Pokemon Makes Tracks Toward Diabetes Prevention: Breaking up prolonged sitting with short bouts of standing or walking improves postprandial markers of cardiometabolic health in women at high risk for type 2 diabetes.
Diabetes Overlooked in Teens: More teens have diabetes than previously known, and many don’t know they have it. Dysglycemia Detection Often Misses the Mark: Researchers investigated the performance of the 2015 USPSTF screening recommendation for prediabetes and diabetes with a retrospective analysis of EHR data from 50,515 adult overweight or obese primary care patients. Call for Gender-specific Diabetes Treatment: Researchers suggest there are clinically important sex and gender differences in patients with type 2 diabetes. High Hypoglycemia Hospitalization Rates Reflect Global Burden: Over 10 years, hospital admissions for hypoglycemia in England increased by 39%. Flu Vaccine Fights Cardiovascular Events: Rates of hospital admissions for certain cardiovascular events are reduced with influenza vaccination of patients with type 2 diabetes.
This release presents results from the New Zealand (complete) period life tables for 2012–14. We have made Pacific ethnic group life tables publicly available for the first time in this release. With the use of our new methods, we have provided uncertainty measures for our life table estimates for the first time.
The total population life tables are characterised by relatively high death rates in the first year of life (about 5 deaths per 1,000 live births). Nearly one-quarter of the gains in life expectancy were due to decreased death rates for both males and females aged 60–69 years. According to Mortality and demographic data 2011, age-standardised death rates from chronic rheumatic heart disease and diabetes were substantially higher for Maori than for non-Maori. Cause-of-death statistics for 2011 (the latest year available) show type two diabetes, chronic ischaemic heart disease, and acute myocardial infarction are the main causes of death for Pacific people (Mortality and demographic data 2011). The 2012–14 life tables indicate that 96 percent of newborn babies can expect to reach 50 years of age.
International rankings can fluctuate from year to year because the life expectancies of many countries are clustered.
In the early 1960s, New Zealand's ranking was about 10th highest for females and 9th for males. Cardiovascular disease is the leading cause of death in patients with chronic kidney disease.  Heart failure may lead to acute kidney injury and vice versa. The case below illustrates a common clinical problem in patients with both acute and chronic cardiac diseases, namely the development of renal dysfunction. A 68-year-old man with ischemic heart disease, type 2 diabetes mellitus, hypertension, and hyperlipidemia had been admitted with a ST segment elevation myocardial infarction three months previously. The term cardiorenal syndrome is an umbrella term for a worse outcome when these two organs fail simultaneously. The development of acute kidney injury as a primary event leading to cardiac dysfunction (CRS type 3) occurs frequently in critically ill patients but has not been systematically studied as much as CRS type 1. CRS type 4 recognizes the extreme burden of cardiovascular disease risk in patients with chronic kidney disease. Human neutrophil gelatinase- associated lipocalin (NGAL), Kidney injury molecule-1 (KIM-1), N-acetyl-D-glucosaminidase (NAG), Ischemia modified albumin (IMA), Renin-angiotensin-aldosteronesystem(RAAS), Sympathetic nervous system(SNS), Myocardial depressant substance (MDS), Brain natriuretic peptide (BNP), N-terminal pro hormone of brain natriuretic peptide (NT-proBNP) , Interleukin-18(IL-18), creatine kinase –MB (CK-MB), Myeloperoxidase (MPO), Pulmonary vasoconstriction (Pulmonary VC), glomerular filtration rate(GFR). CRS type 1 is the most frequent disorder involving the heart and the kidney and is more frequent in patients with acute decompensated heart failure.
Prevention of CRS is important since once the syndrome has started it is difficult to treat, is not completely reversible in some cases, and is associated with poor outcomes. For CRS type 2 angiotensin converting enzyme inhibitors, beta-blockers, angiotensin receptor blockers, and aldosterone antagonists significantly reduce mortality and morbidity in congestive heart failure.41,42 In patients unable to tolerate these agents, hydralazine and nitrates can be used. The development of dysfunction in a second organ (renal) as a consequence of the primary disorder (cardiac) increases morbidity and mortality.
The cardiorenal syndrome classification may help clinicians organize their thinking about pathogenesis and patient management.
Fonarow GC, Abraham WT, Albert NM, Gattis Stough W, Gheorghiade M, Greenberg BH, O’Connor CM, Pieper K, Sun JL, Yancy CW, Young JB. Zannad F, Mebazaa A, Juilliere Y, Cohen-Solal A, Guize L, Alla F,Rouge P, Blin P, Barlet MH, Paolozzi L, Vincent C, Desnos M, Samii K. Owan TE, Chen HH, Frantz RP, Karon BL, Miller WL, Rodeheffer RJ, Hodge DO, Burnett JC Jr, Redfield MM. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Antioxidant Therapies for Hypolipidemia and HyperglycemiaDawei Gao[1] Key Laboratory of Applied Chemistry in Hebei Province, Department of Biological Engineering, Yanshan University, Qinhuangdao,, China1. Search the NHLBI, use the drop down list to select: the entire site, the Health Topics section only, or the News and Resources section. This section presents the results of a critical review of the evidence that atherosclerosis begins in childhood and that this process, from its earliest phases, is related to the presence and intensity of known cardiovascular (CV) disease (CVD) risk factors (see Table 2?1).
