Bariatric procedures generally improve dyslipidemia, sometimes substantially so. Bariatric procedures also improve other major cardiovascular risk factors. This 2-part Scientific Statement examines the lipid effects of bariatric procedures and reflects contributions from authors representing the American Society for Metabolic and Bariatric Surgery (ASMBS), the National Lipid Association (NLA), and the Obesity Medicine Association (OMA). Part 1 was published in the Journal of Clinical Lipidology, and reviewed the impact of bariatric procedures upon adipose tissue endocrine and immune factors, adipose tissue lipid metabolism, as well as the lipid effects of bariatric procedures relative to bile acids and intestinal microbiota. This Part 2 reviews: (1) the importance of nutrients (fats, carbohydrates, and proteins) and their absorption on lipid levels; (2) the effects of bariatric procedures on gut hormones and lipid levels; (3) the effects of bariatric procedures on nonlipid cardiovascular disease (CVD) risk factors; (4) the effects of bariatric procedures on lipid levels; (5) effects of bariatric procedures on CVD; and finally, (6) the potential lipid effects of vitamin, mineral, and trace element deficiencies, that may occur after bariatric procedures.

The National Lipid Association (NLA) Annual Summary of Clinical Lipidology 2015 is a summary of principles important to the patient-centered evaluation, management, and care of patients with dyslipidemia. This summary is intended to be a "living document," with future annual updates based on emerging science, clinical considerations, and new NLA Position and Consensus Statements. The goal is to provide clinicians an ongoing resource that translates the latest advances in medical science toward the evaluation and treatment of patients with dyslipidemia. The 2015 NLA Annual Summary of Clinical Lipidology was founded on the principles of evidence-based medicine and is generally consistent with established national and international lipid guidelines. Topics include a general discussion of the 2014 NLA Recommendations for Patient-Centered Management of Dyslipidemia, genetics, secondary causes of dyslipidemia, biomarkers and "advanced lipid testing," medical nutrition, physical activity, obesity, pharmacotherapy, statin safety, lipid-altering drug interactions, lipoprotein apheresis, dyslipidemia in children and adolescence, dyslipidemia in older individuals, race/ethnicity, and women, health information technology and electronic medical records, as well as investigational lipid-altering drugs in development.

BackgroundAmong the 10 categories of personality disorders (PDs), interventions for antisocial and borderline personality disorder are best studied. However, the remaining PDs also pose major problems in everyday health care settings. People affected often additionally present with Axis-I disorders such as substance-related, mood or anxiety disorders, and are among those most difficult to treat. Cluster A PDs (paranoid, schizoid, schizotypal) are of particular significance as some authors argue that they may be part of a continuum of mental disorders and be considered as sub-syndrome of schizophreniaMethodsIn the context of Cochrane Collaboration reviews for Cluster A, B and C PDs, exhaustive literature searches were completed to identify the current RCT evidence for PD treatments. Retrievals were assessed and evaluated by two reviewers independently and trials for Cluster A PD were identified.ResultsOnly very few (under five) RCTs specifically for Cluster A PDs were identified. Some studies reported on mixed PD samples but it was not always possible to extract data specifically for Cluster A disorders. Participants mostly also suffered from Axis-I disorders. Reported outcomes also focus on Axis-I disorder outcomes or general measures such as overall functioning rather than specific PD symptoms.ConclusionsThe current evidence for psychpathological treatment of Cluster A PD is sparse and does not allow for distinct treatment recommendations. Symptom-driven treatment regimes as suggested by several guidelines are not supported by current evidence.

Objective—To examine CD11c, a 2-integrin, on adipose tissue (AT) leukocytes and blood monocytes and its role in diet-induced obesity. Methods and Results—High-fat diet–induced obese C57BL/6 mice, CD11c-deficient mice, and obese humans were studied. CD11c, leukocytes, and chemokines/cytokines were examined in AT and/or blood by flow cytometry, RNase protection assay, quantitative polymerase chain reaction, or enzyme-linked immunosorbent assay. Obese C57BL/6 mice had increased CD11c in AT and blood compared with lean controls. CD11c messenger RNA positively correlated with monocyte chemoattractant protein 1 in human visceral AT. Obese humans with metabolic syndrome had a higher CD11c level on blood monocytes compared with lean humans. Low-fat diet–induced weight loss reduced blood monocyte CD11c in obese mice and humans. Mouse and human monocyte CD11c levels and mouse AT CD11c messenger RNA correlated with insulin resistance. CD11c deficiency in mice did not alter weight gain but decreased inflammation, evidenced by a lower T-cell number and reduced levels of major histocompatibility complex class II, C-C chemokine ligand 2 (CCL5), CCL4, and interferon in AT, and ameliorated insulin resistance and glucose intolerance associated with diet-induced obesity. Conclusions—Diet-induced obesity increased CD11c in both AT and blood in mice and humans. CD11c plays an important role in T-cell accumulation and activation in AT, and contributes to insulin resistance associated with obesity. (Arterioscler Thromb Vasc Biol. 2010;30:186-192.)

