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Younger people with very high BP levels warranting treatment should bemanaged in the same way as older people with hypertension. In youngerpeople who are judged eligible for a statin on the grounds of either FHor very high lipid levels, the management offered is the same as forolder people. Very importantly, for all patients deemed to suffer withFH, the physician making the management decisions should arrange for FHscreening for family members see section 3a. Age is the dominant driver of cardiovascular risk, and most individuals arealready at very high risk at the age of 65 years see section 2.

Especially in the oldest old, cardiovascular risk management iscontroversial. Opponents argue that risk should not be treated when it isessentially age-driven. Proponents, on the other hand, point out that manypreventive treatments are still effective at advanced age in terms ofpostponing morbidity and mortality.

The Task Force has taken the position that epidemiological evidence ofabsolute risk reduction in clinical trials is the main driver forrecommendations in this guideline. Still, we encourage a discussion withpatients regarding quality of life and life potentially gained, as well asregarding the ethical dilemmas of treating risk inherent to ageing, thetotal burden of drug treatment and the inevitable uncertainties ofbenefit. In this guideline, sections on treatment of the main risk factors containrecommendations or considerations specific to the elderly when evidence isavailable.

Most of the elderly-specific evidence is available for BP section 3a. In general, more lenient treatment targets are advocated in the elderly. The hypertension literature also contains increasing evidence thatbiological rather than calendar age is important. Evidence supporting more lenient glycaemic control targets in the elderlyis also available for DM section 3a. Few areas in CVD prevention are more controversial than the mass use ofstatins in the elderly. On the other hand, thecost-effectiveness of statins in these patients is offset by even smallgeriatric-specific adverse effects.

A recent trial suggested no harm of stopping statins in theelderly with a limited life expectancy. Several obstetric complications, in particular pre-eclampsia andpregnancy-related hypertension, are associated with a higher risk ofCVD later in life. This higher risk is explained, at least partly,by hypertension and DM.

Specific conditions that may occur in females only and may have an impact onCVD risk can be separated into obstetric and non-obstetric conditions. Studies suggest thatpre-eclampsia is associated with an increase in CV risk by a factor1. The rationale for screening these women for theoccurrence of hypertension and DM is, however, quite strong. The risk of developing DM is probablyalso elevated in these women, but exact estimates are not available.

There are no data to suggest that recurrent pregnancy loss is associatedwith an increased CV risk. PCOS has beenassociated with an increased risk for future development of CVD, butlarger studies have produced conflicting results. There are insufficient data to draw conclusions on apossible increased risk of hypertension or DM. The degree to which increased CVD risk associated with several ofthe female-specific conditions occurs independent ofconventional CVD risk factors is unknown.

Information on whether female-specific conditions improve riskclassification in women is unknown. CVD risk varies considerably between immigrant groups. Current risk estimation equations do not provide adequate estimationsof CVD risk in ethnic minorities. First-generation migrants usually display lower CVD mortality rates thannatives of the host country, but with time, migrants tend to approach the CVDrisk in their host country.

Immigrants from South Asia notably India and Pakistan present high CVDrates — and have a much higher prevalence ofDM, , while theprevalence of other CV risk factors is slightly lower than or comparable tonatives of the host country. Management of DM is alsosignificantly worse, while management of high BP and hypercholesterolaemiais better among South Asians than host country natives. Immigrants from China and Vietnam present lower CVD risk than natives of thehost country, although this finding has been challenged. This seems mainly due to the higher prevalence ofsmoking, DM, dyslipidaemia, hypertension and obesity rates.

Immigrants from Morocco present lower CVD rates than natives from the hostcountry. Immigrants from sub-Saharan Africa and the Caribbean present higher CVD ratesthan natives from the host country in some studies, , , but not all. Management of CVD risk factors was worsethan among natives in one study, but not in another. Based on available mortality and prospective data, the following correction factorscould be applied when assessing CVD risk using SCORE among first-generationimmigrants only.

These values reflect the best estimations from availabledata and should be interpreted with caution, but can be used to guide CVrisk management. Alternatively, ethnicity-specificCVD risk equations should be developed. Cognitive behavioural methods are effective in supporting persons inadopting a healthy lifestyle. Individual and environmental factors impedethe ability to adopt a healthy lifestyle, as does complex or confusing advicefrom caregivers. It is important to explore each patient's experiences,thoughts, worries, previous knowledge and circumstances of everyday life.

Individualized counselling is the basis for motivation and commitment. Decision-making should be shared between the caregiver and patient includingalso the individual's spouse and family. In addition, caregivers can build on cognitive behavioural strategies to assessthe individual's thoughts, attitudes and beliefs concerning the perceivedability to change behaviour, as well as the environmental context.

Previous unsuccessful attempts often affect self-efficacy for future change. Acrucial step is to help set realistic goals combined with self-monitoring of thechosen behaviour. Combining the knowledge and skills of caregivers such as physicians, nurses,psychologists, experts in nutrition, cardiac rehabilitation and sports medicine into multimodal behavioural interventions can optimize preventiveefforts.

There is limited evidence to determine which interventions are mosteffective in specific groups e. Treatment of psychosocial risk factors can counteract psychosocialstress, depression and anxiety, thus facilitating behaviour change andimproving quality of life and prognosis. The caregiver—patient interaction should follow the principles ofpatient-centred communication.

Age- and sex-specific psychosocialaspects should be considered. Caregivers in clinical practice are in a unique position to directly supporttheir patients regarding psychosocial risk factors in individuals with high CVrisk or with established disease. Empathic, patient-centred communication helpsto establish and maintain a trustful relationship and is a powerful source ofemotional support and professional guidance in coping with psychosocialstressors, depression, anxiety, CV risk factors and CVD.

Explain essential medical facts in the patient's own language, conveyhope and relief from feelings of guilt and reinforce adaptive thoughtsand actions. In the case of severe mental symptoms, obtain treatment preferences andperform shared decision-making regarding further diagnostic andtherapeutic steps. In addition to the treatment of mood symptoms, there are several other approachesto psychosocial intervention that have proved useful.

Two RCTs , have shown the favourable impact ofstress management and social support groups on the prognosis of clinical CAD. Nurse-led interventions reveal beneficial effects on anxiety, depression andgeneral well-being in CAD patients. In hostile CAD patients, a group-based hostility-control intervention may leadnot only to decreases in behaviourally assessed hostility levels, but also todecreased levels of depression, resting heart rate HR and CV reactivity tomental stress, as well as to increased social support and satisfaction withlife.

