Effects on physical activity, physical fitness and well-being in a 36-months randomized controlled study, comparing a multimodal hospital-based intervention programme for primary cardiovascular prevention with usual care.

BACKGROUND: Cardiovascular disease is a major cause of mortality and morbidity worldwide, and primary prevention efforts are poorly developed in people at high cardiovascular risk. On this background, we performed the Hjerteløftet Study and demonstrated that participation over 36 months in a multimodal primary prevention programme, significantly reduced validated cardiovascular risk scores. In the current substudy we aimed to further explore several elements and effects following the intervention programme. METHODS: A random sample from the original Hjerteløftet Study was included for further examinations (n = 255, 40% women), and these patients were already randomized to an intervention group (IG) (n = 127), or a control group (CG) (n = 128). We compared changes from baseline to 36-months follow-up in physical activity, cardiorespiratory fitness, psychological well-being (WHO-5), cardiovascular medication use, smoking habits, and cardiometabolic risk factors (blood pressure, lipids, blood glucose, HbA1c, Apolipoprotein A-I, Apolipoprotein B and high-sensitive C-reactive protein). RESULTS: Self-reported physical activity increased significantly with absolute difference in mean delta Physical Activity Index score in the IG compared to the CG: 0.90, 95% CI: 0.10 to 1.70, p = 0.028 (ANCOVA). There were no corresponding differences in cardiorespiratory fitness. The participation resulted in psychological well-being improvement in both groups with a larger increase in the IG compared to the CG. The mean difference in delta WHO-5 score was 5.06, 95% CI: 0.68 to 9.45, p = 0.024, and 3.28, 95% CI: -0.69 to 5.25, p = 0.104 when controlled for baseline values (ANCOVA). The use of antihypertensive medication increased significantly more in the CG (p = 0.044). Only minor, nonsignificant changes were observed for traditional risk factors and cardiometabolic variables. CONCLUSIONS: Participation in the Hjerteløftet Study intervention programme resulted in an improved physical activity level, but without changing cardiorespiratory fitness. Participation in the programme also tended to improve psychological well-being, possibly related to increased physical activity, less smoking and less use of cardiovascular medication. Concerning the metabolic status, no major differences were observed, but minor changes may have been concealed by a larger increase in cardiovascular medication use in the control group. TRIAL REGISTRATION: ClinicalTrials.gov (NCT01741428), 04/12/2012.

Randomized trial of cardiovascular prevention in Norway combining an in-hospital lifestyle course with primary care follow-up: the Hjerteløftet study.

AIMS: Cardiovascular risk factor control is suboptimal in Europe, including Norway. The present study examined the efficacy of a multimodal primary prevention intervention programme based on the existing Norwegian health care system. METHODS AND RESULTS: In this open-label randomized controlled trial, adult patients with elevated cardiovascular risk were randomly assigned to an intervention programme including a hospital-based lifestyle course and primary care follow-up or to a control group (CG). The participants were recruited between 2011 and 2015. Primary outcome was change in validated cardiovascular risk scores, national and international (NORRISK, NORRISK 2, Framingham, PROCAM) between baseline and follow-up. Secondary outcomes included major cardiovascular risk factors. After 36 months the NORRISK score was significantly improved in patients assigned to the intervention group (IG) compared to patients assigned to the CG; absolute difference in mean delta score in the IG (n = 305) compared to mean delta score in the CG (n = 296): -0.92, 95% CI: -1.48 to -0.36, P = 0.001. The results for NORRISK 2, Framingham and PROCAM showed similar significant effects. The secondary endpoints including total cholesterol and blood pressure were only minimally, and non-significantly, reduced in the IG, but the proportion of smokers (P = 0.0028) and with metabolic syndrome (P < 0.0001) were significantly reduced. A limited number of cardiovascular events were observed, IG (n = 9), CG (n = 16). CONCLUSION: In subjects with elevated cardiovascular risk, a newly developed prevention programme, combining a hospital-based lifestyle course and primary care follow-up, significantly reduced cardiovascular risk scores after 36 months. This benefit appeared achievable primarily through improvements in metabolic syndrome characteristics and smoking habits.The study protocol was registered in ClinicalTrials.gov (NCT01741428).

Diet, eating behaviour and weight gain in men and women with overweight/obesity receiving varenicline for smoking cessation.