This Roundtable discussion was held to provide a broad discussion of one of the less-well-known lipoprotein risk factors, "lipoprotein little a," or as it is more commonly written, Lp(a). This lipoprotein was identified in 1963 by Kare Berg, MD, PhD, as a lipoprotein antigen that induced antibodies in patients receiving blood transfusions. Initially thought to be an unusual protein found only in some blood donors that induce antibodies in recipients of transfusions, we later learned that all humans have this lipoprotein in the blood. However, the concentration and the structure are highly variable. These differences in structure determined the antigenicity in patients who had different alleles and therefore differing gene products. The later finding that high plasma concentrations of Lp(a) appear to be markers of vascular disease risk has made the assessment of Lp(a) of relevance to all clinicians concerned with risk assessment and treatment. I asked three experts who have extensive experience in assessing and managing lipoprotein-related risk to join me to discuss the issues presented by Lp(a). Dr. Santica Marcovina from the University of Washington in Seattle is an international expert on the structure and laboratory assessment of Lp(a). Drs. Christie Balantyne and Peter H. Jones are well-known experts in lipid management from Baylor College of Medicine in Houston, Texas. ErratumJournal of Clinical LipidologyVol. 4Issue 6PreviewThe incorrect initials are listed for Steven R. Jones, MD in the 10th reference of "Management of Lp(a)" Journal of Clinical Lipidology 2010;4:240–247, by Brown, et al. The citation should read: Jones SR, Blumenthal R. Lipoprotein(a) measurement and determining risk of myocardial infarction. JAMA. 2009;302:1645. Full-Text PDF

Even with optimal statin therapy, many patients with type 2 diabetes mellitus or metabolic syndrome fail to achieve all lipid targets and remain at high risk of cardiovascular events. Add-on lipid-modifying therapy that is effective in improving the triglyceride and high-density lipoprotein (HDL) cholesterol abnormalities characteristic of these conditions is a recommended approach to reduce this risk. Fibrates or niacin is a logical option, supported by clinical studies showing improved lipid control in combination with a statin. Of the fibrates, fenofibrate may offer microvascular benefits in type 2 diabetes-as demonstrated by the Diabetes Atherosclerosis Intervention Study (DAIS) and the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study-as well as a low risk of myopathy when combined with statins compared with gemfibrozil. Although there is good evidence that both agents favorably affect clinical outcome, we need to evaluate their impact against a baseline of statin therapy. We await data from ongoing large-scale studies to evaluate the efficacy and safety of these combinations and to determine the most appropriate option for reducing residual cardiovascular risk in this important patient population. (c) 2008 Elsevier Inc. All rights reserved. (Am J Cardiol 2008;102[suppl]:41L-47L)

How people harness their collective wisdom and power to construct the future in Co-Laboratories of Democracy, by Alexander N. Christakis and Kenneth C. Bausch. Information Age Publishing, 2006. ISBN: 1593114818

Context: Asthma and obesity incidence is increasing worldwide, and asthma is often more severe in the obese. Eotaxin, a CC chemokine, is important in extrinsic asthma, an inflammatory disorder.Objective: Our objective was to examine the relation between eotaxin and obesity.Design: We conducted a comparison study of eotaxin in mice fed high-fat vs. standard chow diet for 26 wk, in obese vs. lean humans, in obese humans before and after 4 - 6 wk of weight loss, and in sc vs. visceral adipose tissue from patients undergoing bariatric surgery.Setting: Our clinical study occurred in an outpatient weight loss program.Patients: Patients were obese adults with metabolic syndrome (n = 40) and nine morbidly obese bariatric surgery patients.Intervention: Intervention was a very-low-calorie diet.Main Outcome Measures: We assessed circulating eotaxin and eotaxin mRNA levels in adipose tissue.Results: Serum eotaxin levels were significantly higher in obese mice, and adipose mRNA levels correlated positively with serum eotaxin levels. Adipose tissue explants from obese mice showed increased secretion of eotaxin compared with explants from lean mice. In obese patients, plasma eotaxin levels were significantly higher than in lean controls and significantly reduced after weight loss, and eotaxin mRNA levels were 4.7-fold higher in visceral than sc adipose tissue.Conclusions: Circulating eotaxin and eotaxin mRNA levels in visceral adipose tissue were increased in obesity in mice and humans. Adipose tissue explants secrete eotaxin, and the stromal/vascular component of adipose tissue seems to be the predominant source of eotaxin. Diet-induced weight loss in humans led to reduction in plasma eotaxin levels, demonstrating that clinical interventions that target obesity can modulate systemic eotaxin levels.