Hence, a reduction of work stress in managers and supervisors mayhave beneficial health effects on the target individuals and may also improveperceived social support in their subordinates. Evidence that treatment of clinically significant depression and anxietyalone will prevent CVD and improve outcomes is inconclusive.

Health providers should assess the PA level in any subject how many days andminutes per day are spent on average doing PA at moderate or vigorousintensity. They should warn against inactivity and help add PA to dailylife. Subjects should be advised on appropriate types of activities and waysof progressing and should be helped to set personal goals to achieve andmaintain the benefits. For a moreeffective behaviour change, clinicians should explore practical ways toovercome barriers to exercise. For this reason, the link between primarycare and local community-based structures for activity, recreation and sportis crucial.

Aerobic PA, the most studied and recommended modality, with a beneficialdose—response effect on prognosis, , , consists of movements of largemuscle mass in a rhythmic manner for a sustained period. It includeseveryday activity, including active travel cycling or walking , heavyhousehold work, gardening, occupational activity and leisure timeactivity or exercise such as brisk walking, Nordic walking, hiking,jogging or running, cycling, cross-country skiing, aerobic dancing,skating, rowing or swimming.

Similar to all other interventions, its prescription can be adjusted interms of frequency, duration and intensity. However, practising PA belowthe lowest recommended levels should be encouraged in individuals unableto meet the minimum or in those sedentary individuals who have juststarted, with a gradual increase in activity level. Moderate or vigorous aerobic exercise should be recommended. This can beexpressed either in absolute or relative terms.

By convention thiscorresponds to 3. Relative intensity is the level of effort required toperform an activity. Less fit individuals generally require a higherlevel of effort than fitter people to perform the same activity. Forindividuals on medication, it is important to consider possiblemodification of HR response and to refer to other relative intensityparameters. Especially for older and deconditioned individuals, arelative measure of intensity is more appropriate.

Classification of physical activity intensity and examples ofabsolute and relative intensity levels. Modified from Howley. PA should occur at a frequency of at least three to five sessions perweek, but preferably every day. Shorterexercise sessions i. Aerobic interval training and high-intensity interval training cannot yetbe broadly recommended until further data on safety and efficacy areavailable. Isotonic PA stimulates bone formation and reduces bone loss; it preservesand enhances muscle mass, strength, power and functional ability, withsome evidence of benefit in lipid and BP control and insulinsensitivity, especially in combination with aerobic exercise.

For older adults at risk of falls, neuromotor exercise helps to maintainand improve balance and motor skills balance, agility, coordination andgait. This includes multifaceted activities such as tai chi and yoga,and recreational activities using paddles or sport balls to challengehand—eye coordination. The optimal volume is not known. Progressive warm-up before and cool-downafter exercise may prevent injuries and adverse cardiac events. With the improvement in exercise tolerance, each subjectprogresses in the level of PA, but increases in any components i.

Before starting more intensive leisure time activities i. Clinical evaluation, including exercise testing, may beconsidered for sedentary people with CV risk factors who intend to engage invigorous PA and sports. The information gathered from exercise tests may beuseful in establishing a safe and effective exercise prescription. Validatedself-assessment questionnaires have been proposed for sedentary individualsentering low-intensity leisure time sports activity or startingmoderate-intensity activities see Table B in web addenda. The lower and upper limit of aerobic PA intensity, duration andfrequency to exert a beneficial effect is unknown.

The effectiveness of PA monitoring vs. There is a strong evidence base for brief interventions with advice tostop smoking, all types of nicotine replacement therapy NRT ,bupropion, varenicline and greater effectiveness of drugs incombination, except for NRT plus varenicline. The most effective arebrief interventions plus assistance with stopping using drug therapy andfollow-up support. Electronic cigarettes e-cigarettes may help in smoking cessation butshould be covered by the same marketing restrictions as cigarettes.

Smoking is a lethal addictive disorder. The year fatal CVD risk is approximately doubled insmokers. Slightly less than half of lifetime smokers will continue smoking untildeath. Although the rate of smoking is declining in Europe, it remains very commonand is increasing in women, adolescents and the sociallydisadvantaged. The survey also foundthat evidence-based treatment for smoking cessation was underused.

The risks associated with smoking show a dose—response relationship with nolower limit for deleterious effects. Tobacco smoke is more harmful when inhaled,but smokers who claim not to inhale the smoke e. Smokeless tobacco is also associated with a smallbut statistically significant increased risk of MI and stroke. Passive smoking increases the risk of CAD.

Major health benefits result from reducedenvironmental tobacco smoke, with public smoking bans in various differentgeographical locations leading to significant decreases in MI rates seesection 3c. Smoking enhances the development of both atherosclerosis and superimposedthrombotic phenomena. Smoking affects endothelial function, oxidativeprocesses, platelet function, fibrinolysis, inflammation, lipid oxidationand vasomotor function. In experimental studies, several of these effectsare fully or partly reversible within a very short time.

Plaque formation isnot thought to be fully reversible and thus smokers would never be expectedto reach the risk level of never smokers concerning CVD. Nicotinereplacement shows no adverse effect on outcomes in patients with cardiacdisease. The benefits of smoking cessation have a large evidence base. Some advantagesare almost immediate; others take more time. CVD risk in former smokers isin between that of current and never smokers.

Significantmorbidity reductions occur within the first 6 months. Smoking reduction has not been shown to increase the probability of futuresmoking cessation, but some advocate nicotine-assisted smoking reduction insmokers unable or unwilling to quit. There is no age limit to the benefits of smokingcessation.

Passive smoking should also be avoided. Professional support can increase the odds of stopping [RR 1.

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Prompting a person to try to quit, briefreiteration of CV and other health hazards and agreeing on a specific planwith a follow-up arrangement are evidence-based interventions see Figure K in web addenda. Smoking cessation programmes initiated during hospital admission shouldcontinue for a prolonged period after discharge. Smokers should be advised about expected weight gain of, on average, 5kg and that the health benefits of tobacco cessation far outweigh the risksfrom weight gain.

Following the failure of advice, encouragement and motivationalinterventions, or in addition to them, NRT, varenicline or bupropion shouldbe offered to assist cessation. The antidepressant bupropion aids long-term smoking cessation with a similarefficacy to NRT. The partial nicotine receptor agonist varenicline at the standard doseincreases the chances of quitting more than two-fold compared with placebo 14 trials, people. Low-dose varenicline four trials, people roughly doubles the chancesof quitting and reduces the number and severity of side effects.

The mainside effect of varenicline is nausea, but this is mostly mild or moderateand usually subsides over time. Clonidine has helped people to quit, but causes side effects and is thereforea second-line agent. It is not clear whether mecamylamine used with NRThelps people to quit. Other treatments did not seem to help. So far,nicotine vaccines are not licensed for use anywhere in the world.


