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By N. Umul. Bethel College, McKenzie, Tennessee. 2018.

The cholesterol-raising properties of saturated fats are attributed to lauric acid (12:0) generic aygestin 5mg mastercard, myristic acid (14:0) buy aygestin 5 mg with visa, and palmitic acid (16:0) aygestin 5 mg online. Stearic acid (18:0) and saturated fatty acids with fewer than 12 carbon atoms are thought not to raise serum cholesterol concentrations (146, 147). The effects of different saturated fatty acids on the distribution of cholesterol over the various lipoproteins are not well known. Trans-fatty acids come from both animal and vegetable sources and are produced by partial hydro- genation of unsaturated oils. Metabolic and epidemiological studies have indicated that trans-fatty acids increase the risk of coronary heart disease (145, 152, 153). It has also been demonstrated that replacing saturated and trans-unsaturated fats with monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease events than reducing overall fat intake (145, 153, 155). Current guidelines recommend a diet that provides less than 30% of calories from dietary fat, less than 10% of calories from saturated fats, up to 10% from polyunsaturated fats, and about 15% from monounsaturated fats (86, 88, 148). Metabolic studies have shown that dietary cholesterol is a determinant of serum cholesterol concentration (156–158). Reducing dietary cholesterol by 100 mg a day appears to reduce serum cholesterol by about 1% (147). However, there is marked individual variation in the way serum cholesterol responds to dietary cholesterol (159); dietary cholesterol seems to have a relatively small effect on serum lipids, compared with dietary saturated and trans-fatty acids (88, 104, 158). Studies have demonstrated that, in controlled conditions, it is possible to modify behaviour, but in daily life the required intensity of supervision may not be practicable. The effects of advice about reducing or modifying dietary fat intake on total and cardiovascular mortality and cardiovascular morbidity in real-life settings were assessed in a systematic review of 27 studies, comprising 30 902 person–years of observation (160). The interventions included both direct provision of food and, in most trials, dietary advice to reduce intake of total fat or saturated fat or dietary cholesterol, or to shift from saturated to unsaturated fat. The pooled results indicate that reducing or modifying dietary fat reduces the incidence of combined cardiovascular events by 16% (rate ratio 0. The reduction in cardiovascu- lar mortality and morbidity was more pronounced in trials lasting at least 2 years. The protective effect of polyunsaturated fats is similar in high- and low-risk groups for both sources (seafood and plants), and in women and men (104, 155, 161, 162). Epidemiological studies and clinical trials suggest that people at risk of coronary heart disease benefit from consuming omega-3 fatty acids (104, 161, 163, 164). The proposed mechanisms for a cardioprotective role include altered lipid profile, reduced thrombotic tendency, and antihypertensive, anti-inflammatory and antiarrhythmic effects (165–168). A systematic review showed a significant benefit of fish-based dietary supplemental omega-3 fatty acids on cardiovascular morbidity and mortality in patients with coronary heart disease (169, 170). Cohort studies analysing omega-3 fatty acid intake and risk of cardiovascular diseases have shown inconsistent findings, however, and a recent large trial of omega-3 fatty acids did not find any benefits (171). In an attempt to clarify their role, an updated meta-analysis has also been conducted (170, 172). Using data from 48 randomized controlled trials and 41 cohort analyses, an assessment was made of whether dietary or supplemental omega-3 fatty acids altered total mortality, cardiovas- cular events or cancers. Pooled trial results did not show a reduction in the total mortality risk or the risk of combined cardiovascular events in those taking additional omega-3 fats. Population studies have demonstrated that high salt intake is associated with an increased risk of high blood pressure (173). Several observational studies have linked baseline sodium intake, estimated from either 24-hour urinary sodium excretion or dietary intake, to morbidity and mor- tality. In a Finnish study, the hazard ratios for coronary heart disease, cardiovascular disease, and all-cause mortality, associated with a 100 mmol increase in 24-h urinary sodium excretion in men and women, were estimated as 1. A prospective study in a Japanese cohort also showed that high dietary salt intake increased the risk of death from stroke (175). A study in hypertensive patients reported an inverse relation between sodium intake and cardiovascular outcomes (176) and suggested a J-curve relationship. This discordant finding has been attributed to methodologi- cal limitations and further study is needed. The efficacy of reduced sodium intake in lowering blood pressure is well established (176, 177). An average reduction of 77 mmol/day in dietary intake of sodium has been shown to reduce systolic blood pressure by 1. Phase 2 of the Trials of Hypertension Prevention Studies has also documented that a reduced sodium intake can prevent hypertension (178). In a meta-analysis of dietary interventions to alter salt intake, which included 17 randomized controlled trials in people with high blood pressure and 11 in people with normal blood