Figure 2-1 depicts the pathologic progression of atherosclerosis with aging, from no visible atherosclerosis at birth to the development of complex plaques with potential rupture and thrombosis in mid- to late adulthood. The most important evidence for the relationship of childhood risk factors to CVD is the establishment of a direct relationship between risk exposure and events. Thus, studies examining the clinical importance of CV risk in childhood must consider end points recognized as intermediate stages in the pathogenesis of CVD. Legend to Figure 2?2: This flow diagram depicts the timeline for development of cardiovascular (CV) risk, atherosclerosis, and CV events along a continuum extending from before birth to adult life. Considered collectively, these studies constitute an evidence chain, with the strength of the body of evidence represented in the evidence grades. Atherosclerosis at a young age was first identified in Korean War and Vietnam War casualties.[5],[6] Two major contemporary studies, the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) and the Bogalusa Heart Study (Bogalusa), have subsequently demonstrated atherosclerosis, indicated by fatty streaks and more advanced lesions, in children, adolescents, and young adults who died as a result of unintentional injury.
Figure 2?3, from the PDAY study, shows the relationship between the number of identified CV risk factors and the pathologic lesions of atherosclerosis by age in the right coronary artery, using maps of arterial segments created by converting pathologically classified lesions to computerized images. These computerized images from the Pathobiological Determinants of Atherosclerosis in Youth study are prevalence maps of fatty streaks and raised lesions, with color intensity reflecting the density and grade of the lesions for the two age groups and the number of risk factors. Measures of subclinical atherosclerosis and end organ injury include the presence of coronary calcium on electron beam computerized tomography (EBCT) imaging, increased medial thickness of the carotid artery assessed with ultrasound (cIMT), reduced endothelium-dependent dilation of the brachial artery with ultrasound imaging (flow-mediated dilation (FMD)), and increased left ventricular mass (LVM) by cardiac ultrasound. Subclinical atherosclerosis imaging studies (coronary calcium by EBCT, cIMT) have been important in demonstrating the importance of childhood risk factors to future atherosclerosis. The most important evidence relating risk in childhood to clinical CVD is the observed association of risk factors for atherosclerosis to clinically manifest CV conditions.
As described above, there is evidence to indicate that hypertension, dyslipidemia, diabetes, obesity, and cigarette smoking—established risk factors for CVD in adults—contribute to the early development of atherosclerosis, with the exception of two risk factors.
CVD has been observed in diverse geographic areas and in all racial and ethnic backgrounds.
Although genetic dyslipidemias and diabetes mellitus are recognized as high-risk states, from a population standpoint, it is the clustering of multiple risk factors that is most commonly associated with premature atherosclerosis.
The relationship of the current obesity epidemic in children to future CVD and diabetes in adulthood is considered one of the most important public health challenges in the United States, particularly given the fact that more than 30 percent of the U.S. Tracking studies from childhood to adulthood exist for all the major risk factors, including obesity, dyslipidemia, diabetes, cigarette smoking, and hypertension. It is important to distinguish between the goals of prevention at young ages and such goals at older ages when atherosclerosis is well-established, morbidity already may exist, and the process is only minimally reversible (Figure 2?2).
The most direct means of establishing evidence for active CVD prevention beginning at a young age would be to randomize young individuals with defined risks to treatment of CV risk factors or to no treatment and then to follow both groups over sufficient time to determine whether CV events are prevented without undue increase in morbidity arising from treatment.
The recognition that evidence from this direct pathway is unlikely to be obtained requires an alternate stepwise approach, linking segments of an evidence chain in a manner that serves as a sufficiently rigorous proxy for the causal inference of a clinical trial. The remaining evidence links pertain to the determination of whether interventions that aim to reduce risk factors will have a health benefit and whether the risk and cost of interventions to reduce risk are outweighed by the reduction in CVD morbidity and mortality. Intervention planning must consider that each risk factor exists within an individual's unique combination of environmental, behavioral, physiologic, and genetic characteristics. For certain behavioral risk factors, limitations in measurement and data collection make the establishment of a causal pathway between the risk factor and disease impossible. Since risk levels in the preadolescent pediatric population with normal weight for height are generally below levels associated with CV events,[113] a critical component of pediatric CVD prevention is understanding those factors associated with the evolution from the low-risk state of childhood to the presence of risk in adulthood. A new consideration is the role of new noninvasive measures of cardiac and vascular injury in the evaluation of evidence.
Thus, for each risk factor discussed in the sections below, recommendations reflect a complex decision process that integrates the strength of the evidence with knowledge of the natural history of atherosclerotic vascular disease, estimates of intervention efficacy and risk, and the physician's responsibility to provide both health education and effective disease prevention and treatment.
They found that targeted diabetes screening based on the new USPSTF criteria may detect only about half of adult community health center patients with undiagnosed dysglycemia, and fewer racial and ethnic minorities than whites. The diagnosis is made at a lower age and body mass index in men, but the biggest risk factor, obesity, is more common in women.
However, admissions for diabetes, length of hospital stay, mortality, and 1-month readmissions decreased. Vaccination was associated with significantly lower admission rates for stroke and heart failure, as well as pneumonia or influenza and all-cause death. We did this to take advantage of new modelling techniques that help with estimation of death rates for small populations. Death rates then decrease as age increases and are at their lowest among ages 5–8 years. However, the fall in death rates for women over 80 years contributed more to their increase in life expectancy than it did for men. Females in particular experienced lower death rates at the older ages (70+), while males made greater improvements than females in ages 20–49 years. Age-standardised death rates were also significantly higher for Maori from lung cancer, cervical cancer, chronic lower respiratory diseases (including chronic obstructive pulmonary disease), and hypertensive disease.
Assuming death rates continue to decrease at all ages, the actual percentage of babies reaching these ages will be higher (see New Zealand cohort life tables). Through the next two decades, longevity increased faster in many other OECD countries than in New Zealand.
Over the period 2008–12, New Zealand ranked about 14th highest for females and 5th for males. Chronic kidney disease may affect the clinical outcomes in patients with cardiovascular disorders. This clinical presentation has been called a cardiorenal syndrome; this construct should lead to a better understanding of the interactions between cardiac and renal disorders and the effect of this interaction on management and outcomes. At this follow up visit he presented with gradually increasing shortness of breath, generalized swelling, and some abdominal distension.