Combining two types of NRT is as effective as using varenicline, and helpsmore people to quit than a single type of NRT. Electronic cigarettes e-cigarettes are battery-operated devices thatsimulate combustible cigarettes by heating nicotine and other chemicals intoa vapour that is inhaled. Electronic cigarettes deliver the addictivenicotine without the vast majority of tobacco chemicals, and are probablyless harmful than tobacco. Evidence on the effectiveness of e-cigarettes is limited due to the smallnumber of trials, low event rates and wide confidence intervals.

Recent evidenceindicates that e-cigarettes, as currently being used, are associated withsignificantly less quitting among smokers. Both individual and group behavioural interventions are effective in helpingsmokers quit. Support from the individual's partner and family is important. There are no reliable data that acupuncture, acupressure, laser therapy,hypnotherapy or electrostimulation are effective for smoking cessation.

Dietary habits influence CV risk, either through an effect on risk factorssuch as cholesterol, BP, body weight and DM, or through othereffects. Most evidence on the relation between nutrition and CVD is based onobservational studies; randomized clinical trials estimating the impact ofdiet on endpoints are scarce. The nutrients of interest with respect to CVD are fatty acids which mainlyaffect lipoprotein levels , minerals which mainly affect BP , vitamins andfibre. For prevention of CVD, the types of fatty acids consumed are more importantthan the total fat content.

The same has notbeen clearly shown for replacement with carbohydrates and monounsaturatedfatty acids MUFAs. The polyunsaturated fattyacids can be divided into two subgroups: omega-6 fatty acids, mainly fromplant foods, and omega-3 fatty acids, mainly from fish oils and fats. They do not changeserum cholesterol levels and, with currently available cardioprotectivetherapies, it is debatable whether they exert a favourable effect onall-cause, CAD, and stroke mortality. The trans fatty acids, a subclass of unsaturated fatty acids, have been shownto be especially harmful due to their unfavourable impact on both totalcholesterol increase and HDL-C decrease.

These fatty acids are formedduring industrial processing hardening of fats and are present in, forexample, margarine and bakery products. The impact of dietary cholesterol on serum cholesterol levels is weakcompared with that of the fatty acid composition of the diet.

Whenguidelines are followed to lower saturated fat intake, this usually alsoleads to a reduction in dietary cholesterol intake. Although the relation between saltintake and BP remains controversial, the totality of evidence warrants saltreduction as an important way to prevent CAD and stroke. Salt reduction can be achieved by making different dietary choices fewerprocessed foods, more basic foods and the reformulation of foods loweringsalt content see Chapter 3c.

Potassium has favourable effects on BP. The main sources of potassium arefruits and vegetables. An inverse statistically significant associationexists between potassium intake and the risk of incident stroke [RR 0. Many case—control and prospective observational studies have observed inverseassociations between levels of vitamin A and E and the risk of CVD.

However,intervention trials have failed to confirm these observational studies.

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Also, for the B vitamins B6, folic acid and B12 and vitamin C, trials haveshown no beneficial effects. Therefore, conclusions about vitamin Dsupplementation [type of supplement D2 or D3 , dosage and duration] for CVprevention cannot yet be drawn. Although themechanism has not been elucidated completely, it is known that a high fibreintake reduces postprandial glucose responses after carbohydrate-rich mealsand lowers total cholesterol and LDL-C levels. Prospective cohort studies have shown a protective effect of theconsumption of fruits and vegetables on CVD, but RCTs are scarce.

The protective effect of fish on CVD is attributed to the n-3 fatty acidcontent. Especially in the rangeof no or very low intake, risk is increased. The public health impact ofa small increase in fish consumption in the general population istherefore potentially large. For fish oil, three randomized controlled prevention trials have beenpublished. A recent meta-analysis of 20trials, mostly prevention of recurrent CV events and mostly using fishoil supplements, showed no benefit of fish oil supplementation on CVoutcomes.

Drinking three or more alcoholic beverages per day is associated withelevated CVD risk. Results from epidemiological studies suggest a lowerrisk of CVD occurring with moderate one to two units per day alcoholconsumption compared with non-drinkers. This association appears not tobe explained by special characteristics of abstainers, although thepotential for residual confounding and reverse causality cannot be fullyexcluded. Moreover, a recent Mendelian randomization study includinganalyses from 59 epidemiological studies has shed doubt on anybeneficial effect of moderate alcohol consumption, suggestingthat the lowest risks for CV outcomes were in abstainers and that anyamount of alcohol is associated with elevated BP and BMI.

Sugar-sweetened soft drinks are the largest single food source ofcalories in the US diet and are important in Europe. Regular consumption of soft drinks has been associated withoverweight, metabolic syndrome and type 2 DM. Substitution ofsugar-sweetened soft drinks with artificially sweetened drinks resultedin less weight gain in children over an month period.

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Regularconsumption of sugar-sweetened beverages i. The cholesterol-lowering effect is in addition to thatobtained with a low-fat diet or use of statins. Further cholesterolreduction can be obtained with higher doses of phytosterols. Studying the impact of a total dietary pattern theoretically shows the fullpreventive potential of diet since it yields a combined estimate of theimpact of several favourable dietary habits. The Mediterranean dietcomprises many of the nutrients and foods that have been discussedpreviously: high intake of fruits, vegetables, legumes, wholegrain products,fish and unsaturated fatty acids especially olive oil ; moderateconsumption of alcohol mostly wine, preferably consumed with meals and lowconsumption of red meat, dairy products and saturated fatty acids.

The biggest challenge in dietary prevention of CVD is to develop moreeffective strategies to make people change their diet bothquantitatively and qualitatively and to maintain that healthy dietand a normal weight. Both overweight and obesity are associated with an increased risk of CVDdeath and all-cause mortality.

Achieving and maintaining a healthy weight has a favourable effect onmetabolic risk factors BP, blood lipids, glucose tolerance and lowerCV risk. There is evidence thatoptimal weight in elderly is higher than in the young andmiddle-aged. In many countries, favourable trends in major risk factors such as bloodcholesterol, BP and smoking prevalence have been observed, translating intoreduced CV mortality. However, BMI has greatly increased in all countriesover recent decades, resulting in a concomitant increase in the prevalenceof type 2 DM. In the USA, it has been projected that if obesity trends from to continue, obesity will increasingly offset the positive effectsof declining smoking rates.