Because trying to quit smoking and not gain weight requires changes in two major behaviours simultaneously we explored eating behaviour in smokers with overweight/obesity making a quit attempt using guideline-based treatment. Participants were randomized to a carbohydrate-reduced or fat-reduced diet. The Three Factor Eating Questionnaire and Binge Eating Scale were completed by 48 of 64 participants in the low-carbohydrate and 47 of 58 in the fat-reduced group at randomization, after 6 and 14 weeks. At 6 weeks, no between group differences were seen in eating behaviour scores thus, we combined the sample for further analyses. In the combined sample, restraint increased (3.94 [95% CI 3.05, 4.83]), disinhibition (uncontrolled eating) decreased (-0.86 [95% CI-1.31, -0.41]) and binge eating decreased (-1.95 [95% CI -2.83, -1.06]), while hunger scores did not change (-0.43 [95% CI -0.89, 0.03]) after 14 weeks. In a general linear model, increase in dietary restraint (P = .012) and decrease in binge eating (P = .040) were associated with lower weight gain (model R2 adj = .147). In a smoking cessation program, dietary support regardless of diet was associated with increased dietary restraint and reduced binge eating. Because smoking cessation causes weight gain these results indicate that dietary support leads to eating behaviour changes that may prevent weight gain.

BMI modifies the effect of dietary fat on atherogenic lipids: a randomized clinical trial.

BACKGROUND: SFA intake increases LDL cholesterol whereas PUFA intake lowers it. Whether the lipid response to dietary fat differs between normal-weight and obese persons is of relevance to dietary recommendations for obese populations. OBJECTIVES: We compared the effect of substituting unsaturated fat for saturated fat on LDL cholesterol and apoB concentrations in normal-weight (BMI ≤ 25 kg/m2) and obese (BMI: 30-45) subjects with elevated LDL cholesterol. METHODS: We randomly assigned 83 men and women (aged 21-70 y) stratified by BMI (normal: n = 44; obese: n = 39) and elevated LDL cholesterol (mean ± SD, normal weight 4.6 ± 0.9 mmol/L; obese 4.4 ± 0.8 mmol/L) to either a PUFA diet enriched with oil-based margarine ( n = 42) or an SFA diet enriched with butter (n = 41) for 6 wk. RESULTS: Seven-day dietary records showed differences of ∼9 energy percent (E%) in SFA and ∼4 E% in PUFA between the SFA and PUFA groups. In the total study population, the PUFA diet compared with the SFA diet lowered LDL cholesterol (-0.31 mmol/L; 95% CI: -0.47, -0.15 mmol/L, compared with 0.32 mmol/L; 95% CI: 0.18, 0.47 mmol/L; P < 0.001) and apoB (-0.08 g/L; 95% CI: -0.11, -0.05 g/L, compared with 0.07 g/L; 95% CI: 0.03, 0.10 g/L; P < 0.001). Tests of the BMI × diet interaction were significant for total cholesterol, LDL cholesterol, and apoB ( P values ≤ 0.009). In normal-weight compared with obese participants post-hoc comparisons found that the respective changes in LDL cholesterol were 9.7% (95% CI: 5.3%, 14.2%) compared with 5.3% (95% CI: -0.7%, 11.2%), P = 0.206, in the SFA group, and -10.4% (95% CI: -15.2%, -5.7%) compared with -2.3% (95% CI: -7.4%, 2.8%), P = 0.020, in the PUFA group. ApoB changes were 7.5% (95% CI: 3.5%, 11.4%) compared with 3.0% (95% CI: -1.7%, 7.7%), P = 0.140, in the SFA group, and -8.9% (95% CI: -12.6%, -5.2%) compared with -3.8% (95% CI: -6.3%, -1.2%), P = 0.021, in the PUFA group. Responses to dietary fat were not associated with changes in polyprotein convertase subtisilin/kexin type 9 concentrations. CONCLUSIONS: BMI modifies the effect of PUFAs compared with SFAs, with smaller improvements in atherogenic lipid concentrations in obese than in normal-weight individuals, possibly supporting adjustment of dietary recommendations according to BMI. This trial was registered with www.clinicaltrials.gov as NCT02589769.

Low Carbohydrate and Moderately Fat-Reduced Diets Similarly Affected Early Weight Gain in Varenicline-Treated Overweight or Obese Smokers.

