Application of short message service to control blood cholesterol: a field trial

Abstract Background Despite recommendations, many middle-age adults neglect to check their blood cholesterol levels. Short message service (SMS, also known as texting) has been seldom studied for preventive education. We estimated how SMS can be a cost-effective method in encouraging people to check their blood cholesterol levels. Methods In a field trial, 3600 cell phone users (age > 30) were randomly assigned to the intervention (N: 1200) and the control groups (N: 2400). An SMS was sent to the intervention group for five rounds every two weeks, which targeted the cognitive and affective learning and finally advised the blood cholesterol level to be checked, if not checked during the past twelve months. Two weeks after the last round, both groups were asked for the time/level of their latest blood cholesterol, family history of early cardiac death and having a family member with coronary heart disease (CHD), and to report their attitude about whether annual blood sampling is worth the cost and time to prevent CHD. Moreover, the intervention group was asked if they remembered the SMS content. The cost-effectiveness was evaluated by estimating the “number needed to treat” (NNT) and calculating the cost of sending SMS to that number of people. Results In the intervention group, 629 individuals (72.0%) recalled the SMS content. The factors associated with cholesterol screening during the past two years were older age, diabetes, family history of coronary disease, higher education, female gender and being non-smoker. In both groups, women were significantly more aware of their blood cholesterol level (68.7% vs. 53.6%). The relative frequency of respondents who believed it was not worth checking their cholesterol annually was significantly lower in the intervention group (P < 0.001). The intervention group was significantly more likely to check its blood cholesterol levels (OR:1.22) after adjustment for age, diabetes, family history of CHD and smoking. The NNT was estimated ≈ 25 for the general population and ≈ 11 for those who received SMS and had a family member with CHD. Conclusions We would postulate that SMS could affect people’s adherence to preventive programs. Relatives of patients admitted with a diagnosis of CHD should be prioritized for superior cost-effectiveness and logistical feasibility

Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management

Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high-density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating triglycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (≥1.7 mmol/L or 150 mg/dL), a marker of TRL and their remnants, and/or low HDL-C (<1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal

Effects of smoking cessation on serum leptin and adiponectin levels

Background: Evidence on the association of leptin and adiponectin and smoking is limited and discordant. Leptin and adiponectin represent the most abundant adipokines in human plasma that play crucial roles in the pathophysiology of metabolic syndrome, atherosclerosis and insulin resistance. Leptin up-regulates the expression of several pro-inflammatory cytokines and is increased upon weight gain. Adiponectin has been shown to possess insulin sensitizing, anti -inflammatory and anti-atherogenic properties and is increased upon weight reduction. Our aim was to assess the effects of smoking cessation on serum leptin and adiponectin levels. Methods: We assessed the changes in serum leptin and adiponectin levels, serum CRP levels and BMI in apparently healthy smokers after 3 and 6 months of abstinence from smoking. Successful cessation was confirmed by an exhaled carbon monoxide measurement. 26 healthy non-smokers were recruited as controls. Results: Among the sample group, 32 subjects had quitted smoking at 3 months and 29 subjects at 6 months. Samples' leptin increased significantly from baseline to three months (mean change 3.76 ng/ml [95 % CI 0.89, 6.64], p = 0.012) and then decreased significantly from three to six months of smoking cessation (mean change -4,29 ng/ml [95 % CI -7.34, -6.64], p = 0.008). Samples' adiponectin increased significantly from baseline to three months of abstinence from smoking (mean change 2.34 [95 % CI -0.05, 4.73], p -0.05). BMI was significantly increased (mean change 2.03 kg/m(2) [95 % CI 1.60, 2.46], p < 0.05), while CRP decreased significantly from baseline to 6 months of smoking cessation (mean change -0.68 mg/dl [95 % CI -1.06, -0.30], p = 0.001). Conclusions: Smoking quitters' leptin levels appear to increase 3 months after smoking cessation and then decrease from 3 to 6 months of abstinence from smoking. Adiponectin levels increase during the first trimester of smoking cessation. The decrease in CRP levels indicates that the low grade inflammation observed in smokers is gradually restored. The alterations of serum leptin and adiponectin after 6 months of smoking cessation suggest the same but do not reach statistically significant levels. Weight gain and changes in fat distribution may attenuate the beneficial effects of smoking cessation

Early Effects of Smoking Cessation and Weight Gain on Plasma Adiponectin Levels and Insulin Resistance

Background Tobacco smoking is a major risk factor for atherosclerotic and cardiovascular disease. Studies have found evidence that smoking cessation is associated with weight gain, which is itself a leading cause of cardiovascular disease. Aim The present study sought to determine how smoking cessation and associated weight gain affect adiponectin levels and insulin resistance. Methods Fifty-two male habitual smokers were treated for 2 months with transdermal nicotine patches, and the 28 subjects who successfully quit smoking were analyzed. Subjects were divided into two sub-groups according to their weight change: weight maintainers and weight gainers. Serum adiponectin levels and the homeostasis model assessment ratio (HOMA-R) were evaluated at the beginning of the study, and at 1 week and 9 weeks after cessation of patch use. Results In weight gainers (n=18), serum adiponection levels tended to increase at 1 week after the end of treatment (mean difference 0.4±1.0 μg/mL, p=0.08). Moreover, after 9 weeks, adiponectin levels were significantly decreased in weight gainers (mean difference between 1 week and 9 weeks 0.8±0.9 μg/mL, p=0.002). In weight maintainers, adiponectin levels increased slightly after smoking cessation, but changes were not significant. In weight gainers, HOMA-R index was significantly increased (mean difference between baseline and 9 weeks 0.4±0.7, p=0.01), while in weight maintainers, HOMA-R index showed no differences throughout the study. Conclusion Our findings suggest that the adverse effects of weight gain attenuate some of the beneficial effects of smoking cessation