Body fat stored in the abdomen intra-abdominal fat carries a higher risk than subcutaneous fat. Several measures of body fatness are available see Table D in the web addenda. Most data are available for BMI, waist:hipcircumference ratio and simple waist circumference. The optimal level formeasurement of waist circumference is midway from the lower rib margin tothe anterior superior iliac crest, in the standing position. The WHOthresholds for waist circumference are the most widely accepted in Europe.

Based on these thresholds, two action levels are recommended:. These thresholds have been calculated based on Caucasians, and it is apparentthat different cut-offs for anthropometric measurements are required indifferent races and ethnicities. Some studies argue that a specific subgroup of obeseindividuals is resistant to metabolic complications such as arterialhypertension and insulin resistance. However, MHO individuals present ahigher all-cause mortality compared with normal weight metabolically healthyindividuals. At the population level, obesity is associated with CVD risk.

However, amongthose with established CAD, the evidence is contradictory. However, this evidence should not bemisinterpreted to recommend higher target BMIs for those with establishedCVD since reverse causality may be operating. Cardiorespiratory fitnessmight influence relationships between adiposity and clinical prognosis inthe obesity paradox.

Normal weight unfit individuals have a higher risk ofmortality than fit individuals, regardless of their BMI. Overweight andobese fit individuals have mortality risks similar to normal weight fitindividuals. Although diet, exercise and behaviour modifications are the mainstaytherapies for overweight and obesity, they are often unsuccessful forlong-term treatment. A recent meta-analysis indicates that patientsundergoing bariatric surgery have a reduced risk of MI, stroke, CV eventsand mortality compared with non-surgical controls. Knowledge and implementation of effective strategies to achieveweight loss and maintain a long-term healthy weight.

Identification of the relative roles of diet, exercise and behaviourmodification in the management of overweight and obese people. Whileaccepting the simplicity of this approach and that it could beuseful in some settings, there is better scientific support for thethree targets matched to level of risk. It should be noted that the evidence for patients withCKD is less strong. The crucial role of dyslipidaemia, especially hypercholesterolaemia, in thedevelopment of CVD is documented beyond any doubt by genetic, pathology,observational and intervention studies.

In blood plasma, lipids such as cholesterol and triglycerides circulate aslipoproteins in association with various proteins apolipoproteins. Themain carrier of cholesterol in plasma LDL-C is atherogenic. The role oftriglyceride-rich lipoproteins is currently under active investigation:chylomicrons and large very-low-density lipoproteins VLDLs appear not tobe atherogenic, but very high concentrations of these triglyceride-richlipoproteins can cause pancreatitis.

Most cholesterol is normally carried in LDL-C. Over a wide range of plasmacholesterol concentrations, there is a strong and graded positiveassociation between total as well as LDL-C and risk of CVD. The evidence that reducing plasma LDL-C reduces CVD risk is unequivocal; theresults of epidemiological studies and trials with and without statins usingangiographic or clinical endpoints confirm that the reduction of LDL-C is ofprime concern in the prevention of CVD.

Every 1. Apolipoprotein B apoB; the main apoprotein of atherogenic lipoproteins levels have also been measured in outcome studies in parallel withLDL-C. Hypertriglyceridaemia is a significant independent CVD risk factor, but theassociation is far weaker than for hypercholesterolaemia. There are, however, no randomized trials to providesufficient evidence to derive target levels for triglycerides. This lipidpattern is also characterized by the presence of small, dense, atherogenicLDL particles. Lipoprotein a [Lp a ] is a low-density lipoprotein to which an additionalprotein called apolipoprotein a is attached.

There is norandomized intervention study showing that reducing Lp a decreases CVDrisk. Apolipoprotein A1 apoA1 is the major apoprotein of high-densitylipoprotein. It is beyond doubt that the apoB:apoA1 ratio is one of thestrongest risk markers. Since the measurement of apolipoproteins is not available toall physicians in Europe, is more costly than currently used lipid variablesand only adds moderately to the information derived from currently appliedlipid parameters, its use is not recommended. Direct methods may beless sensitive to plasma triglyceride levels.

However, recent data showthat the direct methods may also be biased when triglyceride levels arehigh. Also, the values obtained with the different direct methods arenot necessarily identical, especially for low and high LDL-C values.

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Non-HDL-C comprises the cholesterol in low-density lipoprotein,intermediate-density lipoprotein, remnant and VLDL, thus capturing allthe information regarding pro-atherogenic lipoproteins. Therefore, it is certainly abetter measure than calculated LDL-C for patients with increased plasmatriglyceride concentrations, but also has an additional advantage of notrequiring patients to fast before blood sampling.

There is evidence fora role of non-HDL-C as a treatment target. This parameter, however, is not suggested as apredictor or main target for therapy and further population data andclinical studies are awaited. The presence of dyslipidaemias secondary to other conditions must be excludedbefore beginning treatment, as treatment of underlying disease improveshyperlipidaemia without requiring antilipidaemic therapy.

This isparticularly true for hypothyroidism. Secondary dyslipidaemias can also becaused by alcohol abuse, DM, Cushing's syndrome, diseases of the liver andkidneys and several drugs e. If possible, these patients should bereferred for specialist evaluation. In general, RCTs are the ideal evidence base for decisional thresholds andtreatment goals. For treatment goals, this requires RCTs randomly allocatingsubjects to different lipid goal levels. However, most evidence in terms oftreatment goals is derived from observational studies and from post hocanalyses of RCTs and meta-regression analyses thereof randomly allocatingdifferent treatment strategies and not treatment goals.

Hence,recommendations reflect consensus based on large-scale epidemiological dataand RCTs comparing treatment regimens, not on RCTs comparing different lipidgoal levels. In the past, an LDL-C of 2. This goal remains reasonable for most patientswho have an indication for LDL-C-lowering therapy based on calculation ofthe CV risk see section 2. In addition, this is a secondary goal in people with elevatedtriglycerides. There are no differences in the relative reductionbetween men and women and between younger and older age or between thosewith and without DM.

Possible intervention strategies as a function of totalcardiovascular risk and low-density lipoprotein cholesterollevel. Note that risk stratification isnot applicable in familial hypercholesterolaemia, where drugtreatment is recommended, and that, in this table, drugtreatment may be considered at risks lower than the generictreatment thresholds indicated in paragraph 2. If baseline LDL-C in this category is alreadybelow the target level of 1.

If patients with CKD already on ahypolipidaemic therapy enter end-stage renal disease, the therapy may bemaintained. The currently available lipid-lowering drugs include inhibitors of3-hydroxymethylglutaryl-coenzyme A reductase statins , fibrates, bileacid sequestrants anion exchange resins , niacin nicotinic acid ,selective cholesterol absorption inhibitors e.