INTRODUCTION: Weight gain is common when stopping smoking. This study compared the effect of advising smokers to follow a diet low in carbohydrates versus a usual fat-reduced diet on weight gain and nicotine withdrawal. METHODS: In a randomized clinical trial, 122 men and women smokers with body mass index 25-40kg/m(2) were assigned low-carbohydrate versus moderately fat-reduced diets. Within a week thereafter all participants started treatment with a 12-week course of varenicline 10 days prior to the target quit date. Brief dietary and motivational counseling was given at all visits. Self-reported abstinence was validated. RESULTS: Protein intake in the low-carbohydrate versus fat-reduced diets was 26.4% of total energy versus 20.0%, fat 38.2% versus 30.1%, and carbohydrates 29.0% versus 41.7% (all P < .001). Mean weight changes for the low-carbohydrate versus fat-reduced groups were -1.2 (SD 2.2) versus -0.5 (SD 2.0) kg, -0.2 (SD 3.3) versus 0.5 (SD 2.6) kg, and 2.2 (SD 4.5) versus 2.1 (SD 3.9) kg at 4, 12, and 24 weeks after the target quit date, respectively (not statistically significant). Smoking abstinence rates did not differ between diets. In the combined groups, point prevalence abstinence rates were 71.0% at 12 weeks and 46.3% at 24 weeks. The Minnesota Nicotine Withdrawal Symptoms score was lower in the fat-reduced group compared with the low-carbohydrate group at weeks 4 and 12. CONCLUSIONS: In overweight or obese smokers using varenicline a low-carbohydrate diet was no better than a fat-reduced diet in reducing weight gain but may result in more severe nicotine withdrawal symptoms. Compared to previous studies, cessation rates with varenicline were not impaired by dietary counseling. IMPLICATIONS: The study implies that a popular low-carbohydrate diet does not result in greater weight loss than a moderately fat-reduced diet in overweight and obese smokers who are attempting to quit smoking with the aid of varenicline. Dietary counseling combined with varenicline treatment did not appear to unfavorably influence quit rates compared to previous studies in smokers not selected for overweight or obesity. Notably, the withdrawal symptoms score was lower in the fat-reduced dietary group than the low-carbohydrate group, suggesting a venue for further study.

Effect of a low-fat versus a low-gycemic-load diet on inflammatory biomarker and adipokine concentrations.

BACKGROUND: Low-grade inflammation is linked to metabolic syndrome and obesity. We studied the effects of weight loss and dietary composition on serum concentrations of biomarkers of inflammation and adipokines. METHODS: Men and women (n=181) aged 30-65 years with a body mass index (BMI) of 28-40 kg/m(2) (28-35 kg/m(2) for women) and one or more components of metabolic syndrome were randomized to follow one of two hypocaloric diets, a low-fat or low-glycemic-load diet for 3 months. Blood samples were taken pre- and postintervention. Serum concentrations of interleukin-6 (IL-6), tumor necrosis factorα (TNF-α), plasminogen activator inhibitor-1 (PAI-1), monocyte chemoattractant protein-1 (MCP-1), and adipokines (leptin, resistin, and adiponectin) were analyzed using multiplexed microsphere immunoassays. RESULTS: Weight loss was not different in the low-fat (4.4%±3.8%) and low-glycemic-load (4.9%±3.2%) groups. Concentrations of IL-6, TNF-α, PAI-1, and leptin were significantly reduced in both dietary groups with no between-group differences, whereas MCP-1 and adiponectin concentrations did not change. Subjects with full metabolic syndrome (three or more components; n=109) experienced greater weight loss than subjects (n=72) with one to two components and greater reduction in leptin [7.08 (95% confidence interval 5.19, 8.97) vs. 3.46 (0.91, 6.00) ng/mL; p=0.02] and a tendency to greater reduction in TNF-α (1.00 [0.60, 1.44] vs 0.40 [0.02, 0.78] pg/mL; p=0.05). CONCLUSION: Hypocaloric diets improved inflammatory biomarkers and adipokines independently of dietary composition. The response tended to be greater in subjects with three or more components of metabolic syndrome than their counterparts with one to two components.

The influence of long-term awareness of hyperlipidemia and of 3 years of dietary counseling on depression, anxiety, and quality of life.

OBJECTIVE: The purpose of this study is to investigate the long-term effects of participation in a cardiovascular screening program and of dietary counseling on self-reported psychosocial outcomes and health concerns. METHODS: High-risk subjects (n=563) with hyperlipidemia from the Oslo Diet and Antismoking Study (1972-1977) were reexamined after 25 years and randomly assigned to a new 3-year prospective 2x2 factorial placebo-controlled study in 1997 of n-3 polyunsaturated fatty acids and/or dietary counseling. Hospital Anxiety and Depression Scale (HADS), Life Satisfaction Index (LSI), and a new questionnaire on health concerns and behavior in response to risk information were collected at the 25-year follow-up. Hospital Anxiety and Depression Scale and LSI were evaluated at the end of the 3-year Diet and Omega-3 Intervention Trial on atherosclerosis (DOIT) in 505 subjects. RESULTS: Twenty-five years after the screening program, HADS-anxiety was similar to the Norwegian norms (3.3 vs. 3.5), while HADS-depression was significantly lower (3.6 vs. 4.1, P<.01). Patients reported that 25 years of awareness of hyperlipidemia had influenced health concerns through a moderate change in diet habits, some restriction in life conduct, but an improvement of the total life situation. After a novel 3-year intervention in DOIT, there was no difference between the dietary counseling and control group with regard to anxiety, depression, or life satisfaction, but HADS-anxiety increased significantly (4.0 vs. 3.3, P<.001) in both groups. CONCLUSION: Compared to the general population, screening-positive subjects did not have increased mental distress 25 years after screening, and beneficial health behavior persisted. Dietary counseling did not affect psychosocial outcomes.

