We aimed to evaluate the effect of statin treatment initiation on lipoprotein(a) [Lp(a)] levels in patients with dyslipidemia, and the interactions with the apolipoprotein(a) [apo(a)] phenotype, LPA single nucleotide polymorphisms (SNPs) and change in LDL cholesterol. The study population consisted of patients with dyslipidemia, predominantly familial hypercholesterolemia, who first initiated statin treatment (initiation group; n = 39) or were already on stable statin treatment for at least 4 months (control group; n = 42). Plasma Lp(a) levels were determined with a particle-enhanced immunoturbidimetric assay before and at least 2 months after start of statin treatment in individuals of the initiation group, and at two time points with an interval of at least 2 months in the control group. High and low molecular weight (HMW and LMW, respectively) apo(a) phenotype was determined by immunoblotting, and the common LPA SNPs rs10455872, rs3798220 and rs41272110 by Taqman assay. Plasma Lp(a) levels did not increase significantly in the initiation group (median 20.5 (IQR 10.9-80.7) to 23.3 (10.8-71.8) mg/dL; p = 0.09) nor in the control group (30.9 (IQR 9.2-147.0) to 31.7 (IQR 10.9-164.0) mg/dL; p = 0.61). In patients with the LMW apo(a) phenotype, Lp(a) levels increased significantly from 66.4 (IQR 23.5-148.3) to 97.4 (IQR 24.9-160.4) mg/dL (p = 0.026) in the initiation group, but not in the control group and not in patients characterized by the HMW apo(a) phenotype. Interactions with common LPA SNPs and change in LDL cholesterol were not significant. Statins affect Lp(a) levels differently in patients with dyslipidemia depending on the apo(a) phenotype. Statins increase Lp(a) levels exclusively in patients with the LMW apo(a) phenotype.

Background: Obesity is a multifactorial, chronic, progressive disease associated with decreased health-related quality of life, comorbidities, and increased mortality risk. Lifestyle interventions, focusing on dietetics, physical exercise, and behavioral therapy, are a cornerstone of therapy. Despite this very multidisciplinary treatment approach, the definition of treatment success is often based only on a weight loss of ≥ 5%. However, the heterogeneous nature of obesity may necessitate a more comprehensive approach to assessing treatment effects. Objectives: Here, we describe changes in physiological, psychological, and behavioral health after a multidisciplinary combined lifestyle intervention (CLI). Additionally, we investigated whether these changes were related to weight loss. Methods: This prospective observational longitudinal study comprised 96 adults with obesity (73 women, 81 Caucasian) participating in a CLI at the Obesity Center CGG, Erasmus University Medical Center, Rotterdam, the Netherlands. The 1.5-year intervention comprised multidisciplinary professional guidance towards a healthy diet, increased physical activity, and included cognitive behavioral therapy. Physiological health outcomes, psychological well-being, eating behavior, and physical activity were assessed after ten weeks and 1.5 years and compared to baseline. Results: An average of 5.2% weight loss (-6.0 kg) was accompanied by a mean 9.8% decrease in fat mass (-5.9 kg; both P < 0.001) and significant improvements in metabolism, hormonal status, and immune parameters (all P < 0.05). Moreover, we observed decreased psychopathology, increased quality of life, and decreased disordered eating (all P < 0.05). Weight loss correlated with most metabolic changes (all P < 0.05) but not with most psychological/behavioral changes. Conclusions: Combined lifestyle intervention in patients with obesity was accompanied by significant improvements in body weight and body composition along with cardiometabolic, endocrine, immunological, psychological, and behavioral improvements. Interestingly, most changes in psychological and behavioral health occurred independently of weight loss. Obesity treatment success should be evaluated based on a combination of physical and patient-reported outcomes rather than weight loss alone.

