Statistics from Altmetric.com
The metabolic benefits associated with stopping smoking.
The effect of different types of diet on metabolic profile and clinical outcomes.
The protective components of diet.
The benefits associated with exercise.
Chapters 2.7.1 and 2.7.2 of the ESC curriculum.
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in Europe and worldwide.1 The major modifiable risk factors (obesity, hypertension, smoking, dyslipidaemia and diabetes) are well known and guidelines regarding their management have been issued.2–6 All guidelines focus on the importance of lifestyle changes, which should be implemented before or in conjunction with drug therapy. Still, most studies show that implementation of a healthy lifestyle is far from optimal, a significant percentage of patients with CVD risk factors reporting no change at all.7 8
The effects of lifestyle changes, alone or in conjunction with medical treatment, on CVD risk factors are seldom put forward. In this paper, we will make a brief overview of the effect of lifestyle changes (smoking cessation, adopting a healthier diet and increasing physical activity (PA)) on CVD risk factors (high blood pressure (BP), dyslipidaemia and hyperglycaemia) and compare them with the effect of pharmacological treatment. As smoking cessation per se is the most powerful lifestyle determinant of CVD,9 only the effects of smoking cessation on other risk factors will be assessed.
The results of lifestyle changes and of antihypertensive drug treatments on BP levels are summarised in table 1, and comparison between lifestyle and drug effects is provided in figure 1A (for systolic blood pressure (SBP)) and figure 1B (for diastolic blood pressure (DBP)).
Weight loss led to a consistent reduction in BP levels,10 and interventions leading to a weight loss ≥5% had a stronger effect on BP levels than interventions leading to a lower percentage of weight loss.11 Intermittent fasting had no benefits relative to continuous fasting.12 Drug-induced weight loss decreased BP levels,13 14 but the magnitude of the effect was lower than using lifestyle interventions (table 1).
Smoking cessation leads to an increase in BP levels in several studies, mostly related to weight gain.15–17 Conversely, other studies reported a decrease in BP levels among quitters despite weight gain.18 19 No deleterious effect of smoking cessation drugs on BP levels has been reported.20 Overall, the results suggest that smoking cessation might slightly improve BP levels, provided adequate measures to prevent weight gain are implemented.
Reducing salt intake leads to a decrease in BP levels.21–23 This decrease is mostly seen among hypertensive and non-white subjects,23 while the effect on normotensive subjects is limited and restricted to SBP. Potassium supplementation in hypertensive subjects decreases BP levels.24–26 Fat modification or reduction, or increased consumption of omega-6, omega-3 or nuts, does not seem to influence BP levels.27–30 Decreasing sugar intake led to a decrease in DBP levels,31 but shifting to a low glycaemic index diet did not.32 Increasing fibre intake led to a reduction in BP levels,33 while advice to eat more fruits and vegetables only influenced SBP levels.34 Vitamin D supplementation led to a reduction in DBP in one study,35 an increase in SBP in another36 and no effect in another.37 Vitamin E supplementation reduced SBP alone.38
The Mediterranean diet reduced BP levels in one study39 but not in another.40 Conversely, the Nordic diet (ie, a diet rich in fatty fish and shellfish) reduced BP levels.41 The Dietary Approach to Stop Hypertension (DASH) diet consistently reduced BP levels,42 and a meta-analysis concluded that most dietary interventions lead to a small but consistent reduction in BP levels, the magnitude of the effect varying according to the type of diet.43 Conversely, high-intensity diet counselling had no effect on BP levels.44 Overall, the results of the different meta-analyses show that diets including low-fat meat, fish, a variety of fruits and vegetables, high fibre and low salt intake can reduce SBP by 3–5 mm Hg and DBP by 1–4 mm Hg, namely in hypertensive subjects. The effect of those diets in normotensive subjects, or of fat manipulation or vitamin supplementation, is not warranted.
Increasing PA or endurance training decreased BP levels in hypertensive subjects, while no effect was observed for resistance training.45 Overall, a decrease of 10 mm Hg for SBP and 3 mm Hg for DBP could be achieved by exercise,46 while the effect in normotensive and diabetic subjects is not warranted. It is likely that the effects of aerobic or endurance training on BP levels are partly associated with weight control.47
Overall, lifestyle modifications achieve BP reductions close to those obtained by antihypertensive monotherapy, but lower than achieved by antihypertensive drug combinations.5 Based on meta-analysis data,46 combining different lifestyle changes (ie, smoking cessation, a healthier diet and aerobic exercise) could theoretically reduce SBP by 10 mm Hg and DBP by 8 mm Hg, a value close or equal to some antihypertensive drug combinations.5
The results of lifestyle changes and of hypolipidaemic drug treatments on lipid levels are summarised in table 2.
Any weight loss decreased low-density lipoprotein (LDL)-cholesterol but had no effect on triglycerides.48 Compared with interventions leading to <5% weight loss, interventions leading to a weight loss ≥5% had a stronger effect on LDL-cholesterol levels but no effect on the other lipid levels (including triglycerides) was found.11 Intermittent fasting had no benefit relative to continuous fasting.12 Drug-induced weight loss led to a slight decrease in lipid levels,13 Orlistat exerting a stronger effect than the other drugs13 14 (table 2).
