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Effect of Smartphone-Based Lifestyle Coaching App on Community-Dwelling Population With Moderate Metabolic Abnormalities: Randomized Controlled Trial.
Cho, SMJ, Lee, JH, Shim, JS, Yeom, H, Lee, SJ, Jeon, YW, Kim, HC
Journal of medical Internet research. 2020;22(10):e17435
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Metabolic disorders are established precursors to cardiovascular disease. The aim of the study was to evaluate the longitudinal effect of smartphone-based health care app on metabolic parameters in a sample of the general population with moderate metabolic abnormalities. The study is a single-blind 3-arm parallel-design randomized controlled trial delivering a 6-month primary prevention program via mobile app. One hundred twenty-nine smartphone users, aged between 30-59 years with at least 2 metabolic abnormalities, have been recruited. Results showed that the simultaneous diet/exercise logging and lifestyle coaching yielded greater body weight reduction, specifically via body fat mass reduction. On the other hand, the systolic blood pressure did not change notably between the 3 groups at any follow-up examinations. Authors conclude that future studies focusing on comparative effectiveness using alternative study designs are needed to integrate these apps in everyday lives and clinic practice.
Abstract
BACKGROUND Metabolic disorders are established precursors to cardiovascular diseases, yet they can be readily prevented with sustained lifestyle modifications. OBJECTIVE We assessed the effectiveness of a smartphone-based weight management app on metabolic parameters in adults at high-risk, yet without physician diagnosis nor pharmacological treatment for metabolic syndrome, in a community setting. METHODS In this 3-arm parallel-group, single-blind, randomized controlled trial, we recruited participants aged 30 to 59 years with at least 2 conditions defined by the Third Report of the National Cholesterol Education Program expert panel (abdominal obesity, high blood pressure, high triglycerides, low high-density lipoprotein cholesterol, and high fasting glucose level). Participants were randomly assigned (1:1:1) by block randomization to either the nonuser group (control), the app-based diet and exercise self-logging group (app only), or the app-based self-logging and personalized coaching from professional dieticians and exercise coordinators group (app with personalized coaching). Assessments were performed at baseline, week 6, week 12, and week 24. The primary outcome was change in systolic blood pressure (between baseline and follow-up assessments). Secondary outcomes were changes in diastolic blood pressure, body weight, body fat mass, waist circumference, homeostatic model of assessment of insulin resistance, triglyceride level, and high-density lipoprotein cholesterol level between baseline and follow-up assessments. Analysis was performed using intention-to-treat. RESULTS Between October 28, 2017 and May 28, 2018, 160 participants participated in the baseline screening examination. Participants (129/160, 80.6%) who satisfied the eligibility criteria were assigned to control (n=41), app only (n=45), or app with personalized coaching (n=43) group. In each group, systolic blood pressure showed decreasing trends from baseline (control: mean -10.95, SD 2.09 mmHg; app only: mean -7.29, SD 1.83 mmHg; app with personalized coaching: mean -7.19, SD 1.66 mmHg), yet without significant difference among the groups (app only: P=.19; app with personalized coaching: P=.16). Instead, those in the app with personalized coaching group had greater body weight reductions (control: mean -0.12, SD 0.30 kg; app only: mean -0.35, SD 0.36 kg, P=.67; app with personalized coaching: mean -0.96, SD 0.37 kg; P=.08), specifically by body fat mass reduction (control: mean -0.13, SD 0.34 kg; app only: mean -0.64, SD 0.38 kg, P=.22; app with personalized coaching: mean -0.79, SD 0.38 kg; P=.08). CONCLUSIONS Simultaneous diet and exercise self-logging and persistent lifestyle modification coaching were ineffective in lowering systolic blood pressure but effective in losing weight and reducing body fat mass. These results warrant future implementation studies of similar models of care on a broader scale in the context of primary prevention. TRIAL REGISTRATION ClinicalTrials.gov NCT03300271; http://clinicaltrials.gov/ct2/show/NCT03300271.