pres- sure, a reduction of 100 mmol (6 g) per day in salt intake was associated with a fall in blood pressure of 7. This information strongly supports other evidence that a modest, long-term reduction in population salt intake would immediately reduce stroke deaths by about 14% and coronary deaths by about 9% in people with hypertension, and by approximately 6% and 4% in those with normal blood pressure. This review has been pro- duced and updated as a Cochrane systematic review (180). The authors concluded that, in trials of four or more weeks duration, a reduction in salt intake had a significant and, from a population viewpoint, important effect on blood pressure in individuals with normal or high blood pressure. In individuals with elevated blood pressure, the median reduction in 24-h urinary sodium excre- tion was 78 mmol (equivalent to 4. In individuals with normal blood pressure, the median reduction in 24-h urinary sodium excretion was 74 mmol (4. This demonstrates a cor- relation between the magnitude of salt reduction and the magnitude of blood pressure reduction. These findings may, however, exaggerate the reductions achievable in routine clinical practice.

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In all patients long-term strict and thus stroke aygestin 5mg with visa, paraplegia (due to spinal artery in- blood pressure control is needed order aygestin 5 mg on line. Myocardial infarction may occasionally be due to dis- section involving the coronary arteries discount aygestin 5 mg on line. Incidence r Chest X-ray may show a widened mediastinum: di- Commonest vascular emergency. Chapter 2: Hypertension and vascular diseases 81 Sex kinase and myoglobin, which can cause acute renal fail- M > F urebyadirecttoxiceffect(rhabdomyolysis). Incasesofembolifurtherpost- of atrial fibrillation or post-infarction) or from ab- operative investigation is required to establish the source normal, infected or prosthetic heart valves. Hypo- Following assessment and resuscitation treatment in- volaemia or hypotension often precipitates complete volves the following: occlusion. Less commonly thrombosis may arise in r Heparintominimisepropagationofthrombus,invery non-atherosclerotic vessels as a result of malignancy, mild cases this will be sufficient. Loss of arterial blood supply causes acute ischaemia and r Acute occlusion with signs of severe ischaemia is irreversible infarction occurs if the occlusion is not re- treated with emergency surgery. Aftertheocclusionisrelievedthere mbectomy is usually performed with a Fogarty bal- maybesecondarydamageduetoreperfusioninjury. This loon catheter under local anaesthetic if possible, and is due to the production of toxic oxygen radicals, which complex cases may require arterial reconstruction. Clinical features Prognosis Patients present with a cold, pale/white and acutely Acute upper limb ischaemia tends to have a better prog- painfullimb,whichbecomesweakandnumbwithlossof nosis, as there is better collateral supply. Unfortunately, sensation and paraesthesiae, which starts distally (pain acute lower limb arterial occlusion is more common. Paraesthesiae or reduced muscle power are as high as 20%, depending on the degree of ischaemia at signs of severe ischaemia. Complete loss of muscle power with tender, firm muscles is a sign of muscle infarction. Deep vein thrombosis Definition Complications A thrombus forming in a deep vein most commonly Compartment syndrome may occur (muscle swelling within the lower limb. Muscle stasis, vascular damage or hypercoagulability (Virkoff’s necrosis leads to the release of high quantities of creatine triad). Other risk factors include increasing age, malignant dis- ease, varicose veins and smoking. Varicose veins Definition Pathophysiology Distended and dilated lower limb superficial veins as- The starting point for thrombosis is usually a valve sinus sociated with incompetent valves within the perforating in the deep veins of the calf, primary thrombus adheres veins. Incidence Common Clinical features The condition is often silent and pulmonary embolism Age may be the first sign. Familial predisposition, obesity, pregnancy and prolonged standing are estab- Investigations lished aetiological factors. Ultrasound or Doppler ultrasound scans can be used to confirm the diagnosis; below-knee thromboses cannot Pathophysiology be easily seen and may only be diagnosed with venogra- r Primary varicose veins are common and show a fa- phy. Alternatively, in patients with a low clinical risk for milial tendency, which may either be due to intrinsic deepveinthrombosismaybescreenedusingtheD-dimer valve incompetence or loss of elasticity in the veins. If the D-dimer is normal no further investigation is r Secondary varicose veins develop after valve function required. The valves in the perforating Management veins are disrupted, so that blood refluxes from the Bedrestandcompressionstockings;patientswithabove- deep veins to the superficial veins. These changes are referred to as lipodermatoscle- patients with a large iliofemoral thrombosis. Chapter 2: Hypertension and vascular diseases 83 Clinical features Clinical features Patients complain of cosmetically unsightly veins and The pain may be dull or burning, usually superficial and aching, heavy legs. There may be a family history or his- on examination there may be one or more visible cord- tory of previous deep vein thrombosis. The superficial veins are prone Complications to thrombus formation due to stasis, causing tender, If