Since the current literature provides more information on CRS type 1, our discussion emphasizes this syndrome. Although CRS is less frequent in acute coronary syndrome patients, it is associated with longer hospital stays and with higher in-hospital mortality in these patients. Vasodilators and loop diuretics are frequently used in cases of acute decompensated heart failure with CRS type 1.36 However, loop diuretics predispose patients to electrolyte imbalance and hypovolemia leading to neurohumoral activation, reduced renal glomerular flow, and higher serum urea and creatinine levels. The Study of Heart and Renal Protection (SHARP) trial included 3,023 end stage renal disease patients and 6,247 chronic kidney disease patients not on dialysis, and preliminary results showed a significant benefit with the combination of simvastatin and ezetimibe.46 In another study, 245 patients were randomized to three times weekly (conventional) or six times weekly (frequent) hemodialysis and followed up for 12 months.
Associated cardiac and renal complications warrant appropriate therapy as indicated on an individual basis. Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure.
The complexity and cost of drug regimens of older patients hospitalized with heart failure in the United States, 1998–2001. Characteristics and outcome of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE). Role of diminished renal function in cardiovascular mortality: marker or pathogenetic factor?
Congestion in chronic systolic heart failure is related to renal dysfunction and increased mortality.
Incidence, predicators at admission and impact of worsening renal function among patients hospitalized with heart failure.
Urinary neutrophil gelatinase associated lipocalin (NGAL), a marker of tubular damage, is increased in patients with chronic heart failure.
Tubular damage in chronic systolic heart failure is associated with reduced survival independent of glomerular filtration rate. Relationship between pulmonary hemodynamics and arterial pH and carbon dioxide tension in critically ill patients. Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-alpha.
Association of single measurements of dipstick proteinuria, estimated glomerular filtration rate, and hematocrit with 25-year incidence of end-stage renal disease in the multiple risk factor intervention trial. Comparative impact of multiple biomarkers and N-Terminal pro-brain natriuretic peptide in the context of conventional risk factors for the prediction of recurrent cardiovascular events in the Heart Outcomes prevention  Evaluation (HOPE) Study. Correlation and prognostic utility of B-type natriuretic peptide and its aminoterminal fragment in patients with chronic kidney disease.
Long term risk of mortality and end-stage renal disease among the elderly after small increases in serum creatinine level during hospitalization for acute myocardial infarction. Prevalence and impact of worsening renal function in patients hospitalized with decompensated heart failure: results of the prospective outcomes study in heart failure (POSH). The prognostic importance of different definitions of worsening renal function in congestive heart failure. Long term outcomes of Medicare beneficiaries with worsening renal function during hospitalization for heart failure.
The relationship between transient and persistent worsening renal function and mortality in patients with acute decompensated heart failure. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. Loop diuretics can cause clinical natriuretic failure: a prescription for volume expansion. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. Clinical profile, contemporary manag- ement and one-year mortality in patients with severe acute heart failure syndromes: The EFICA study. The effects of lowering LDL with simivastatin plus ezetimibe in patients with chronic renal disease (Study of Heart and Renal Protection): a randomized placebo-controlled trial. Flow cytometric analysis of Nrf2 expression in the liver tissues of lactic acid bacteria treated mice and control mice. Each risk factor exists within a behavioral, environmental, physiologic, and genetic context that provides the rationale for its consideration as a risk factor that could be used to identify persons who are at elevated risk or who may be the target of intervention. This evidence is best obtained from long-term observational studies beginning in childhood, with risk factors measured and related to CVD outcomes later in life.
The chart flows in one direction with arrows pointing downward and lateral arrows to one or more boxes. Studies evaluated for the Guidelines may have examined single links in the chain of evidence, may have connected several links simultaneously, or may have evaluated the consequences of specific interventions for risk-benefit analysis. In the Bogalusa study, CV risk factors (lipids, blood pressure, body mass index (BMI), tobacco use) were measured as part of a comprehensive school-based epidemiologic study of a biracial community.
These are displayed as prevalence maps of fatty streaks and raised lesions, with color intensity reflecting the density and grade of the lesions.[13] In 15- to 24-year-old subjects, the maps demonstrate the impact of increasing numbers of risk factors on both the presence and severity of the atherosclerotic process. Genetic disorders related to high cholesterol are the biologic model for risk factor impact on the atherosclerotic process.
As demonstrated in the PDAY, CARDIA, Young Finns, and Bogalusa studies and as shown in Figure 2?3, the presence of multiple risk factors is associated with striking evidence of an accelerated atherosclerotic process. At middle age and older, the goals are to prevent clinical events from occurring and to minimize the risk of future events in those with existing morbidity.

This direct approach is attractive because atherosclerosis prevention would begin at the earliest stage of the disease process, thereby maximizing benefit. Figure 2?2 demonstrates the components of this evidence chain, with links comprising a series of critical studies leading from risk beginning before birth, to risk acquisition during childhood, to risk modification by reduction strategies, and finally to clinical disease in adulthood. There is unlikely to be a study comparing the effect of a lifetime of whole-milk consumption with fat-free milk consumption, or a study comparing daily physical training for decades with a lifetime of inactive television watching on the amount of atherosclerosis or rates of myocardial infarction. The well-established factors on this environmental-behavioral axis are initiating tobacco use and becoming obese. These recommendations for providers of health care to children will be most effective when complemented by a broader public health strategy, as discussed in Section XVI.
One cornerstone of pediatric care is placing clinical recommendations in a developmental context.