Smoking cessation increased lipid levels in one study.15 This increase was likely due to weight gain, as in another study this increase disappeared after adjusting for weight gain.17 A study conducted in overweight/obese subjects treated with varenicline and dietary counselling showed an improvement in lipid levels while no weight gain was found.49 Two studies reported improvements in lipid levels despite weight gain,18 19 and a meta-analysis concluded that smoking cessation led to an increase in high-density lipoprotein (HDL)-cholesterol levels, while no effect was found for the other lipid markers.50 Importantly, no deleterious effect of smoking cessation drugs on lipid levels has been reported20 Overall, the results suggest that smoking cessation might reduce lipid levels, provided adequate measures to prevent weight gain are implemented.
Salt reduction increased total cholesterol and triglyceride levels.23 Conversely, fat reduction or modification decreased total and LDL-cholesterol levels without influencing HDL-cholesterol and triglyceride levels.27 28 30 51 Among fats, only increased omega-3 significantly reduced triglyceride levels.52 Decreasing sugar intake reduced total and LDL-cholesterol and triglyceride levels, but had no effect on HDL-cholesterol,31 while decreasing the glycaemic index of the diet did not influence lipid levels.32 53 Increased fibre intake reduced total, LDL and HDL-cholesterol levels but did not impact triglycerides,33 while advice to eat more fruits and vegetables had no impact in lipid levels.34 Vitamin D supplementation, increased eicosapentaenoic acid or docosahexaenoic acid intake had no effect,37 54 while increased phytosterol (plant-derived sterols or stanols structurally similar to cholesterol) intake reduced LDL-cholesterol levels55 and red yeast rice reduced total and LDL-cholesterol and triglyceride levels, but had no effect on HDL-cholesterol.56 The Mediterranean diet reduced triglycerides but did not influence HDL-cholesterol levels,39 while the Nordic diet reduced total and LDL-cholesterol levels without influencing HDL-cholesterol and triglycerides.41 The DASH diet reduced total and LDL-cholesterol levels without influencing HDL-cholesterol and triglycerides,42 while high-intensity diet counselling led to a reduction in total cholesterol levels.44 Overall, diets poor in saturated fats and sugars could achieve the strongest reductions in lipid levels. Such diets could be achieved by replacing butter by vegetal fats57 or excluding high-fructose corn syrup beverages.58 Specific dietary supplements could be considered,59 although phytosterols provided in capsules are not better than phytosterol-enriched foods in decreasing lipid levels.60
Increased PA led to a decrease in triglyceride levels in two studies61 62 and to an increase in HDL-cholesterol in one.62 Neither resistance nor aerobic training appeared to influence lipid levels.63 64
Overall, the results suggest that dietary changes might be more effective in decreasing lipid levels than smoking cessation or PA. A simulation of a multiple lifestyle intervention associating a 10% reduction in saturated fatty acid, a 15–20 g increase in dietary fibre, a 5 kg weight reduction and increased consumption of phytosterol-rich foods concludes that the corresponding decrease in LDL-cholesterol levels could be as much as 35%,65 a value slightly lower than achieved by statin monotherapy.
Hyperglycaemia and diabetes risk
The results of lifestyle changes and of antidiabetic drug treatments on glucose and glycated haemoglobin levels are summarised in table 3 and comparison between lifestyle and drug effects is provided in figure 2.
Weight loss decreased both fasting plasma glucose and HbA1c,48 but this effect was limited to interventions leading to a weight loss of ≥5%.11 Intermittent fasting had no benefit relative to continuous fasting.12 No effect of pharmacologically induced weight loss was found (table 3).
A low-carbohydrate diet reduced HbA1c, together with SBP and triglyceride levels, while increasing HDL-cholesterol levels in patients with diabetes.68 A low-glycaemic index diet failed to reduce glucose and HbA1c in non-diabetic subjects,32 53 while it reduced HbA1c in patients with diabetes.69 The Mediterranean diet and high-intensity diet counselling reduced glucose levels, while their effect on HbA1c was not reported.39 44 Finally, no effect of the DASH diet was found regarding glucose levels.42 Overall, dietary interventions reduced glucose or HbA1c levels in patients with diabetes, while being less effective in non-diabetic subjects.
Exercise reduced HbA1c levels but not glucose levels in two studies,61 62 the decrease in HbA1c levels being stronger in patients with diabetes.61 A study found no effect of aerobic exercise on glucose levels in overweight or obese subjects,64 and another found no difference between aerobic and resistance training regarding glucose or HbA1c levels in patients with diabetes.70 Structured (ie, planned and supervised) exercise, either aerobic or resistance, reduced HbA1c levels in patients with diabetes, while simple PA advice failed to do so.71 Overall, interventions focusing on exercise reduced HbA1c levels in patients with diabetes and were less effective in non-diabetic subjects. The effect of exercise appeared to be stronger than of dietary interventions.
