a multicomponent primary care package of behavioral interventions to reduce parental distress caused by excessive infant crying in the first 6 months of life. A systematic review was performed to determine whether behavioral interventions for sleep, when applied by parents to infants younger than 6 months, improve maternal and infant outcomes. Searches of PubMed, CINAHL, and Cochrane Database of Systematic Reviews were conducted to identify systematic reviews, meta-analyses, clinical trials, and cohort studies investigating the effects of behavioral sleep interventions in infants younger than 6 months (January 1993-March 2013). The evidence is critically analyzed, according to PRISMA guidelines. Cry-fuss, feeding, and sleep problems emerge out of multiple dynamically interacting and co-evolving variables in early life and are for this reason generically referred to as regulatory problems. Studies that link behavioral interventions for sleep in the first 6 months with positive effects on maternal and infant health demonstrate 3 methodological constraints. They fail to identify and control for feeding difficulties, fail to distinguish between the neurodevelopmentally different first and second halves of the first year of life, and apply reductive analyses to evaluations of complex interventions. Despite substantial investment in recent years in implementation and evaluation of behavioral interventions for infant sleep in the first 6 months, these strategies have not been shown to decrease infant crying, prevent sleep and behavioral problems in later childhood, or protect against postnatal depression. In addition, behavioral interventions for infant sleep, applied as a population strategy of prevention from the first weeks and months, risk unintended outcomes, including increased amounts of problem crying, premature cessation of breastfeeding, worsened maternal anxiety, and, if the infant is required to sleep either day or night in a room separate from the caregiver, an increased risk of SIDS. The belief that behavioral intervention for sleep in the first 6 months of life improves outcomes for mothers and babies is historically constructed, overlooks feeding problems, and biases interpretation of data.

Commentary: Structure or agency? The importance of both for addressing social inequalities in health

In their paper entitled ‘Rose’s population strategy of prevention need not increase social inequalities in health’, McLaren et al. offer a cogent response to our earlier paper ‘The inequality paradox: the population approach and vulnerable populations’. It is a pleasure, and was indeed our goal, to see a lively debate sparked by our initial musings. It is therefore an equal pleasure to respond to their paper as part of a further debate. McLaren et al.’s argument rests in part on the idea that not all population prevention interventions influence social inequalities in health to the same extent. They argue that their influence depends on whether the strategy is what they call structural or agentic; the former targets the conditions in which behaviours occur, the latter, behaviour change among individuals. They conclude that structural interventions are less likely to worsen social inequalities in health than agentic strategies. While this distinction is interesting it may be somewhat distracting given that social inequalities in health, we have argued in the past, arise due to the interplay of ‘both’ structure and agency. While McLaren et al. rightly cite Anthony Giddens as an important 20th century thinker with respect to the structure/agency debate, they fail to mention that among Giddens’ most important contributions to sociology has been his structuration theory. Structuration theory is based on the idea that both agency, defined as the ability to deploy a range of causal powers, and structure, objectified as the rules and resources in society, give rise to people’s social practices, which are the activities that make and transform the world we live in (referred to by people in public health as behaviours). Using the heuristic of collective lifestyles, it has been argued that an adequate tackling of inequalities in health should address all three aspects of structuration theory (agency, social structure and social practices) rather than structure or agency alone. Indeed, we thank the authors for bringing us back to some of our earlier reflections with regard to the structure/agency relationship as it plays a crucial role in our new argument regarding vulnerable populations. By using the term vulnerable populations, we sought to move away from risk factor epidemiological thought, which tends to focus largely on behaviour alone, and suggest that some groups are vulnerable with regard to their agency, their position with regard to the social structure and their social practices. It is only by focusing on all three that one would be able to reduce social inequalities in health, as all three are at the base of these inequalities. However, we agree with McLaren et al. that the use of the term vulnerable populations is not without problems, including potential stigmatization. One might consider instead the concept of exclusionary process developed by the Social Exclusion Knowledge Network of the WHO Commission on the Social Determinants of Health. Their critique of the notion of vulnerability is that it emphasizes a state without identifying causes, and that it becomes a characteristic of people and not the result of a process. On the contrary, an exclusionary process originates in the unequal distribution of four types of resources: material, cultural, social and political. It is the unequal distribution of these resources that reproduces health inequalities. This notion of exclusionary processes points to the importance of working upstream in order to address some of the original causes that led to the unequal distribution of these resources. A final note is warranted regarding our perspective on participation. The authors suggest that participatory strategies may ultimately be agentic if structural conditions are not addressed. It is true that the public health literature tends to be ideological and offers little theoretical breadth with regard to the conditions required in the participatory process. In our view participatory planning is a political process. This process Published by Oxford University Press on behalf of the International Epidemiological Association