there is a portal of entry, e. Investigations The site of the incompetent valve can be identified by the Investigations TrendelenbergtourniquettestorbyDopplerultrasound. No investigations are necessary, except to diagnose un- derlying deep venous insufficiency. Management Elderly patients are managed conservatively with weight reduction, regular exercise and avoidance of constricting Management garments. Sclerotherapy and laser therapy can be used The condition usually responds to symptomatic treat- for small varices, but only surgery is effective if there ment with rest, elevation of the limb and non-steroidal is deeper valve incompetence. After the acute attack, treatment of underlying r To interrupt incompetent connections between deep chronic venous insufficiency may be necessary, scle- and superficial veins. The sapheno-femoral junction rotherapy or laser therapy may be used as treatment for is visualised and the saphenous vein is ligated and varicose veins. Definition Ulceration of the gaiter area (lower leg and ankle) due to venous disease. Superficial thrombophlebitis Definition Incidence Inflammation of veins combined with clot formation. Aetiology/pathophysiology r Thrombophlebitis arising in a previously normal vein Age may result from trauma, irritation from intravenous Increases with age. Aggravating factors include old age, obesity, re- current trauma, immobility and joint problems.

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It is important to use an effective disinfectant discount 5 mg aygestin overnight delivery, such as 5% phenol generic aygestin 5mg without a prescription, iodine solutions with a high concentration of available iodine best 5mg aygestin, or glutaraldehyde, as M. On infected farms rodent control may be advisable given these species may become infected and may be able to transmit infection more widely. Livestock The insidious, chronic nature of this disease makes prevention or early detection and control imperative. In collaboration with the authorities conduct routine diagnostic tests and report suspected cases and dead animals. Control of wildlife reservoirs or means by which to isolate livestock from the reservoir. A badger entering a cattle shed, and a badger-proofed shed, which is a relatively straightforward means by which contact between livestock and wildlife can be reduced (Fera). Wildlife However desirable, there are many difficulties in controlling the disease in wildlife. Control can be achieved to some extent by using a combination of surveillance and management to monitor and control the spread and occurrence of the disease. This might be achieved in various ways including use of physical barriers to restrict wildlife access to domestic animal housing. In some wildlife populations reducing population density and/or changing social behaviour can help to reduce risk. This may be achieved in a number of ways including not providing supplementary food which can maintain animals above a carrying capacity for an area and not using feeding stations (for e. Vaccination is a possibility for control of the disease in wildlife (primarily to reduce risk to livestock). Humans Humans should protect themselves by wearing protective clothing (including gloves, masks) when dealing with infected animals as infections in humans are difficult to treat. Cooking meat thoroughly or pasteurisation of milk and other dairy products reduces risk of infection. Presence of the disease may also lead to loss of consumer confidence in milk and beef products. Potential human health risks in the developing world, in particular, and the additional potential for infection in a wide range of hosts including free-roaming wildlife increases the need for control in domestic situations. Effect on humans Public health concerns arise from the possibility of human infection with M. Incidence appears higher in personnel that work closely with cattle such as farmers and abattoir staff. It has also been documented that humans can be infected by exposure to other species, including goats, farmed elk and even rhinoceros. In countries where bushmeat is eaten wildlife species may be a particular source of infection. In some communities the close contact of humans and animals may facilitate disease transmission, for example, in some African countries cattle are an integral part of life and are present at ceremonies representing wealth and animals working in agriculture. A review of tests available for use in the websites diagnosis of tuberculosis in non-bovine species. Revue Scientifique et Technique de l’Office International des Épizooties, 24 (3): 1039-1059 www. A chronic and contagious bacterial disease of domestic and wild animals that may be transmitted to humans. In humans, it causes influenza-like symptoms which can be severe and last for months and can be confused with malaria and typhoid. Species affected Many species of terrestrial and marine mammals, particularly cattle, swine, bison, elk Cervus canadensis, deer, goats, sheep, other ruminants and humans. Wildlife reservoirs do exist and can include feral pigs, bison, and elk amongst others. Geographic distribution Present to varying degrees in most countries of the world. High risk areas are the Mediterranean Basin (Portugal, Spain, Southern France, Italy, Greece, Turkey, North Africa), South and Central America, Eastern Europe, Asia, Africa, the Caribbean, and the Middle East. Direct contact with infected animals or with an environment that has been contaminated with