Response to all therapy varies widely among individuals and thereforemonitoring the effect on LDL-C levels is recommended. Data indicate that combination therapy with ezetimibe also brings a benefitthat is in line with the Cholesterol Treatment Trialists' CTT Collaboration meta-analysis supporting the notion that LDL-C reduction iskey to the achieved benefit independent of the approach used. Increased levels of liver enzymes in plasma occur occasionally during statintherapy, and in most cases are reversible.

Routine monitoring of liverenzyme values is not indicated. Because statins are prescribed on a long-termbasis, possible interactions with other drugs deserve particular andcontinuous attention, as many patients will receive pharmacological therapyfor concomitant conditions. In general, the safety profile of statins is acceptable, and earlierobservations that lipid-lowering treatment may contribute to an increase innon-CV mortality e. For non-statin treatments, selective cholesterol absorption inhibitors e.

They arerecommended as combination therapy with statins in selected patients when aspecific goal is not reached with the maximal tolerated dose of astatin. Bile acid sequestrants also decrease total cholesterol and LDL-C but arepoorly tolerated and tend to increase plasma triglyceride concentrations. They are therefore not recommended for routine use in CVD prevention. In those rare patients with severe primaryhypertriglyceridaemia, specialist referral must be considered.

Whether this approach results in thepredicted reduction in CV events is being addressed in large outcome trials;preliminary evidence suggests that this is the case. Patients with dyslipidaemia, particularly those with established CVD, DM orasymptomatic high-risk individuals, may not always reach treatment goals,even with the highest tolerated statin dose. Therefore, combinationtreatment may be needed. It must be stressed, however, that the onlycombination that has evidence of clinical benefit one large RCT is that ofa statin combined with ezetimibe.

Combinations of niacin and a statin increase HDL-C and decrease triglyceridesbetter than either of these drugs alone, but flushing is the main adverseeffect of niacin, which may affect compliance. Furthermore, there is noevidence of clinical benefit for this combination. Fibrates, particularly fenofibrate, may be useful, not only for decreasinghigh triglyceride concentrations and increasing low HDL-C, but for loweringLDL-C further when used with a statin. There is limited evidence for thiscombination in terms of a reduction in CVD events. Other drugsmetabolized through cytochrome P should be avoided when this combinationis prescribed.

Fibrates should preferably be taken in the morning andstatins in the evening to minimize peak dose concentrations and decrease therisk of myopathy. Patients have to be instructed about warning symptoms myalgia , even though such adverse effects are very rare. Gemfibrozilshould not be added to a statin treatment, because of the high potential forinteractions. If target levels cannot be reached even on maximal doses of lipid-loweringtherapy or drug combinations, patients will still benefit from treatment tothe extent that the dyslipidaemia has been improved.

In these patients,increased attention to other risk factors may help to reduce total risk. Whether functional foods and food supplements with a lipid-loweringeffect can safely reduce the risk of CVD. Lifestyle management to aid weight control by sustainable dietary changesand increased PA levels should be central in the management of patientswith type 2 DM. Intensive management of hyperglycaemia reduces the risk of microvascularcomplications and, to a lesser extent, the risk of CVD.

However, targetsshould be relaxed in the elderly, frail, those with long-duration DM andthose with existing CVD. Intensive treatment of BP in DM, with a target of mmHg systolic forthe majority, reduces the risk of macrovascular and microvascularoutcomes. A lower SBP target of mmHg further lessens the risks forstroke, retinopathy and albuminuria and should be applied to selectedpatients. Recent evidence points to sizeable reductions in CVD mortality in DMpatients via improvements in risk factor management, although theincreasing worldwide DM prevalence will create major challenges.

Moreshould be done to prevent DM. Clear reductions have occurred inCVD death rates in DM consistent with better management of risk factors,although the increasing prevalence of DM continues to create pressures on allhealth care systems. The targets, especially the glycaemic and in some cases lipids, should be lessstringently implemented in older people with DM, those with a longer duration ofDM, those with evidence of CVD and the frail.

Except for glucose management, prevention of CVD follows the same generalprinciples as for people without DM. Many treatmenttargets are more stringent for patients with DM. Typically, patients with type 2DM have multiple CVD risk factors, each requiring treatment according toexisting guidelines. The ESC and European Association for the Study of Diabetes scientificstatements advocate lifestyle management as a first measure for theprevention and management of DM.

Several dietary patterns can be adopted where thepredominance of fruits, vegetables, wholegrain cereals and low-fat proteinsources is more important than the precise proportions of total energyprovided by the major macronutrients. Salt intake should be restricted. Specific dietary recommendations include limiting saturated and trans fatsand alcohol intake, monitoring carbohydrate consumption and increasingdietary fibre.

A Mediterranean-type diet is acceptable, where fat sourcesare derived primarily from monounsaturated oils. A combination of aerobic and resistance exercise training is effective in theprevention of the progression of DM and for the control of glycaemia. Littleis known about how to promote and sustain PA; however, reinforcement byhealth care providers to patients to find sustainable ways to increase PA iscrucial. Smoking increases the risk of DM, CVD and premature death andshould be strongly discouraged see section 3a.

This recommendationreflects greater lifetime vascular risk trajectories in these individuals. However, a proportion of DM patients at 40—50 years of age may have a low 10year risk of CVD due to normal BP and lipid levels and being non-smokers,and in such cases there remains a role for physician judgement. The UK Prospective Diabetes Study UKPDS established the importance ofintensive glucose lowering with respect to CVD risk reduction in newlydiagnosed patients with DM but not treated with modern BP- or lipid-loweringtherapies, with the best evidence to support metformin, leading to itsposition as first-line therapy.

Three trials were conducted to see if CVevents could be reduced further with more intensive glycaemia treatment andlower target HbA1c levels. The results prompted concerns about the safety of intensiveglucose lowering and the appropriateness of pursuing tight glucose control,particularly in older people with DM and in those with existing CVD. Moreresearch on understanding the trial results is needed.

Hypertension is more common in patients with type 2 DM compared with thegeneral population. Combination treatment is commonly needed to lower BP effectively in DM. AnACE-I or an angiotensin receptor blocker ARB , where tolerated, shouldalways be included as first-line therapy because of the evidence of superiorprotective effects against initiation or progression of nephropathy.

While the most common lipid abnormality in type 2 DM is elevated triglycerideand low HDL-C, trials examining possible CVD benefits of lipid mainlytriglyceride lowering with fibrates in DM have not been positive.