Rose's population strategy of prevention need not increase social inequalities in health

Geoffrey Rose's 1985 paper, Sick individuals and sick populations, continues to spark debate and discussion. Since this original publication, there have been two notable challenges to Rose's population strategy of prevention. First, identification of high-risk individuals has improved considerably in accuracy, which some believe obviates the need for population-wide prevention strategies. Secondly, and more recently, it has been suggested that population strategies of prevention may inadvertently worsen social inequalities in health. We argue that population prevention will not necessarily worsen social inequalities in health, and the likelihood of it doing so will depend on whether the prevention strategy is more structural (targets conditions in which behaviours occur) or agentic (targets behaviour change among individuals) in nature. Also, there are potential drawbacks of approaches that focus on discrete populations (i.e. high risk or vulnerable) that need to be considered when selecting a strategy. Although Rose's ideas need to be continually scrutinized, his population strategy of prevention still holds considerable merit for improving population health and narrowing social inequalities in health.

Prevention strategies for sexually transmitted infections: importance of sexual network structure and epidemic phase

This article explores the relationship between sexual network structure and epidemic phase in sexually transmitted disease epidemiology, and discusses how this may be used to inform prevention strategies at the...

A maternalistic approach to prevention

One of the fundamental goals of public health is the prevention of disease to reduce human suffering. Identifying risk factors for diseases is an important milestone towards prevention, but influencing global health often requires converting such findings into behavioural modifications. We are painfully aware how difficult behavioural changes are, and consequently many insights into disease causation remain scientific discoveries that do not translate into substantial reductions of the global burden of disease. Can we more effectively convert our knowledge into successful prevention using a population strategy of prevention that circumvents the individual’s choice? Or does our society favour the freedom of the individual’s choice even at the expense of a conscious self-destruction of health, thus increasing the burden of disease and the cost to society? In this issue of the journal, Adams and White focus on one possibly problematic aspect of the population approach to prevention, its effect on individuals with the lowest risk when a J-shaped curve characterizes the relation between risk factor and disease. 1 Adams and White point out an issue that Geoffrey

The strategy of preventive medicine

Part 1 The Objectives of Preventive Medicine: The scope for prevention. Why seek to prevent?: the economic and humanitarian arguments. Priorities: a matter of choice Part 2 What needs to be prevented?: Sick individuals: a continuum of disease severity case definitions. A continuum of risk: the prevention paradox mass and individual measures. A unified approach Part 3 The Relation of Risk to Exposure: The dose-effect relationship. The limitations of research methods. Small but widespread risks: a public health disaster? Part 4 Prevention for Individuals and the High-risk Strategy Prevention and clinical care The high-risk strategy. Identifying risk-screening. Strengths and weaknesses of the high-risk strategy Part 5 Individuals and Populations: Individual variation: genetic, social and behavioural determinants of diversity. Variation between populations. Sick and healthy populations Part 6 Some Implications of Population change: Effects of the population average on the occurrence of deviance examples from mental health. Health implications for the population as a whole: cardiovascular disease body weight birth weight early development and adult health Down's Syndrome alcohol osteoporosis and fractures occupational and environmental health other fields of application. Safety Part 7 The Population Strategy of Prevention: Principles: the sociological, moral and medical arguments scope proximal and underlying causes. Strengths. Limitations and problems 8. In Search of Health: How do populations change?: the alcohol example. Scientific justification for change. Social engineering versus individual freedom. Freedom of choice. Role of governments. Who takes the decisions? The largest threat to public health: war. Social and economic deprivation. Responsibility for health.