BACKGROUND The complex pathology of disease has sparked the development of novel protein expression profiling techniques that require validation in clinical settings. This study focuses on multiplexed analyses of adipocytokines and biomarkers linked to the metabolic syndrome, diabetes, and cardiovascular disease. METHODS Multiplexed immunoassays using fluorescent microspheres and the Luminex-100 system were performed on plasma from 80 obese patients (40 with the metabolic syndrome) before and after 6-8 weeks of diet-induced weight loss. Leptin, insulin, C-peptide, monocyte chemoattractant protein-1 (MCP-1), eotaxin, interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and IL-6 concentrations measured with multiplex panels from 3 different manufacturers were compared with results from commercial ELISAs. Detection limits and between- and within-run imprecision were determined for each analyte. Bland-Altman analysis was used to determine agreement between multiplexed immunoassays and ELISAs. RESULTS Correlation between the Luminex multiplexed assays and ELISAs was good for leptin (Linco), insulin (Linco), MCP-1 (Biosource and Upstate), and eotaxin (Biosource) with correlation coefficients of 0.711-0.895; fair for eotaxin (Upstate) and C-peptide (Linco) with correlation coefficients of 0.496-0.582; and poor for TNF-alpha, IL-8, and IL-6 (Linco, Biosource, Upstate, and R&D) with correlation coefficients of -0.107 to 0.318. Within- and between-run imprecision values for the multiplex method were generally <15%. Relative changes in plasma leptin and insulin concentrations after diet-induced weight loss were similar whether assessed by multiplex assay or ELISA. CONCLUSION Although this technology appears useful in clinical research studies, low assay sensitivity and poor correlations with conventional ELISA methods for some analytes with very low plasma concentrations should be considered when using the Luminex platform in clinical studies.

Cardiovascular disease (CVD) is the leading cause of death in the United States as well as in other highly developed countries. It is also the leading cause of death in people with diabetes, a disease becoming rapidly more prevalent. This article reviews a series of clinical trials showing the benefits of lipid-lowering agents in reducing CVD risk. It also provides a review of the recent treatment guidelines, including the Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Pressure in Adults and focuses on the primary prevention in patients with multiple risk factors. Additionally, appropriate management of special populations is analyzed, including patients with the metabolic syndrome, elderly patients, those with low levels of high-density lipoprotein cholesterol, and those with coronary artery syndrome. Also analyzed is the risk assessment value of the high-sensitivity C-reactive protein assay in clinical practice. Overall, this article provides evidence that lipid treatment should be part of the overall approach to managing CVD risk factors. (Adv Stud Med. 2004;4(5A):S372-S381)

Introduction Much of the increased coronary heart disease risk in obese individuals [1] is mediated by an increased prevalence of type 2 diabetes mellitus (T2DM), hypertension, elevated plasma triglycerides and low HDL cholesterol [2]. T2DM is characterized by progressive resistance to the effects of insulin, followed by an eventual failure of the b cell to compensate by further increasing insulin secretion. Obesity has increased dramatically in North America over the last 20 years [3] and is a major etiological factor in the development of insulin resistance. With few exceptions, a degree of adiposity is necessary for the development of T2DM [4], but the vast majority of patients with a body mass index in the obese category (430 kg/m) are not diabetic and, indeed, have fasting and postprandial blood glucose and HbA1c levels in the normal range. Of particular relevance are genes and gene products involved in adipocyte free fatty acid (FFA) metabolism, adipocytokine expression and secretion, insulin signaling and its downstream effectors of glucose transport in skeletal muscle and adipose tissue, and regulation of oxidative metabolism and mitochondrial function in skeletal muscle [5]. This review will focus on the central role of adipose tissue in the etiology of insulin resistance. Role of the adipocyte in insulin resistance and type 2 diabetes mellitus Adipose tissue triglyceride is an energy reserve for longterm metabolic needs. Adipocytes also play an important role in the control of circulating levels of FFAs, mediating the rapid clearance of FFAs in the postprandial phase and the release of FFAs during lipolysis of the core lipid droplet. FFAs play an important role in insulin resistance by inhibiting muscle glucose transport and oxidation via effects on serine/threonine phosphorylation of insulin receptor substrate-1 (IRS-1) [6–8]. Chronic exposure to elevated concentrations of FFAs impairs insulin secretory responses to glucose [9] and Carpentier and coworkers [10] demonstrated that insulin secretion in response to glucose fails to compensate for increased insulin resistance induced by a prolonged elevation of FFAs in healthy individuals. The capacity of the adipocyte for FFA uptake and storage is controlled at a number of levels including regulation of preadipocyte differentiation, synthesis and secretion of lipoprotein lipase, regulation of fatty acid and glucose transporters, triglyceride synthesis and lipolysis. Although visceral fat accounts for only about 10% of total body fat, this depot is most strongly related to insulin resistance [11], in part related to higher lipolytic activity and the capacity to release FFAs directly to the liver via the portal circulation [12].