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Association of Major Food Sources of Fructose-Containing Sugars With Incident Metabolic Syndrome: A Systematic Review and Meta-analysis.
Semnani-Azad, Z, Khan, TA, Blanco Mejia, S, de Souza, RJ, Leiter, LA, Kendall, CWC, Hanley, AJ, Sievenpiper, JL
JAMA network open. 2020;3(7):e209993
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Fructose is a type of sugar that has been implicated as a contributor to the development of metabolic syndrome (MetS), which is a condition where large waist circumference, high blood pressure and elevated blood lipid levels may all coexist. However, it remains unclear as to the role of fructose containing foods in the development of MetS. This systematic review and meta-analysis of 13 prospective cohort studies aimed to determine the association of several fructose containing foods and drinks with MetS. The results showed that sugary drinks containing fructose increased the risk of MetS, whereas no associations were found with mixed fruit juice, 100% fruit juice, honey, ice cream or confectionary. Interestingly fruit and yoghurt containing fructose decreased the risk of developing MetS. It was concluded that fructose containing food and drinks are not all equal in their biological effects. Sugary drinks increased the risk of developing MetS but yoghurt and fruit had a protective effect against development. Reasons for this could be due to a generally unhealthier lifestyle in those who consume sugary drinks or may be due to the increased protective effects associated with the vitamins and minerals in fruit and yoghurt. This study could be used by healthcare professionals to recommend a diet eliminating sugary drinks and containing regular fruit and yoghurt intake.
Abstract
Importance: Sugar-sweetened beverages (SSBs) are associated with increased risk of metabolic syndrome (MetS). However, the role of other important food sources of fructose-containing sugars in the development of MetS remains unclear. Objective: To examine the association of major food sources of fructose-containing sugars with incident MetS. Data Sources: MEDLINE, Embase, and Cochrane Library were searched from database inception to March 24, 2020, in addition to manual searches of reference lists from included studies using the following search terms: sugar-sweetened beverages, fruit drink, yogurt, metabolic syndrome, and prospective study. Study Selection: Inclusion criteria included prospective cohort studies of 1 year or longer that investigated the association of important food sources of fructose-containing sugars with incident MetS in participants free of MetS at the start of the study. Data Extraction and Synthesis: Study quality was assessed using the Newcastle-Ottawa Scale. Extreme quantile risk estimates for each food source with MetS incidence were pooled using a random-effects meta-analysis. Interstudy heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic). Dose-response analyses were performed using a 1-stage linear mixed-effects model. The certainty of the evidence was assessed using GRADE (Grading of Recommendations, Assessment, Development, and Evaluation). Results were reported according to the Meta-analysis of Observational Studies in Epidemiology (MOOSE) and Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guidelines. Main Outcomes and Measures: Pooled risk ratio (RR) of incident MetS (pairwise and dose response). Results: Thirteen prospective cohort studies (49 591 participants [median age, 51 years; range, 6-90 years]; 14 205 with MetS) that assessed 8 fructose-containing foods and MetS were included. An adverse linear dose-response association for SSBs (RR for 355 mL/d, 1.14; 95% CI, 1.05-1.23) and an L-shaped protective dose-response association for yogurt (RR for 85 g/d, 0.66; 95% CI, 0.58-0.76) and fruit (RR for 80 g/d, 0.82; 95% CI, 0.78-0.86) was found. Fruit juices (mixed and 100%) had a U-shaped dose-response association with protection at moderate doses (mixed fruit juice: RR for 125 mL/d, 0.58; 95% CI, 0.42-0.79; 100% fruit juice: RR for 125 mL/d, 0.77; 95% CI, 0.61-0.97). Honey, ice cream, and confectionary had no association with MetS incidence. The certainty of the evidence was moderate for SSBs, yogurt, fruit, mixed fruit juice, and 100% fruit juice and very low for all other food sources. Conclusions and Relevance: The findings of this meta-analysis suggest that the adverse association of SSBs with MetS does not extend to other food sources of fructose-containing sugars, with a protective association for yogurt and fruit throughout the dose range and for 100% fruit juice and mixed fruit juices at moderate doses. Therefore, current policies and guidelines on the need to limit sources of free sugars may need to be reexamined.