Based on the results of the evidence review, the Guidelines provide recommendations for preventing the development of risk factors and optimizing CV health beginning in infancy. Comparison of coronary heart disease risk factors in autopsied young adults from the PDAY Study with living young adults from the CARDIA study. Risk factors related to carotid intima-media thickness and plaque in children with familial hypercholesterolemia and control subjects. Usefulness of electron beam tomography in adolescents and young adults with heterozygous familial hypercholesterolemia. Carotid artery intimal-medial thickness and left ventricular hypertrophy in children with elevated blood pressure.
Intima media thickness in childhood obesity: relations to inflammatory markers, glucose metabolism, and blood pressure.
Left ventricular geometry and severe left ventricular hypertrophy in children and adolescents with essential hypertension. Vascular function and carotid intimal-medial thickness in children with insulin-dependent diabetes mellitus. Endothelial dysfunction and increased arterial intima-media thickness in children with type 1 diabetes.
Early atherosclerosis in childhood type 1 diabetes: role of raised systolic blood pressure in the absende dyslipidaemia. Increased carotid intima-media thickness in children, adolescents and young adults with a parental history of premature myocardial infarction. Parental occurrence of premature cardiovascular disease predicts increased coronary artery and abdominal aortic calcification in the Framingham Offspring and Third Generation cohorts. Endothelium-dependent dilatation is impaired in young healthy subjects with a family history of premature coronary disease. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults.
Study authors suggested that playing Pokemon Go, the immensely popular reality game that involves walking long distances, could help remedy the physical inactivity associated with diabetes and obesity. In a recent JAMA study, the prevalence was 0.8%—with 29% undiagnosed—and the prevalence of prediabetes was 18%.
Women are at greater risk for cardiovascular risk, myocardial infarction, and stroke mortality, but when dialysis therapy is initiated, mortality is comparable.
Given the continuous rise of diabetes prevalence, an aging population, and the associated costs, researchers suggested initiatives are needed to reduce the burden of hospital admissions for hypoglycemia. The 2012–14 results discussed in this publication refer to the median results unless otherwise stated. In contrast, Maori had lower age-standardised death rates than non-Maori from melanoma, and pneumonia and influenza.
The chance of survival decreases rapidly at the oldest ages, with just 7 in every 100 boys expected to live to age 95, and 13 in every 100 girls. Since the mid-1980s, faster-than-average gains in life expectancy in New Zealand, particularly for males, have improved New Zealand's relative position. Renal impairment with any degree of albuminuria has been increasingly recognized as an independent risk factor for cardiovascular events and heart failure hospitalizations, while chronic heart failure may cause chronic kidney disease. We have reviewed this topic by discussing the definitions, prevalence, pathophysiology, and treatment of cardiorenal syndromes.
Both acute heart failure leading to acute kidney injury and chronic heart failure leading to progressive renal insufficiency and chronic kidney disease represent conditions that may seem interchangeable.
Depending upon pre-existing comorbidity and the underlying etiology, left ventricular assist devices can be used as a bridge to transplantation or cardiac surgery. The core management of CRS type 3 is intravascular and extravascular volume control with either use of diuretics and various forms of renal replacement therapy or extracorporeal therapy and solute removal. For example, removal of the source of infection, antibiotic therapy, and other supportive measures in early goal directed therapy are indicated in patients with septic CRS type 5. Cardiac resynchronization therapy with biventricular pacing improves renal function in heart failure patients with reduced glomerular filtration rate. Introduction, the literature search for these Guidelines addressed 14 critical questions (I.
The progression of atherosclerosis is exacerbated and intensified by the presence of risk factors. Because of the time course of atherosclerosis, studies of 50 to 60 years' duration linking early risk to CV events are impractical, although studies exist in which risk was measured in early adulthood and outcomes were measured much later in life.
Studies describing environmental or behavioral factors that affect the process are shown on the left side, and potential pathophysiologic or medical actions are shown on the right.
Below, the flow chart is described as lists in which the possible next steps are listed beneath each box label. Although each study is graded individually in the evidence tables, the Expert Panel assigned summary grades for the body of evidence reviewed in developing each recommendation. Prevention of atherosclerosis development receives greater emphasis in children and young adults. Findings were related to atherosclerosis measured at autopsy after accidental death, and strong correlations were shown between the presence and intensity of risk factors and the extent and severity of atherosclerosis.[3],[7] In the PDAY study, risk factors and surrogate measures of risk factors were measured post mortem in 15- to 34-year-olds who died accidentally of external causes. Comparison with 25- to 34-year-olds shows the impact of both age and multiple risk factors. Alex McMahan for the Pathobiological Determinants of Atherosclerosis in Youth Study Group, unpublished observation. Studies directly relating fitness levels in childhood to future atherosclerosis have not been performed. Several longitudinal cohort studies referenced extensively in these Guidelines (Bogalusa, PDAY, Coronary Artery Risk Development in Young Adults (CARDIA)) examine biracial populations, although longitudinal data for Hispanic, Native American, and Asian children are lacking. The two most prevalent multiple risk combinations are tobacco use with one other risk factor[74] or the development of obesity, which often is associated with insulin resistance (as opposed to elevated blood sugar in adults), elevated triglycerides, reduced HDL?C, and elevated blood pressure. Among the many studies demonstrating this tracking,[72],[92],[93],[94] one of the most recent is a report from the Bogalusa study, which followed more than 2,000 children from 5 to 14 years of age at initial evaluation to adult followup at a mean age of 27 years.
At a young age, historically there have been two goals of prevention: (1) prevent the development of risk factors (primordial prevention) and (2) recognize and manage those children and adolescents at high risk due to the presence of one severe risk factor or multiple risk factors (primary prevention).
That does not diminish the critical importance of public health measures to CVD prevention. Studies evaluated for these Guidelines may examine single links in this evidence train, connect several links simultaneously, or evaluate the consequences of specific interventions to allow risk-benefit analysis.