Aims: This systematic review and meta‐analysis evaluates the additional effect of exercise to hypocaloric diet on body weight, body composition, glycaemic control and cardio‐respiratory fitness in adults with overweight or obesity and type 2 diabetes.Methods: Embase, Medline, Web of Science and Cochrane Central databases were evaluated, and 11 studies were included. Random‐effects meta‐analysis was performed on body weight and measures of body composition and glycaemic control, to compare the effect of hypocaloric diet plus exercise with hypocaloric diet alone.Results: Exercise interventions consisted of walking or jogging, cycle ergometer training, football training or resistance training and duration varied from 2 to 52 weeks. Body weight and measures of body composition and glycaemic control decreased during both the combined intervention and hypocaloric diet alone. Mean difference in change of body weight (−0.77 kg [95% CI: −2.03; 0.50]), BMI (−0.34 kg/m² [95% CI: −0.73; 0.05]), waist circumference (−1.42 cm [95% CI: −3.84; 1.00]), fat‐free mass (−0.18 kg [95% CI: −0.52; 0.17]), fat mass (−1.61 kg [95% CI: −4.42; 1.19]), fasting glucose (+0.14 mmol/L [95% CI: −0.02; 0.30]), HbA_1c (−1 mmol/mol [95% CI: −3; 1], −0.1% [95% CI: −0.2; 0.1]) and HOMA‐IR (+0.01 [95% CI: −0.40; 0.42]) was not statistically different between the combined intervention and hypocaloric diet alone. Two studies reported VO_2max and showed significant increases upon the addition of exercise to hypocaloric diet.Conclusions: Based on limited data, we did not find additional effects of exercise to hypocaloric diet in adults with overweight or obesity and type 2 diabetes on body weight, body composition or glycaemic control, while cardio‐respiratory fitness improved.

This proof-of-concept study tested whether an adjuvant eucaloric very-low-carbohydrate diet for 2 weeks added to first-generation somatostatin receptor ligand therapy would reduce IGF-I concentrations in patients with uncontrolled acromegaly. The diet appeared to result in IGF-I control in such patients.

Background: Obesity is of major pathogenetic importance to type 2 diabetes, it contributes to poor glycemic control and increases the risk of cardiovascular disease. Over 80% of patients with diabetes type 2 are overweight. To achieve a more favourable risk profile, changes in diet and lifestyle are needed. However, current treatment programs for obese DM type 2 patients are not effective in the long term. In this RCT, we compare the effectiveness of a Combined Psychological Intervention (CPI) and usual care in maintaining the favourable effects on weight and risk profile during 2 years of follow-up after a Very Low Calorie Diet (VLCD).Methods and design: In a randomised parallel group intervention study, 140 patients with type 2 diabetes and overweight (BMI>27 kg/m2) will be recruited from the outpatient department of the Erasmus Medical Centre.After obtaining ≥5% of weight loss with a VLCD, participants will be randomly assigned to CPI or usual care for 10 weeks. CPI consists of cognitive behaviour therapy, problem solving therapy and proactive coping.Primary outcome measure is weight change (kg).Other outcome measures are Body Mass Index (BMI = weight (kg)/length (m)2), waist circumference (cm), systolic blood pressure (mmHg), HbA1c (mmol/mol), lipid levels (LDL, HDL, TG (mmol/l) and chol/HDL-ratio), antidiabetic agents and doses, cardiovascular risk profile (UKPDS), lifestyle and quality of life (EuroQol EQ-5D). Psychosocial parameters are also studied, as secondary outcomes as well as determinants for weight loss.When successful, we want to conduct an analysis of the cost effectiveness of the intervention as compared to usual care.Discussion: We expect that a CPI after a VLCD will be effective in maintaining weight loss and improving cardiovascular risk and glycaemic control, while being cost-effective and improving quality of life in patients with type 2 diabetes.Clinical trials registration: trialregister.nl NTR2264

The term "ketogenic diet" (KD) is used for a wide variety of diets with diverse indications ranging from obesity to neurological diseases, as if it was the same diet. This terminology is confusing for patients and the medical and scientific community. The term "ketogenic" diet implies a dietary regimen characterized by increased levels of circulating ketone bodies that should be measured in blood (beta-hydroxybutyrate), urine (acetoacetate) or breath (acetone) to verify the "ketogenic metabolic condition". Our viewpoint highlights that KDs used for epilepsy and obesity are not the same; the protocols aimed at weight loss characterized by low-fat, low-CHO and moderate/high protein content are not ketogenic by themselves but may become mildly ketogenic when high calorie restriction is applied. In contrast, there are standardized protocols for neurological diseases treatment for which ketosis has been established to be part of the mechanism of action. Therefore, in our opinion, the term ketogenic dietary therapy (KDT) should be reserved to the protocols considered for epilepsy and other neurological diseases, as suggested by the International Study Group in 2018. We propose to adjust the abbreviations in VLCHKD for Very Low CarboHydrate Ketogenic Diet and VLEKD for Very Low Energy Ketogenic Diet, to clarify the differences in dietary composition. We recommend that investigators describe the researchers describing efficacy or side effects of KDs, to clearly specify the dietary protocol used with its unique acronym and level of ketosis, when ketosis is considered as a component of the diet's mechanism of action.