AIM:Individuals with the metabolic syndrome (MS), a clustering of risk factors [triglycerides, glucose, high-density lipoprotein cholesterol, blood pressure (BP), abdominal obesity] defined by the National Cholesterol Education Program (NCEP), are at high risk for coronary heart disease and type 2 diabetes mellitus, and may benefit from aggressive lifestyle modification.METHODS:We reviewed 1 year of consecutive patients' charts to determine the prevalence of the MS in obese individuals enrolled in a medically supervised rapid weight loss programme, the correlation of weight change with the components of the MS, and response to diet-induced weight loss.RESULTS:Out of 185 individuals, 125 (68%) met the NCEP definition of the MS. A moderate decrease in weight (6.5%) induced by a very low calorie diet (VLCD) resulted in substantial reductions of systolic (11.1 mmHg) and diastolic (5.8 mmHg) blood pressure (BP), glucose (17 mg/dl), triglycerides (94 mg/dl) and total cholesterol (37 mg/dl) at 4 weeks (all p < 0.001). These improvements were sustained at the end of active weight loss (average 16.7 weeks; total weight loss 15.1%), with further significant reductions in BP and triglycerides. Weight loss was related to the changes in each criterion of the metabolic syndrome.CONCLUSIONS:The MS is prevalent in two-thirds of obese individuals enrolling in a structured weight loss programme. Moderate weight loss with a VLCD markedly improved all aspects of the MS.

Atherosclerotic cardiovascular disease is a major health problem in the United States. In particular, coronary heart disease (CHD) is the leading cause of death in men and women in the United States, as well as in other industrialized countries. Extensive observational epidemiologic data within and between populations have strongly linked such various factors as untreated hypertension, diabetes, cigarette smoking, and lipid abnormalities to the development of CHD. With respect to lipoprotein parameters, elevated total and low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C) have been strongly associated with CHD risk. Emerging evidence suggests that other lipoprotein abnormalities also are associated with premature CHD, including elevated levels of lipoprotein(a), triglyceride-rich lipoproteins such as small very-low-density lipoproteins and intermediate-density lipoproteins, small and dense LDL particles, and the magnitude of postprandial lipemia. Extensive primary and secondary clinical trial evidence has established that favorably altering dyslipidemias through diet and a variety of pharmacologic agents produces clear improvements in CHD end points. The extent of this benefit depends on the presence or absence of clinical atherosclerotic disease, as well as other CHD risk factors, and the severity of one or more lipoprotein abnormalities. CHD patients and individuals with multiple risk factors, but free of clinical CHD, derive the greatest absolute benefit from lipid treatment directed at reducing LDL-C. The dyslipidemias that impart high risk are severely elevated LDL-C (> 200 mg/dL), combined high LDL-C and low HDL-C (< 35 mg/dL), and combined hyperlipidemias (non-HDL-C > 200 mg/dL with low HDL). The purpose of this review is to aid the primary care physician in identifying these important dyslipidemias and to critically analyze the relative importance of various lipoproteins on atherosclerotic risk.

Collaboration of health care professionals is likely beneficial in modifying patient behavior in the treatment of hyperlipidemia. The purpose of this study was to determine whether limited instruction and demonstration of collaborative management of hyperlipidemia in a continuing medical education (CME) would change physicians' office practices, as determined 1 year later by questionnaire. Collaborative practice was defined as physicians working with other allied health care professionals as a team to increase patients' medication compliance and other behavioral outcomes. A 19-credit hour CME Lipid Disorders Training Program (LDTP) was offered emphasizing the collaborative approach to hyperlipidemia patient management. Physicians (n = 196) were surveyed 1 year after LDTP. The response rate was 52.5%, nonrespondents were similar in locations. About 51% of respondents reported increased collaborative practice; of these respondents, 68% reported saving time, 78% reported improved patient outcomes, 76% improved office efficiency, and 90% increased patient satisfaction. According to self-reporting by these physicians, increased collaboration practices after attending the LDTP course led to improved patient outcomes.