Introduction, Table 1?1, questions 9?14), which are addressed subsequently in the evidence review of each risk factor. A family history showing multiple members affected by clinical CVD at a young age suggests the need to investigate both genetic risk and toxic environmental exposure and to consider early risk reduction.
What is important about diet and exercise in childhood is the relationship of healthful behaviors to the development of future risk factors, including obesity, diabetes mellitus, hypertension, and dyslipidemia.
Although the evidence for a heart healthy diet and physical activity in the treatment of established risk factors is strong, less strong but emerging evidence suggests that an energy-balanced, nutrient-dense diet and consistent routine levels of physical activity that promote physical fitness prevent risk factor acquisition over the course of decades. For adults, the primary use of these technologies has been in event prediction; that is, whether the presence of one of these markers increases the likelihood of a future CV event beyond that expected from conventional risk factor assessment. As opposed to virtually universal recommendations that apply to nearly all adults, pediatric recommendations must consider not only the relationship of age to disease expression but also the ability of the child and the family to understand and implement medical advice and the safety of the intervention modality. Pediatric care providers—pediatricians, family practitioners, nurses and nurse practitioners, physician assistants, and registered dietitians—are ideally positioned to reinforce these CV health behaviors as part of routine care. Authors suggest a need for improved screening among adolescents because diabetes in youth is associated with early onset of risk factors and complications. The bidirectional nature of these disorders contributes to the complexity and the composite definitions of cardiorenal syndromes. In some cases it difficult to distinguish between the two entities without the necessary time based information in the clinical history of the patient.
Aronson et al reported that persistent worsening renal function after admission for acute decompensated heart failure was more likely in those with worse baseline kidney function. In a randomized trial involving patients hospitalized for acute decompensated heart failure, worsening renal function, and persistent congestion, Bradley found that a stepped pharmacologic-therapy algorithm was superior to ultrafiltration for the preservation of renal function. In the setting of acute kidney, prevention of left ventricular volume overload is critical to maintain adequate cardiac output and systemic perfusion and also to protect against the vicious cycle that will worsen both cardiac and renal function. Important improvements in serum phosphate, control of hypertension, and avoidance of intradialytic hypotension were also noted in the frequent dialysis group. Clinical trials of voluntary risk exposure, in which children would be randomized at birth to become, for example, chronic smokers, to determine the likelihood of future heart attack decades later, would be both impractical and unethical. Also relevant are studies of factors associated with the development of risk factors, such as a high-fat diet and a physically inactive lifestyle. The complexity of the evidence development process is apparent in the multiple interrelationships between risk factors that change and evolve throughout the history of each individual from childhood to adulthood. The many evidence pathways pursued in preventive cardiology research and included in the evidence reviewed for the Guidelines are displayed in Figure 2?2. In older adults, importance is placed on factors associated with the progression of atherosclerosis and factors associated with acute events, such as predisposition to thrombosis or plaque instability. Strong relationships were demonstrated between atherosclerotic severity and extent and the presence and intensity of known risk factors, including higher age, higher non-high-density lipoprotein cholesterol (non-HDL?C), lower HDL cholesterol (HDL?C), hypertension (determined by renal artery thickness), tobacco use (thiocyanate concentration), diabetes mellitus (glycohemoglobin), and obesity in males. Risk, particularly the presence of multiple risk factors, accelerates the development of atherosclerosis.
Clinically important differences in the prevalence of risk factors exist by race and gender, particularly with regard to tobacco use rates, obesity prevalence, hypertension, and dyslipidemia. This latter combination, known as the metabolic syndrome in adults, has become increasingly prevalent in childhood.
Based on BMI percentiles derived from the study population, 84 percent of those with a BMI in the 95th to 99th percentiles as children were obese as adults.[95] For obesity, increased correlation is seen with increasing age at which the elevated BMI is obtained.
With the development of measures of subclinical atherosclerosis, left ventricular hypertrophy, and endothelial function, the potential to assess a third goal has emerged: documentation of the prevention of the early stages of atherosclerosis and other forms of CV pathology. For risk factors such as tobacco use and physical inactivity, public health measures are critical for risk reduction. Such a study would be extremely expensive and would require a high level of adherence and participant retention over several decades, during which time changes in environment and medical practice would diminish the relevance of the results.
Some studies encompass the entire lifespan, whereas others examine the impact of interventions on intermediate states. The best evidence for answering these questions derives from randomized trials showing event reduction in adults, randomized trials in children showing risk reduction with change in subclinical measures of atherosclerosis or target organ damage and patient safety, genetic studies that provide a model for the adverse effects of sustained exposure to risk, and long-term observational studies demonstrating the benefit of maintenance of low risk on health and all-cause mortality. Consequently, recommendations must include studies that examine the impact of interventions on risk factor development and reduction rather than studies that only examine the effects on subclinical disease measures or clinical events. The Guidelines also offer specific guidance on primary prevention, with age-specific, evidence-based recommendations for individual risk factor detection. Patients and families expect physicians, nurses, dietitians, and other health care providers and counselors to provide accurate health information. However, the most important clinical trials in heart failure tend to exclude patients with significant renal dysfunction. The pathophysiology of CRS type 1, renal dysfunction in patients with decompensated heart failure, is complex.
Untreated uremia affects myocardial contractility through the accumulation of myocardial depressant factors and can cause pericarditis.17 Partially corrected or uncorrected acidemia produces pulmonary vasoconstriction, which in some patients contributes to right-sided heart failure. He investigated this outcome in a cohort of 467 patients admitted with acute decompensated heart failure.