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Patients with type 1 or type 2 DM have an increased tendency to developthrombotic phenomena. The role of aspirin in patients without CVD remains unproven. A meta-analysisof six RCTs found no statistically significant reduction in the risk ofmajor CV events or all-cause mortality when aspirin was compared withplacebo or no aspirin in people with DM and no pre-existing CVD.

In patients with DM and hypertension,microalbuminuria—even below the current threshold values—predicts CV events,and a continuous relationship between CV as well as non-CV mortality andurinary protein:creatinine ratios has been reported. Microalbuminuria can bemeasured from spot urine samples due to inaccuracy in sampling, 24 h ornight-time urine collection is discouraged by indexing the urinary albuminconcentration to the urinary creatinine concentration 2. There is a need to examine whether a type 2 DM CV risk score based oneither 10 year or lifetime risk helps to improve targeting ofpreventative therapies and leads to a reduction in CV risk or a gainin lifetime years free from disease.

Further trial data are needed to establish if the empagliflozinoutcome findings hold for other classes of SGLT2 inhibitors and tobetter understand the mechanisms of benefit. More research on the benefits of glucagon-like peptide 1 GLP-1 receptor agonists on CVD risk is needed and trials are due to bereported in subsequent years. Key messages Type 1 DM is the result of a lack of insulinproduction in the pancreas, confirmed by absent or virtually absentC-peptide levels. Type 1 DM should be suspected in any patientwho progresses to insulin within the first year of diagnosis.

A largecontemporary study in Scotland observed a relative risk for CVD events of2. The presence of proliferative retinopathy andautonomic neuropathy also signalled an elevated CVD risk. CVD and mortality risks have decreased in type 1 DM patients butremain unacceptably elevated in those with very poor glycaemiccontrol or any evidence of kidney disease.

Intensive management of hyperglycaemia in DM reduces the risk ofmacrovascular complications and premature mortality; a target of6. The Diabetes Control and Complications Trial DCCT established theimportance of tight glucose control to lessen the risks of bothmicrovascular and macrovascular disease. A 27 year follow-up of this trialshowed that 6. The use of insulin analogues, insulin pumps and continuousglucose monitoring to improve glycaemic control while minimizinghypoglycaemia is the subject of intense research, as is the use of agents e.

The CTT suggested lipid lowering with statins is as equally effective in type1 patients as in type 2. Younger patients with multiple risk factors orevidence of end organ damage albuminuria, low eGFR, proliferativeretinopathy or neuropathy should be considered for statin therapy. As morepatients with type 1 DM are living to older age, SBP targets may need to berelaxed mmHg in some to avoid side effects. Further studies are needed on metformin and GLP-1 receptor agonistsin subgroups of patients with type 1 DM to determine whether theyimprove glycaemic control, aid in weight reduction and improveclinical outcomes.

There is a need for a CVD risk score in type 1 DM to better guideinitiation of preventative therapies in younger patients. High BP is a leading risk factor for disease burden globally, accounting for9. The risk of death from either CAD or stroke increases progressivelyand linearly from BP levels as low as mmHg systolic and 75 mmHgdiastolic upwards, although for absolute risk the curves flatten in thelower BP ranges.

Office BP is recommended for screening and diagnosis of hypertension, whichshould be based on at least two BP measurements per visit and on at leasttwo visits. If BP is more markedly elevated or accompanied by targetorgan damage, other CV factors or established CV or renal disease, repeatedBP measurements are required within a shorter period in order to maketreatment decisions.

Auscultatory or oscillometric semi-automatic sphygmomanometers should bevalidated and checked periodically. If feasible, automated recording of multiple BP readings inthe office, with the patient seated in an isolated room, might be consideredas a means of improving reproducibility and matching office BP values closerto those provided by daytime ambulatory BP monitoring ABPM or home BPmeasurements HBPMs.

The following general principles and remarks should be taken into account: i the procedure should be adequately explained to the patient, with verbaland written instructions; ii interpretation of the results should takeinto account that the reproducibility of out-of-office BP measurements isreasonably good for 24 h, day and night BP averages, but less so for shorterperiods; iii ABPM and HBPM provide somewhat different information on thesubject's BP status and risk, and the two methods should thus be regarded ascomplementary rather than competitive; iv devices should be validated andregularly calibrated, at least every 6 months.

Clinical indications for the use of out-of-office blood pressuremeasurements home blood pressure measurement, ambulatory bloodpressure measurement. Laboratory tests should include haemoglobin, fasting plasma glucose HbA1c ifnot fasting and serum tests for total cholesterol, HDL-C, triglycerides,potassium, uric acid, creatinine and calculated renal function andthyrotropin in postmenopausal women.

Urinalysis should includealbumin:creatinine ratio, dipstick test, sediment and quantitativeproteinuria if the dipstick test is positive. Echocardiography andfundoscopy can be considered. The decision to start pharmacological treatment depends not only on the BPlevel but also on total CV risk, outlined in section 2.

Promises, promises, and precision medicine

The decision to start antihypertensive treatment depends on the BP level andtotal CV risk. Lifestyle changes are recommended in all patients withsuboptimal BP, including masked hypertension. Prompt initiation of drugtreatment is recommended in individuals with grade 3 hypertension with anylevel of CV risk. Lifestyle changes only with close BP monitoring should be the recommendationin young individuals with isolated moderate elevation of brachialSBP andin individuals with high-normal BP who are at low or moderaterisk. Drug treatment may also be considered in white coathypertensive patients with a higher CV risk because of metabolicderangements or in the presence of organ damage.

Lifestyle interventions, weight control and regular PA alone may besufficient for patients with high-normal and grade 1 hypertension, andshould always be advised for patients receiving BP-lowering drugs, asthese may reduce the dosage of BP-lowering drugs needed to achieve BPcontrol. The lifestyle intervention specific to hypertension is saltrestriction.

At the individual level, effective salt reduction is by nomeans easy to achieve. As a minimum, advice should be given to avoidadded salt and high-salt food. As the BP-lowering effect of increasedpotassium has been well documented in the DASH diet rich in fruits,vegetables and low-fat dairy products with a reduced content of dietarycholesterol as well as saturated and total fat , patients withhypertension should generally be advised to eat more fruits andvegetables and to reduce their intake of saturated fat andcholesterol.

The large number of randomized trials of BP-lowering therapy, both thosecomparing active treatment vs. Some aspects should be considered for each of theBP-lowering drug groups. Thiazide diuretics also have dyslipidaemic and diabetogenic effects,particularly when used in high doses. Evidence concerning the benefits of other classes of agents is much morelimited. All of these agents have frequentlybeen used as added drugs in trials documenting CV protection and canthus be used for combination treatment in addition to the recommendedcombinations see below.