birthing tissues or, most commonly, fluids from infected animals (e. Animals may lick those materials or the genital area of other animals or ingest the disease-causing organisms with contaminated food or water. Venereal transmission is the most common means of spread but the bacteria can also be found in milk, blood, urine and semen. How does the disease Brucellosis is usually spread from one animal group to another by an spread between groups infected or exposed animal, e. Brucellosis can also be spread by contaminated objects (fomites) such as equipment, clothing, shoes, feed or water. Person-to- person transmission is very rare but has occurredthrough transplants, sexual intercourse, or from mother to child. Milk production may be reduced, and other signs include an apparent lowering of fertility with poor conception rates, retained afterbirths with resulting uterine infections, and (occasionally) enlarged, arthritic joints. Recommended action if Contact and seek assistance from appropriate animal health professionals. Disinfection and sanitation Livestock The disease in livestock may be avoided by employing good sanitation and animal management practices e. Preventing the introduction of infection through movement controls, testing and quarantine. Detecting any infected animals in the population as early as possible through surveillance, and thoroughly investigating all suspect cases. Eliminating any confirmed infection found in livestock through the slaughter of infected and exposed animals. Cleaning and disinfection of calving areas and other places likely to become contaminated with infective material.

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A typical large American hospital may have as many as three dozen separate computer systems discount 5mg aygestin with amex, ranging in age from near-Technicolor- quality youth to green-screened senility 5 mg aygestin free shipping. That is 5 mg aygestin otc, a patient may be a different person in the emergency room than he or she is in the clinical laboratory, in the surgical suite, and yet again in the doctor’s office just a day earlier. Each of these different sites of care within the same organization maintains a different medical record of its encounters with same patient. These separate systems were primarily built to bill for each department’s services, not to guide patient care. There is also a nearly impermeable barrier between the hospital’s records and those of the physicians who direct the care. In the typical community hospital, it is impossible for the doctor or any other care worker to access the doctor’s office records from any site other than that doctor’s office because more than 80 percent of those office records are still in paper form. Furthermore, most doctors in private medical practice have been unwilling to support shared digital record-keeping systems with their hospitals because of a profound lack of trust and poor communication with hospital management. Even where it is possible to link all of these fragments of a pa- tient’s history and medical situation electronically, a considerable feat of software engineering is required to move this information around quickly enough that it can actually be used by the physician in making important care decisions. When information reaches a digital dead end, it is printed out and piled up in various in-boxes or paper filing systems. Thus, vital information remains locked up in paper, or in people’s short-term memories, and cannot flow through wire or fiber or the air to where it is needed to make timely and accurate medical decisions. As long as the source documents detailing patient care remain in paper form, the only way to determine whether particular clinical decisions contributed to a positive health outcome is to hire squads of graduate students or nurses to cull the records by hand months later and tabulate the results. The fact that we know so little about 4 Digital Medicine what actually works in medical treatment can be attributed in large part to the prison of paper we have constructed around the care process. Public research in- vestments through the National Institutes of Health and private equity investment, including research and development expendi- tures by the nation’s pharmaceutical and biotechnology firms, are creating new medical knowledge at a stunning pace. In 2001, nearly $51 billion was invested in creating new knowl- edge in medicine just in the United States. The logistics of medical practice itself have become so dauntingly complex that physicians barely have time for their families, let alone time to keep pace with the exciting advances in their own fields. A monthly continuing medical education session at the hospital or local medical society and periodic visits from pharmaceutical salespeople are the principal conduits of new knowledge to most practicing physicians. A visit to a physician’s personal office typically reveals piles of unread medical journals, pink telephone message slips, and scattered samples of new drugs from the last pharmaceutical sales representa- tive to visit the office. The computer in the office is probably turned off, is likely at least three years old, and is surely not configured to The Information Quagmire 5 reach or retain data about current medical practice. Physicians know they are not keeping up, and this both frustrates and frightens them. Professional training and culture in medicine conditioned physi- cians to rely principally on direct peer contact