Weight loss at 96 hours was similar with the two approaches, but ultrafiltration was associated with higher rates of adverse events.38 An earlier ultrafiltration vs. Diabetes mellitus (DM) can be defined as a group of syndromes due to defects in pancreatic secretion of insulin or insulin action, which characterized by hyperglycemia, altered metabolism of lipids, carbohydrates and proteins along with an increased risk of complications from vascular disease (Taskinen et al., 2002). Of these, the first nine pertain to evidence that atherosclerosis begins in childhood and that early atherosclerosis is associated with the presence and intensity of identified risk factors; it is this evidence that is reviewed here.
Except in rare circumstances, atherosclerotic disease is subclinical for the first two to three decades of life. Atherosclerosis develops more rapidly as the number and the intensity of risk factors increase.
Finally, and most importantly, Figure 2?3 demonstrates that the absence of identified risk factors is associated with a virtual absence of advanced atherosclerotic lesions (American Heart Association Grades IV and V) in 15- to 34-year-olds.
In adults, lower HDL levels are consistently shown to be associated with increased risk for CVD. In adults, the influence of obesity on CV risk may vary by ethnicity.[73] Low SES in and of itself confers substantial risk. For risk factors such as hypertension, diabetes mellitus, obesity, and dyslipidemia, public health measures will affect prevalence, but without medical recognition and treatment, effective risk reduction cannot occur. Many scenarios could arise in which the ethics of such a trial could be questioned, including undue exposure to risk in one of the trial arms, the discovery of novel treatments of improved efficacy during the conduct of the trial, environmental changes or shifts in priorities of the funding entity that complicate its completion, and the potential withholding of effective therapy to a generation of youths with identified risk who do not receive treatment. Many of these evidence links come from the epidemiologic studies described in this entire section and provide answers to the first nine critical questions of the evidence review: atherosclerosis begins in childhood, atherosclerosis is related to risk factors that can be identified in childhood, and the presence of these risk factors in a given child predicts an adult with risk factors.
Recommendations to intervene must consider not only the relationship of the risk factor to future disease but also whether reduction of that risk factor will result in an appreciable decline in subclinical disease or in adverse clinical events with an acceptable safety profile. That this behavior is highly addictive means that the use of tobacco alone is an indication for smoking cessation counseling. Management algorithms provide staged care recommendations for risk reduction within the pediatric care setting and identify risk factor levels requiring referral to a specialist.
The childhood health maintenance visit provides a useful context for effective delivery of the CV health message.
Optimization of fluid, avoidance of nephrotoxic agents, and correction of underlying disorders are the basic principles.
A conceptual model for CVD prevention by pediatric care providers beginning in childhood was developed based on the evidence review. The studies that make up the pathways in Figure 2?2 provide evidence addressing the key questions critical to this evidence review—including associations between exposures and outcomes, efficacy of screening for conditions of interest, the presence of adverse consequences of screening, the efficacy of interventions on outcomes, and the adverse consequences of interventions. Evidence is not adequate for the recommendations provided in these Guidelines to be specific to racial or ethnic groups or to SES. Individuals who develop obesity have been shown to be more likely to develop hypertension or dyslipidemia as adults.[72],[94] Tracking data on physical activity are more limited. The presence of a risk factor may confer a high relative risk of a future CV event, but intervention may not be warranted if actual event rates in the next several decades are low; conversely, a lower relative risk may be acceptable for intervention if the likelihood of an adverse event related to that risk factor is high.
In contrast, recommendations to treat elevated blood pressure are based on multiple elevated measures over time because of the intrinsic variability of blood pressure and the possibility of significant modification through diet and exercise. Rather than predicting clinical events, future research may show that a positive test signals the transition to more advanced atherosclerosis or the presence of CV target organ damage.
The Guidelines also identify specific medical conditions, such as diabetes and chronic kidney disease, which are associated with increased risk for accelerated atherosclerosis. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathway, and arginine-vasopressin release.

Free radicals react with lipids and cause peroxidative changes that result in enhanced lipid peroxidation (Girotti, 1985). This evidence inquiry is limited by the absence of reports of cost-effectiveness analyses of the screening and intervention strategies to lower CV risk in childhood.
The timing and safety profile of pharmacologic interventions are important considerations for CVD prevention. Studies of subclinical atherosclerosis and LVM have been important in establishing the relationship of risk in childhood to evidence of CV injury. Recommendations for ongoing CV health management for children and adolescents with these diagnoses are provided.
The office of the pediatric care provider provides an effective setting for the health care team to engage children and families in the initiation of behavior change to reduce the risk of CVD and promote lifelong CV health.
These mechanisms cause fluid and sodium retention, peripheral vasoconstriction, and volume overload. These markers reflect activation of hormonal, immunologic, inflammatory, and oxidative processes and are associated with an increased risk deterioration in renal function.15,16 These biomarkers have the potential to identify cardiorenal syndromes and predict outcomes and need more study.
This trial showed that ultrafiltration produces greater weight and fluid loss than intravenous diuretics and reduces 90-day heart failure rehospitalizations and emergency department visits in patients with acute decompensated heart failure.
The level of lipid peroxidation in cells is controlled by various cellular defense mechanisms consisting of enzymatic and nonenzymatic scavenging systems. In contrast to adult guidelines, the challenge of preparing evidence-based guidelines for CV risk reduction in childhood is augmented by the scarcity of evidence pertaining to the impact of preventive interventions on mortality, morbidity, and quality of life. The lifetime risk of disease associated with high risk in childhood may identify candidates for more aggressive intervention. The presence of multiple risk factors represents a powerful stimulus for accelerated atherosclerosis, and knowledge of this situation affects treatment decisions. Monitoring of LVM has been incorporated into treatment algorithms for hypertension in childhood.[113] However, only a few studies in the pediatric age group have used these measures as clinical end points.
Therapy to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardiorenal syndrome.
Patients with chronic heart failure can develop chronic renal failure (CRS type2) through a similar pathophysiology. These results support the hypothesis that removal of isotonic fluid by ultrafiltration rather than hypotonic urine by intravenous diuretics may explain the improved clinical benefits of ultrafiltration.40 However, ultrafiltration increases the complexity of care.