Drugs with 24 h efficacy are preferred. Simplification of treatmentimproves adherence to therapy, and effective 24 h BP control isprognostically important in addition to office BP control. Long-actingdrugs also minimize BP variability, which may offer protection againstprogression of organ damage and the risk of CV events. Any all-purpose ranking of drugs for general BP lowering is infeasibleand no evidence is available that different choices should be made basedon age or sex except for caution in using ACE-Is and ARBs in women ofchildbearing age because of possible teratogenic effects.

Combination treatment is needed to control BP in most patients. Theaddition of a drug from another class should thus be regarded as arecommended treatment strategy unless the initial drug needs to bewithdrawn because of side effects or the absence of any BP-loweringeffects.

The extra BP reduction from combining drugs from two differentclasses is approximately five times greater than doubling the dose ofone drug andmay reduce the side effects associated with either drug. The combinationof two drugs may also offer advantages for treatment initiation,particularly in patients at very high risk in whom early BP controlmay be desirable.

Trial evidence of outcome reduction has been obtained,particularly for the combination of a diuretic with an ACE-I, an ARB ora calcium antagonist. The most rational combinations appear to bea blocker of the renin—angiotensin system, a calcium antagonist and adiuretic at effective doses. There are only a few randomized clinical trials comparing different treatmenttargets. Hence any recommendation on target levels largely derives fromobservational studies and post hoc analyses of RCTs, which have mostlycompared different treatment regimens and reported achieved BP levels.

Nevertheless, it should beconsidered that DBP values between 80 and 85 mmHg are generally safe andwell tolerated. Post hoc analyses of large-scale trials e. However, significantly higher rates of serious adverse events, hypotension,syncope, electrolyte abnormalities and acute kidney injury or failure, butnot injurious falls, were observed in the intensive-treatment group.

Thefact that the study was open label in a strategy close to usual care withfrequent visits may have helped to adjust the antihypertensive treatment ifserious side effects occurred and thus minimized the risk of events. Large meta-analyses confirm that treatment is highly beneficial in theelderly hypertensive patient.

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Infrail elderly patients, it is recommended to be careful and reach adecision based on monitoring of the clinical effects of treatment. Resistant hypertension isassociated with a high risk of CV and renal events. I just do the functional liver detoxification profile and get their livers working properly to get rid of the chemicals. You need to stick with science as much as possible. Theme 3: The environmental exposure history is the most important clinical tool It was agreed by all clinicians that the environmental exposure history is by far the most important clinical tool for assessing toxicant exposures.

Table 3 The environmental exposure history is the most important clinical tool. IP History, history, history is the most important tool to use. The first thing is to have an awareness of the possibility of toxicant exposure. The second is to ask a good history. And then trying to find out what tests could be done and what treatments could be used or who to refer to. Challenges of long consultations OEP In 90 minutes you can actually really get to understand a person and their risk of exposures and whether in fact this might be something that is related to occupational or environmental exposures.

IP 90 minutes allows me to give an hour to the history taking portion and half an hour for examination. So, that is a big problem. And if you claim for a long consultation, they complain. Occupational history OEP You need to go through what is this person exposed to through the whole course of their working life. I would tease it out, detail by detail, according to the history given, whether it was volatile organic solvents, whether it was dust, whether it was asbestos, whether it was diesel fumes.

So it would become an individualized, personal question-and-answer, to get a measure of what the exposure has been, in both the long-term and in the short-term, resulting in the symptoms as expressed by the individual. You ask people what they are exposed to, then you look at specific heavy metals or chemicals in the workplace. If somebody was making or refurbishing old thermometers, then test for mercury.

So you tailor it to the environment. If you were a painter, preparing, or getting rid of lead paint in old houses, first of all you scrape the old paint and then you burn it. You need to investigate the house for lead paint, or eating antique furniture, being bathed in an old bath. Where were you born, where did you grow up, what were your early life experiences and exposures, or potential exposures, to toxins, what was your health like in childhood, early adulthood and adulthood? I get them to map out on Google maps where they live, go to school and where they work.

I draw a sausage shape around their home, and go half a kilometre sideways and one kilometer each end-wise and find out what is the vicinity of golf courses, industrial areas, service stations, main roads, airports, farms, bowling greens, parks…? What are the prevailing summer and winter winds? And so, we basically just stare at the map on the places where they used to live and work, and where they currently do live and work.

What school did you go to, where was it? Lots of the toxicological assaults come from the schools, which can be situated on hills, or beside main roads and kids get plenty of exposure to cleaning agents and traffic fumes, pesticides and just about everything there. And then, half the schools seem to have the old, unflued gas heating systems through all of winter… volatile organic chemical exposure and respiratory irritants are high.

Dietary history IPs So tell me a bit about the chemical reaction you are concerned about. When was it, how long was it, how long after the exposure, the duration of the effects. What did those effects, i. And then I just try and map it out. Then you go on to the next one. What was the next environmental reaction which your child had. And then you just slowly build up a picture of the person, and then I go through the artificial chemicals and colors, additives and preservatives as well as the natural colors, flavors, preservatives, like salicylates.

I look for genetic predisposition and for chemical sensitivity. And the typical child, you know, the blond-haired, blue-eyed freckly, or red-head, Theme 4: Patients with environmental sensitivities are increasing, have unique phenotypes, are complex to treat and rarely regain full health Where IPs treated patients with chronic idiopathic environmental sensitivities, OEPs were more likely to attribute symptoms to psychological factors on the basis that linear dose-response relationships could not explain their symptoms.

Table 4 Patients with environmental sensitivities have unique phenotypes, are complex to treat, rarely regain full health and are becoming more prevalent. You have to be a little bit careful in this area otherwise you can get a bad reputation. Dose-response relationships are important. And then the rest of us are in the rest of the bell-shaped. Could it be overexposure therefore causation because the dosage was high enough, or could it be failure of elimination, because in the genetic diversity of the human race, some people are just crappy at clearing drugs, pills, potions and pesticides out of their system.

But other things are there as a toxic record, if you like. Toxic Load. The whole ADHD has been kind of like a tsunami in the making in recent times. The increased number of people with mold-related illness… I do see more of what I now appreciate biotoxin exposures, rather than all pesticides, poisons and other types of toxins.

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The biggest thing that has changed is the degree of education. The patients are much more aware and now they are far more likely to seek advice and tend to come earlier. OEP Greater awareness of the population generally I think GPs are becoming more aware of things like MCS and fibromyalgia… and for which patients were often rubbished thirty years ago. Observations of phenotypes of patients with environmental sensitivities OEP The majority of people with Multiple Chemical Sensitivity have got some sort of an allergic, or highly reactive predisposition.