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Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. Relation with obesity-associated cardiometabolic risk.
Frühbeck, G, Catalán, V, Rodríguez, A, Gómez-Ambrosi, J
Adipocyte. 2018;7(1):57-62
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Obesity is medically defined as a condition of abnormal or excessive fat accumulation in adipose tissue, of sufficient extent to produce adverse health consequences. Presently, adipose tissue has emerged as an extremely active endocrine organ, based on its ability to secrete a plethora of biologically active adipokines [a class of cytokine mediators that are predominantly secreted by adipose cells] such as leptin and adiponectin. Furthermore, obesity is characterized by an increase in circulating leptin concentrations, in parallel to a decrease in blood levels of adiponectin. Thus, the adiponectin/leptin ratio has been suggested as a marker of adipose tissue dysfunction. A dysfunctional adipose tissue, evidenced by a lower adiponectin/ leptin ratio, is a clear contributor to the low-grade chronic inflammation associated with metabolic syndrome. Authors conclude that this ratio is highly and negatively correlated with markers of low-grade chronic inflammation emerging as a useful estimator of obesity- and metabolic syndrome- associated cardiometabolic risk.
Abstract
Obesity is currently the most extended metabolic disturbance worldwide favoring the development of cardiometabolic alterations such as type 2 diabetes, hypertension, and dyslipidemia. Obesity and the metabolic syndrome (MS) are characterized by an increase in circulating leptin concentrations, in parallel to a decrease in blood levels of adiponectin. Consequently, the adiponectin/leptin ratio has been suggested as a maker of adipose tissue dysfunction. This emerging biomarker correlates with insulin resistance better than adiponectin or leptin alone, or even HOMA and is decreased with increasing number of metabolic risk factors having been proposed as a predictive marker for the MS. Moreover, the adiponectin/leptin ratio is negatively correlated with markers of low-grade chronic inflammation. In this sense, an increase in this ratio has been related with reduced atherosclerosis risk as well as with a decreased risk of some types of cancer in epidemiological studies. In this commentary we propose new cutoffs to estimate obesity- and MS-associated cardiometabolic risk according to the adiponectin/leptin ratio and discuss different therapeutic strategies to increase this promising biomarker of metabolic risk.
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Fructose metabolism and metabolic disease.
Hannou, SA, Haslam, DE, McKeown, NM, Herman, MA
The Journal of clinical investigation. 2018;128(2):545-555
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Sugar consumption is thought to be a contributing factor in the increase in diabetes and obesity and the associated risk of cardiovascular disease worldwide. Sucrose (table sugar) and high fructose corn syrup contain almost equal amounts of fructose and glucose and are commonly added to processed foods. Whilst long-term studies are lacking, some short-term intervention studies show that fructose can impair lipid metabolism and insulin sensitivity in humans. This article reviews the biochemistry and molecular genetics of fructose metabolism as well as potential mechanisms by which excessive fructose consumption contributes to cardiometabolic disease. Fructose absorption in the human intestine is saturable, and there is a large range in capacity to absorb fructose between individuals, and unabsorbed fructose may contribute to gastrointestinal symptoms including pain and bloating. Fructose concentrations in the blood can increase 10-fold after consumption, but are rapidly cleared, mostly by the liver, where it provides substrate for metabolic processes, but may also be involved in signalling functions. Fructose may enhance glucose uptake by the liver and storage as glycogen and lipids. It may also increase production of uric acid which is implicated with gout. Excessive fructose consumption affects lipid metabolism and may contribute to fat accumulation in the liver and increase circulating triglycerides, a risk factor for heart disease. In animal models it also induces increased insulin levels. Fructose is one of the sweetest sugars which may affect appetite and overeating. It may also induce addiction-like behaviours such as binging and dependence in part by stimulating dopaminergic pathways. It also appears to induce leptin resistance which further increases food intake and obesity.
Abstract
Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.