The efficiency of the antioxidant defense mechanism is altered in diabetes (Wohaieb and Godin, 1987).
As described throughout these Guidelines, recommended strategies for intervention should consider environmental, behavioral, physiologic, and genetic attributes, as well as the efficacy and safety of potential treatment modalities, in selecting the type and timing of any intervention and in measuring outcomes. It is expected that research using these intermediate end points will be used to clarify knowledge gaps identified in the evidence review for these Guidelines; the clinical importance of these new studies in adults and children remains to be fully established.
Increased free radical production exerts cytotoxic effects on the membrane phospholipid, resulting in formation of toxic products such as MDA. The antioxidant scavenging enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) offer protection to cells and tissues against oxidative injury (Bonnefont-Rousselot et al., 2000). There are various reports indicating the bene?cial effects of antioxidant supplementation in preventing dyslipidemia. Some herbal drugs are a good source of natural antioxidants, and increased utilization of medicinal plants became a World Health Organization policy on 1970.
Bor (Chinese Name: Hong jing tian) is a traditional Tibetan pharmacology, which distributed in Eastern Europe and Western Asia (altitude 3500-5000 meters).
We found that RS could significantly stimulate insulin secretion, and possess antioxidative and antidiabetic potentials.
Ligustrum lucidum Ait (LLA) is a traditionally Chinese medicinal plant, known with a local name as “Nv zhenzi”.
It has been used to treat cancer whose tumor inhibitory rate was 46.15% (Xiang and Gu, 2002). The hypoglycemic effect of oleanolic acid (OA) isolated from LLA was identified in streptozotocin-induced diabetic rats, at the same time, the ability of LLA stimulating secretion of insulin was disclosed in our study (Gao et al., 2007).
In order to reveal the efficacy of LLA in alloxan-induced diabetic rats, the effects of OA from LLA were estimated on hypoglycemia, lipids modulating and antioxidant efficacy in alloxan-induced diabetic rats. Meanwhile, we investigate the effect of OA on serum level of hepatic enzymes and tissue level of lipid peroxidation and antioxidant enzymes in alloxan-induced diabetic rats.Nuclear factor erythroid 2-related factor 2 (Nrf2) controls the antioxidant response element (ARE)-dependent gene regulation in response to oxidative stress. Nrf2 regulates the transcriptional activation of more than 200 antioxidant and protective genes that constitute the so-called phase II response. A number of Lactobacillus species, Bifidobacterium sp, Saccharomyces boulardii, and some other microbes have been proposed as and are used as probiotic strains, i.e.
Fermented cabbages, one of the most important foods in the traditional Chinese diet, hold a wide variety of LAB which may have interesting features for application in health. Fermented cabbages have made up a significant part of food intake in Asia countries for several centuries, including China, Japan, Korea, and so on. In our study, 28 LAB strains were isolated from pickled cabbage, and two strains with high acid tolerance and bile salt resistance were screened, which were Lactobacillus plantarum and Lactobacillus brevis. Activities of antioxidant enzymes in liver and kidney tissues were observed, parameter of blood lipid was examined, and their effects of hypoglycemia and hypolipidemia were analyzed. The experiment was designed to determine whether the antioxidative effects of lactic acid bacteria from fermented cabbage are mediated, at least in part, by the activation of Nrf2. We analysed the scavenging effects of superoxide anion radicals and hydrogen peroxide of the strains isolated from fermental cabbages in vitro, and evaluate liver antioxidative activities related to the elimination of reactive oxygen species in L.plantarum-treated high-fat diet mice. Meanwhile, the Nrf2-mediated antioxidant defense pathway and immune status of the lactic acid bacteria-treated mice were investigated.The present study was performed to investigate the antioxidant therapeutic effects and mechanism of R.
We found that they could significantly stimulate lipid metabolizing, and possess antioxidative, hypolipidemic and hypoglycemic potentials. Antidiabetic and antioxidative potentials of Rhodiola sachalinensis polysaccharideRhodiola sachalinensis has been used as one of Tibet traditional herbs, which possesses anti-fatigue, anti-lacking oxygen, anti-microwave radiation and anti-caducity potentials. In the study, we examined the antidiabetic effect and probable mechanisms of Rhodiola sachalinensis root extract (RS), its main compound was polysaccharide. The levels of serum total cholesterol (TC) and triglcerides (TG) of RS-treated diabetic rats were lower than control diabetic rats. A significant enhancement in the serum insulin levels of diabetic rats following RS treatment was also observed. Furthermore, RS treatment decreased malondialdehyde (MDA) level, while increased SOD, CAT and GSH-px activities of the liver and kidney of diabetic rats. At the same time, RS has not expressed significant toxicity in LD50 test and single cell gel electrophoresis assay. These results indicate that RS has the hypoglycemic and hypolipidemic activities, which is an effective scavenger of free radicals to inhibit the lipid peroxidation. The abilities of antioxidation and protecting pancreatic ? cells might be the main mechanisms of RS on antidiabetic effect. After filtering the residue was air-dried and then refluxed again with 80% ethanol to remove monosaccharide and oligosaccharide. After filtering and centrifuging, the precipitate was collected and vacuum-dried, obtaining light brown extracts, named RS.
The extract was examined by thin layer chromatography (TLC) analysis to identify the main compounds. Nine kinds of indicator system were used to identify the compounds of RS, and different color spots were visualized (Gao et al., 2009). The results were shown on Table 1, which indicated that the main compound in RS was polysaccharide, meanwhile including a little of flavone, saponin and organic acid, but no alkaloide, anthraquinone, hydroxybenzene, terpene, steroid and lignin were detected. These results have indicated that polysaccharide is the main ingredient of the extract of R. Preparation of STZ-induced diabetic ratsMale wistar rats weighing 180-200 g were obtained from the animal department of Beijing institute of traditional medical and pharmaceutical sciences.