Overall, the results suggest that smoking cessation might increase glucose and HbA1c levels, namely due to weight gain. Exercise might be more effective than diet in decreasing HbA1c levels, although this effect occurs mostly among patients with diabetes. The magnitude of the HbA1c-lowering effect of lifestyle interventions is close to that of some antidiabetic drugs.
Implications for practice
Adequately implemented, changes in lifestyle achieve reductions in CVD risk factors close to those of single-drug therapies, with major public health impact.72 As indicated in the European Society of Cardiology (ESC) guidelines, a healthy lifestyle should be implemented in all subjects with CVD risk factors before and after initiating drug treatment, and should be maintained throughout life.2–5 Importantly, the introduction of drug treatment should not lead to a lowering of the lifestyle intervention, and adherence to a healthy lifestyle should be continuously implemented, as it rarely exceeds 70%.73
Smoking cessation should be systematically proposed, as it leads to a considerable reduction in CVD risk per se and has additional benefits in BP, lipid and glucose levels, provided adequate measures against weight gain—such as increased PA—are implemented. Smoking cessation aids can be used, as they increase success rates and have no influence on cardiovascular risk factors.
Weight loss decreased most risk factors, the magnitude of the effect being proportional to the percentage of weight lost. Indeed, all ESC guidelines recommend overweight or obese subjects to lose weight for CVD risk factor management.2–5 No specific weight loss method is recommended, both PA and/or dietary-based methods being adequate. Regarding diets, no specific diet is recommended, as most diets have shown to exert the same effect.74 Most importantly, realistic goals and a personalised dietary approach should be implemented.75 Finally, if a pharmacological approach is to be introduced, Orlistat might provide better results regarding lipid levels.
The EAT-Lancet Commission76 defined a healthy diet as composed of a diversity of plant foods, unsaturated fat, and small amounts of animal foods, refined grains and highly processed and sugary foods. This healthy diet is in line with the guidelines for CVD and risk factor prevention2–5 and should be safe, adapted to the cultural background of the patient and agriculturally sustainable. It should be noted that some elements of a healthy diet may be beyond the reach of low and middle-income populations in some countries,77 either because of the low availability of these food groups in certain regions (ie, food desserts),78 or because of the high availability of cheap, unhealthy foods (ie, food swamps).79 Further, several individual or societal barriers might hamper the adoption of a healthy diet,80 as well as insufficient knowledge from doctors.81 Hence, whenever possible, dietary counselling should be provided by trained dieticians/nutritionists.82
Increased PA should be proposed to all subjects, taking into account individual limitations and societal or environmental constraints.4 5 PA should be progressively incremented and consist mainly of aerobic activities. A target of 150 min/week of moderate-intensity PA (3–6 metabolic equivalents (METs)) or 75 min/week of vigorous-intensity PA (>6 METs) is recommended, corresponding to an energy expenditure of approximately 1000 kcal/week.83 Brisk walking is the best option for sedentary people, while cycling will suit environmentally conscious people, provided adequate cycling infrastructures are available. The use of exercise prescription aids such as the EXPERT tool is recommended.84
Finally, the best approach will be to combine smoking cessation, healthy diet and increased PA, as their combined effect outweighs the effect of a single intervention.85 86
Adequately implemented, changes in lifestyle achieve reductions in cardiovascular risk factors close to those of single-drug therapies and should be systematically proposed to all subjects with cardiovascular risk factors. Multidisciplinary teams including doctors, dieticians and sport specialists are recommended.
Blood pressure (BP): weight loss, reducing salt and sugar intake, increasing potassium and fibre intake, and increased aerobic exercise decrease BP levels. The magnitude of the decrease is stronger among patients with hypertension.
Lipids: weight loss decreases low-density lipoprotein (LDL)-cholesterol levels; smoking cessation increases high-density lipoprotein-cholesterol levels; dietary changes reduce total and LDL-cholesterol levels.
Glucose and diabetes risk: weight loss decreases glucose and HbA1c levels, while smoking cessation might increase them, namely due to weight gain. Exercise might be more effective than diet in decreasing HbA1c levels, mainly among patients with diabetes.
Adequately implemented, the effect of lifestyle intervention might be half to almost equal to the effect of pharmacological treatment.
CME credits for Education in Heart
Education in Heart articles are accredited for CME by various providers. To answer the accompanying multiple choice questions (MCQs) and obtain your credits, click on the ‘Take the Test’ link on the online version of the article. The MCQs are hosted on BMJ Learning. All users must complete a one-time registration on BMJ Learning and subsequently log in on every visit using their username and password to access modules and their CME record. Accreditation is only valid for 2 years from the date of publication. Printable CME certificates are available to users that achieve the minimum pass mark.
The author thanks Mrs Pollyanna Patriota, PhD, for scientific advice in the nutrition part of the manuscript.
Collaborators Pollyanna Patriota.
Contributors PMV conceived the work, acquired and interpreted the data, wrote the manuscript and gave his final approval. PMV is accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article
Author note References which include a * are considered to be key references.
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.