One-fifth of the population who are already predisposed, develop this neuropathic pain, for which they have become a hypervigilant responder. They will give you a history of childhood asthma, maybe long-standing hay fever, working out in the farm areas with their exposures there. The blond-haired, blue-eyed freckly, or red-haired child of Scottish or Irish descent whose got behavioral problems are much more prone to salicylate sensitivity. People of Scottish-Irish descent are much more sensitive to gluten than other people. The Irish for celiac disease, the Chinese for lactose intolerance is quite common.

These are the individuals who come in wearing white gloves and masks over their face. Sensitivity to smells and sensitivity to sound, to all of the senses, out of a group has an extraordinary advantage: that you hear the tiger, you know the poison in the plum, you become, effectively, the early warning radar.

Observations of genotypes of patients with environmental sensitivities IP Some people are just crappy at clearing drugs, pills, potions and pesticides out of their system. And those who have it remain for a long period of time, may have vulnerabilities. A reaction to chemicals implies they have some sort of genetic defect in their Phase II detoxification pathways. Difficulties treating environmental sensitivities IP The more symptoms and systems involved and the more chronic the illness, the more challenging it is; especially people with multiple chemical sensitivity, because then they have difficulty tolerating the treatment as well.

Complicated chronic fatigue together with chemical sensitivity and pain… and severe neuroimmune dysfunctions. Those are the hardest to treat. Autism is clearly the hardest of the neurodevelopmental problems, complex neurodevelopmental disorders. Older severely autistic are the most challenging and also the severely allergic, especially with anaphylactic type reactions.

Table 5 Educational and clinical resources in environmental medicine are lacking. There is no one single organization I think of as the best. The resources just cover fragments and they specialise in one area. I find it very hard to find one organisation who does the whole picture. You have to put the fragments together. Recently-admitted fellows would not have very much training in chemical exposures, even at workplaces. Limited in their scope. We need a lot more in-depth teaching. Journals OEP Many of the things that come up as an expert witness in court require me to do quite a bit of research with Dr.

Google and the online journals. I usually do searches and just try and pick up general articles when I am researching a particular topic. Is there one? About fifty to sixty other doctors would gather and talk and get lectured to and then go out and try to apply that elsewhere. So, the education was primarily through that group. I still have a long way to go. I teach general practitioners to listen much more to the patient, rather than get into your standard position of physical medicine.

IP I have my little army of a few thousand chemically sensitive, chemically poisoned, affected people. Table 6 Websites used as a resource by clinicians on EM. Environmental Health Criteria Monographs. Table 7 Books on EM. Volume 4. A chronicle of individual, industrial and governmental carelessness. The chelation therapy handbook. Blaurock Busch. MTM Publishing. The basic science of poisons. Discussion EM is a divided profession It appears that EM is divided between bottom-up patient-based approaches and top-down population-based approaches to medicine.

Clinical assessment of toxicant exposures is challenging, and the exposure history is the most important clinical tool Whilst these differences give an appearance of a divided profession, there were strong similarities across all clinicians including agreement that an exposure history is the most important clinical tool, that EM is an emerging science with few established experts and that chemical risk assessment is challenging in the absence of standardised data-collection tools or guidelines for toxicant testing.

Patients with environmental sensitivities are increasing, have unique phenotypes, are complex to treat and rarely regain full health Clinicians acknowledged that patients with environmental sensitivities often have unique phenotypes and that patients presenting with allergies food and aeroallergens , neurodevelopment disorders and mould-related disorders appear to be increasing.

Limitations Whilst this paper has identified clear themes, our research is limited by inherent limitations of qualitative research which include the biases we bring as clinician researchers who decide on the questions to ask and how responses are interpreted. Conclusions EM is relevant to all fields of medicine yet is currently divided between integrative medical practitioners using patient-centred approaches in private-practice settings and occupational and environmental physicians using public-health approaches in workplace settings.

Acknowledgements The authors would like to acknowledge the Jacka Foundation for providing the first author with a PhD scholarship. Competing interests The authors declare that they have no competing interests. Contributor Information Nicole Bijlsma, Email: ua. References 1. Bijlsma N, Cohen M. Environmental chemical assessment in clinical practice: unveiling the elephant in the room. Zachek CM, et al. J Pediatr Hematol Oncol. A scoping review of maternal and child health clinicians attitudes, beliefs, practice, training and perceived self-competence in environmental health.

Environmental and occupational medicine. LaDou J, Harrison R. Current diagnosis and treatment. Occupational and environmental medicine. New York: McGraw-Hill; Consolidated criteria for reporting qualitative research COREQ : a item checklist for interviews and focus groups. Int J Qual Health Care. Principles of exposure measurement in epidemiology: collecting, evaluating and improving measures of disease risk factors. Oxford: Oxford University Press; Kilpatrick N, et al. Environ Health Perspect. Prescott S, Allen KJ. Food allergy: riding the second wave of the allergy epidemic. Pediatr Allergy Immunol.

Platts-Mills TA. The allergy epidemics: — J Allergy Clin Immunol. Wang XD, et al. An increased prevalence of self-reported allergic rhinitis in major Chinese cities from to Ellwood P, et al. The Global Asthma Network rationale and methods for phase I global surveillance: prevalence, severity, management and risk factors. Eur Respir J. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab. Polanczyk GV, et al. ADHD prevalence estimates across three decades: an updated systematic review and meta-regression analysis. Int J Epidemiol. Thomas R, et al.

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Herr C, Eikmann T. Environmental health practice: environmental medicine A2 - Nriagu, J. O, in Encyclopedia of Environmental Health. Burlington: Elsevier; Integrating environmental health into medical education. Am J Prev Med. Turner MC, et al. Assessing the exposome with external measures: commentary on the state of the science and research recommendations.

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The emergence of environmental health literacy—from its roots to its future potential. Support Center Support Center. External link. Please review our privacy policy. The patients that I see have seen seven or eight different doctors and have been examined to death and nothing has come out of that. Mainly chronic neck pains and chronic back pains from a work injury.

The basis of my practice is chronically ill people, who do not fit into a clear medical diagnostic category… [they] suffer [from] persistent inflammation, immunological dysregulation and neurological responses which are hyper-responses. The environment means different things to different people. It would be great to have a standardized data-collection tool for environmental exposure history. The frustrating thing with EM is actually trying to find the tests which can actually show that what they the patient have got is real.