A randomized clinical trial on n-3 polyunsaturated fatty acids supplementation and all-cause mortality in elderly men at high cardiovascular risk.

BACKGROUND: The benefit of n-3 polyunsaturated fatty acids (PUFA) supplementation for mortality and cardiovascular events after myocardial infarction is well documented, but the effect of n-3 PUFA in Caucasians without established cardiovascular disease is not known. Our aim was to examine the influence of supplementation with eicosapentaenoic acid and docosahexaenoic acid on all-cause mortality and cardiovascular events in elderly men at high-risk of cardiovascular disease. DESIGN: In the Diet and Omega-3 Intervention Trial, 563 Norwegian men, 64-76-year old and 72% without overt cardiovascular disease, were randomized to a 3-year 2×2 factorial designed clinical trial of diet counseling and/or 2.4 g n-3 PUFA supplementation. The n-3 PUFA arm was placebo-controlled (corn oil). METHODS: Demographic parameters and classical risk factors were obtained at baseline. Deaths and cardiovascular events were recorded through 3 years, and the effects of n-3 PUFA-intervention on these outcomes were evaluated in pooled groups of the n-3 PUFA-arm. RESULTS: There were 38 deaths and 68 cardiovascular events. The unadjusted hazard ratios of all-cause mortality and cardiovascular events were 0.57 (95% confidence interval: 0.29-1.10) and 0.86 (0.57-1.38), respectively. Adjusted for baseline age, current smoking, hypertension, body mass index and serum glucose, hazard ratios were 0.53 (0.27-1.04, P=0.063) and 0.89 (0.55-1.45, P=0.641), respectively. CONCLUSION: We observed a tendency toward reduction in all-cause mortality in the n-3 PUFA groups that, despite a low number of participants, reached borderline statistical significance. The magnitude of risk-reduction suggests that a larger trial should be considered in similar populations.

No effect of increased water intake on blood viscosity and cardiovascular risk factors.

Observational data have suggested that increased water intake decreases the risk of CHD. A postulated mechanism is that increased water ingestion reduces blood viscosity. The aim of the present study was to assess the effect of increased fluid intake on blood viscosity. Men (n 67) and postmenopausal women (n 27) with one or more risk factors for CVD who reported intake of < or =0.5 litres water daily were randomised to a control group (n 31), an intervention group (n 32) that increased their daily water intake by 1 litre/d and an intervention group (n 31) that ingested 1 litre blueberry juice/d. All were encouraged to continue their usual diet and lifestyle. Whole-blood viscosity and blood and urine chemistries were measured by standard techniques after 2 and 4 weeks. Urine volume increased (by a median of 872 and 725 ml in the water and blueberry juice groups, respectively, v. 10 ml in the control group; P< or =0.002), confirming the subjects' adherence to the protocol. Urine osmolality and urinary levels of Na, K and creatinine decreased in the water and blueberry juice groups v. the controls (P<0.05). No change was seen in whole-blood viscosity or in levels of fibrinogen, total protein, lipids, glucose, insulin, C-peptide or other chemistry and haematology variables. In conclusion, a postulated protective effect of increased water or fluid intake is not explained by a change in blood viscosity and increased fluid intake does not influence CVD risk factors in the short term.

[How to identify individuals with elevated cardiovascular risk?]. / Hvordan identifisere personer med høy risiko for kardiovaskulaer sykdom?

In spite of a substantial decline in the morbidity and the mortality from coronary heart disease in Norway since 1970-1975, cardiovascular disease remains the leading cause of death. The prevention of premature cardiovascular disease includes a mass strategy as well an individual strategy. While the first aims at changing life habits in the whole population, the latter is directed towards individuals with elevated cardiovascular risk. Non-pharmacological and pharmacological modes of treatment have been demonstrated to be effective in reducing cardiovascular events. However, the value of such measures depends on our ability to identify high-risk individuals. This paper describes different approaches in preventive medicine, from population screening to the screening of relatives of patients with premature disease. While doctors previously focused on whether blood pressure or cholesterol levels were above the defined limits, a global risk assessment is now recommended. Information regarding family history, smoking and exercise habits, lipid values, blood pressure, and the presence of diabetes must be obtained in a proper risk assessment. In some individuals with intermediate risk, additionally non-invasive tests may be of value in order to ensure that sufficient information has been obtained for a recommendation of preventive measures.