and what they can carry around in their memories to support their advice to patients. The channels by which new information reaches physicians in prac- tice are dangerously narrow and lack the bandwidth and intelligence to organize and transmit the flood of new medical knowledge in a way that it can be absorbed and used in practice. Although major journals have digitized their articles and made them available online, medical knowledge is still largely paper driven. Unless physicians have a good relationship with a medical librarian or, as do a lucky few senior physicians in teaching hospitals, have residents and fellows to research issues for them, the large number of important questions about a patient’s health that occur to a physician during a typical practice day never get answered. How- ever, the reality is that the lack of timely and accurate information at the point of care is a major contributor to patient deaths and injuries, as well as resulting in a waste of time and money. As a vehicle for applying medical knowledge to solving problems, the healthcare system has become increasingly cumbersome, user- unfriendly, and expensive. When the Internet opened up new channels for consumers to access medical knowledge directly, it was rapidly flooded with users. According to a recent Harris poll, roughly 110 million Americans used the Internet to seek health information in 2002. According to Peter Drucker (see Note 1), large healthcare institutions, like urban academic health centers, may be the most complex organizations in human history. Not only do the medical problems presented at the point of service vary tremendously, but no inventory exists; health services are, for the most part, custom manufactured for individual patients on a “just in time” basis. For most healthcare, there is no template on which physicians can rely to make decisions about health. This is because professional consensus on what best practice is or ought to be is only now emerging. Perhaps most significantly, more complex, highly trained health professionals collide at the point of care than in any other business in our economy. Each profession has its own unique view of the patient’s needs, its own language for describing those needs, and an intensely territorial view of its involvement in care. Collaboration The Information Quagmire 7 among professionals is vital to effective care, yet professions compete for resources and control over patients. It is on the verge of revolutionizing medi- cal practice, dramatically improving communication among physi- cians and between physicians and patients. Whereas hospitals and major insurers have been connected elec- tronically for years through dedicated, high-bandwidth telephone conduits called T1 lines, the advent of the Internet has recently brought affordable broadband connect ivity to doctors and patients. The Internet has not only brought new options for physicians and patients to connect with one another, it has made possible con- nectivity to and networking with thousands of colleagues and tens of thousands of patients worldwide. Complex software can now be maintained efficiently at a single site on remote servers, which hospital and physician users can reach by way of a web browser and high-speed 8 Digital Medicine Internet connections.

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The results presented in this chapter suggest that a global goal for preventing chronic disease is needed to generate the sustained actions required to reduce the disease burden discount aygestin 5mg. The target for this proposed goal is an additional 2% reduction in chronic disease death rates annually over the next 10 years to 2015 5 mg aygestin overnight delivery. The indicators for the measurement of success towards this goal are the number of chronic disease deaths averted and the number of healthy life years gained purchase 5 mg aygestin. This target was developed based on the achievements of several coun- tries, such as Poland, which achieved a 6–10% annual reduction in cardiovascular deaths during the 1990s (8). Similar results have been realized over the past three decades in a number of countries in which comprehensive programmes have been introduced, such as Austra- lia, Canada, New Zealand, the United Kingdom, and the United States (9–11). This global goal aims to reduce death rates in addition to the declines already projected for many chronic diseases – and would result in 36 million chronic disease deaths averted by 2015. This represents an increase of approximately 500 million life years gained for the world over the 10-year period. Cardiovascular diseases and cancers are the diseases for which most deaths would be averted. Most of the deaths averted from specific chronic diseases would be in low and middle income countries as demonstrated by the top figure, opposite (12). Chronic diseases: causes and health impacts Projected cumulative deaths averted by achieving the global goal, by World Bank income group, 2006–2015 40 Low and middle income countries High income countries 35 30 25 20 15 10 5 0 Chronic Cardiovascular Cancer Chronic Diabetes diseases diseases respiratory diseases Every death averted is a bonus, but the goal contains an additional positive feature: almost half of these averted deaths would be in men and women under 70 years of age (see figure below). Extending their lives for the benefit of the individuals concerned, their families and communities is in itself the worthiest of goals. It also supports the overall goal of chronic disease prevention and control, which is to delay mortality from these diseases and to promote healthy ageing of people everywhere. Chronic disease deaths, projected from 2005 to 2015 and with global goal scenario, for people aged 70 years or less 20 2005 2015 baseline 2015 global goal 18 16 14 12 10 8 6 4 2 0 Chronic Cardiovascular Cancer Chronic Diabetes diseases diseases respiratory diseases This goal is ambitious and adventurous, but it is neither extravagant nor unrealistic. The means to achieve it, based on the evidence and best practices from countries that have already made such improvements, such as the United Kingdom and the other countries referred to above, 59 are outlined in Parts Three and Four of this report. Confusion and long-held misunderstandings about the nature of chronic diseases, their prevalence, the popula- tions at risk, and the risk factors themselves are barriers to progress and prevention. What might have been true – or thought to be true – 30, 20 or even 10 years ago is no longer the case. The health of the world is generally improving, with fewer people dying from infectious diseases and therefore in many cases living long enough to develop chronic diseases. Increases in the causes of chronic diseases, including unhealthy diet, physical inactivity and tobacco use are leading to people developing chronic diseases at younger ages in the increasingly urban environments of low and middle income countries. Disturbing evidence of this impact in many of these countries is steadily growing. They are ill equipped to handle the demands for care and treatment that chronic diseases place on their health systems and so people die at younger ages than in high income countries. Individuals and their families in all countries struggle to cope with the impact of chronic diseases, and it is the poorest who are the most vulnerable. Chronic diseases and poverty Chronic diseases and poverty » The chronic disease burden is concentrated among the poor Chronic diseases and poverty » Poor people are more vulnerable are interconnected in a vicious for several reasons, including cycle. This chapter explains how, increased exposure to risks and decreased access to health in almost all countries, it is the services poorest people who are most » Chronic diseases can cause at risk of developing chronic poverty in individuals and diseases and dying prematurely families, and draw them into a from them. Poor people are more downward spiral of worsening disease and poverty vulnerable for several reasons, » Investment in chronic disease including greater exposure to prevention programmes is risks and decreased access to essential for many low and health services. Once again, it is people and families who are already poor who are most likely to suffer, because chronic diseases are likely to ruin a family’s economic prospects. Poverty can be divided into extreme (when households cannot meet basic needs for survival), moderate (in which basic needs are barely met), and relative poverty (in which household income is less than a proportion of average national income). Poverty is found in every country, but unlike moderate and relative poverty, extreme poverty occurs mainly in low income countries (13). Wealth enables people to avoid most of the risks of developing chronic disease, and to obtain access to health care. However, even within high income countries, psychosocial factors, for example lack of social support and perceived lack of control, are strongly related to the risk of chronic diseases (14 ). At the same time, in some countries, evidence clearly links growing national income with increases in obesity and high cholesterol levels across the population. Alarmingly, the evidence also reveals that this trend occurs at an earlier stage of socioeconomic development than has been previously assumed. As countries develop economically, some risk factors appear to affect wealthier populations first, although they quickly concentrate among the poor. In some countries at an early stage of economic development, wealthy members of society report more chronic disease than poorer members – it is unclear, however, whether this is because they develop more chronic diseases, or because they survive with them longer owing to their ability to access health services. In all countries, poor people are more likely to die after developing a chronic disease. In most countries, health inequalities have been widening over recent decades (15, 16). Once disease is established, poor people are more likely to suffer adverse consequences than 62 Chapter Two. This is especially true of women, as they are often more vulnerable to the effects of social inequality and poverty, and less able to access resources. In Denmark, England and Wales, Finland, Italy, Norway, and Sweden inequalities in mortality increased between the Material deprivationMaterial deprivation 1980s and the 1990s. These widening inequalities have been attributed and psychosocial stressand psychosocial stress to two important changes. The first is that cardiovascular disease death rates declined among Constrained choicesConstrained choices wealthy members of these societies, explaining about half of the widening and higher levels ofand higher levels of risk behaviourrisk behaviour gap. This might have been a result of faster changes in health behaviour in these groups and/or better access to health-care interventions.

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