Following one week of acclimation, eight rats were randomly assigned as normal control group, and the rest rats, treated with STZ, became the diabetic model rats according to the standard method (Gao et al., 2007). Blood samples were taken at 30, 60, 90, and 120 min intervals following glucose administration, and blood glucose levels were measured at various time points.
However, the blood glucose levels in diabetic control rats declined after 90 min, but it was still high during the experiment.
On days 0, 10, 20, 30 and 40, the blood samples were collected from rat’s tail veins and measured, followed by an overnight fast. Changes of plasma glucose level as a result of RS treatment for 40 days are shown in Figure 2. They were consistently staying at similar levels within the experimental course in NC & DC groups. In a healthy person, plasma glucose concentrations are maintained within a fairly narrow range in the fasting state, even if no food is ingested for many days. However, after glucose intake an acute increase in plasma glucose is seen, the concentration peaking generally within 1 h. Plasma glucose then decreases and fasting levels are regained by 2 h post ingestion (Choi, et al., 2008). Determination of effects of RS treatment on blood biochemical parametersAt the end of the experiment, the blood samples of fasted tested rats were collected from the eyes under ether anaesthesia, to determine the levels of TG, TC and insulin, according to commercial advice by the Automatic Biochemical Analyzer. The situation of insulin secretion of the diabetic rats has been ameliorated by RS treatment (Figure 3). The levels of serum lipids are usually raised in diabetes mellitus (Sakatani et al., 2005).
The increase of blood glucose is accompanied with the rise of TC and TG (Sharma et al., 2003). The significant rise of blood glucose, TC and TG levels has been observed in STZ-induced diabetic rats, whereas those were significantly decreased by RS treatment. Our results suggested that RS not only possess significant hypoglycemic ability but also have remarkable hypolipidemic effect. RS also enhanced serum insulin release in STZ-diabetic rats by 40 days treatment, which was obviously different with the diabetic control rats. We presume that RS appears the hypoglycemic effect in diabetic rats is partly attributed to its stimulation of insulin secretion.
Determination of tissue antioxidative enzyme activitiesThe animals were sacrificed under ether anaesthesia. Their liver and kidney tissues were immediately removed, washed using chilled saline solution, homogenized in 4 volumes of Tris-HCl buffer (pH 7.4). The protein concentrations of the homogenates were determined by the Bradford method using bovine serum albumin as the standard (Bradford et al., 1976). The levels of SOD, MDA, CAT and GSH-px were measured by commercial suggestion of the kits, and the results are shown in Table 3. In STZ-diabetic animals, STZ generates nitric oxide, which is a powerful free radical oxidant (Kwon et al., 1994) resulting in an increase in blood glucose level. Free radicals can diffuse intracellularly and result in mitochondrial enzyme damage and DNA break, impair cellular function and contributes to the pathophysiology of diabetes (Bonnefont-Rousselot et al., 2000).
Several reports have shown the alterations in the antioxidant enzymes during diabetic condition (Preet et al., 2005). The antioxidative defense system like SOD and CAT showed lower activities in liver and kidney during diabetes.
The decreased activities of SOD and CAT may be a response to increased production of H2O2 and O2– by the auto oxidation of excess glucose and non-enzymatic glycation of proteins (Argano et al 1997). Pigeolet et al (1990) have reported the partial inactivation of these enzyme activities by hydroxyl radicals and hydrogen peroxide. The decreased activity of SOD and CAT could also be due to their decreased protein expression levels in the diabetic condition as reported recently in liver (Sindhu et al 2004). GSH is often regarded as antioxidant agents, since they protect protein –SH groups against oxidation and can scavenge oxygen radicals and some other reactive species (Robertson, 2004).
In these reactions, two GSH molecules transform into one molecule of oxidized glutathione (GSSG). In our research, the level of SOD, GSH-px and CAT was increased and the concentration of MDA was decreased after RS treatment, which suggests that RS has effective antioxidative properties and could scavenge well excess free radicals, which may prevent the oxidative damage of the tissues and can increase a protective effect on improving diabetic complications.
It is a rapid, simple, visual and sensitive technique for measuring DNA breakage in individual mammalian cells.Single cell gel electrophoresis (SCGE) experiment was made.
The blood samples were collected from five rats, then lymphocytes were separated from whole blood using a Ficoll Paque lymphocytes separation medium, then suspended in PBS (Collins and Dusinska, 2002). Electrophoresis was conducted at 25 V for 20 min, and then the slides were washed gently to remove alkali and detergents with Tris-buffer, rinsed with dH2O, and stained with ethidium bromide.
Four different cultures were analyses under a fluorescence microscope, the tail lengths of 300 cells per culture evaluated and categorized. In our study, the results showed that RS had not toxic effect to the cultured lymphocytes’ DNA, which were similar with dH2O-treated.
Visual classification of DNA damage, accoding to the relative proportion of DNA in the tail (cells 0-4), obtained by single-cell gel electrophoresis. Antidiabetic and antioxidant effects of oleanolic acid in diabetic ratsOur study evaluates the antidiabetic and antioxidant effects of oleanolic acid (OA) from Ligustrum lucidum Ait in alloxan-induced diabetic rats. The levels of serum TC, TG and low-density lipoprotein cholesterol (LDL-c) of OA-treated diabetic rats were lower, and the high-density lipoprotein cholesterol (HDL-c) level was higher than control diabetic rats. Furthermore, OA treatment decreased MDA level, while increased SOD and GSH-Px activities of the liver and kidney in diabetic rats. These results indicate that OA has the hypoglycemic, hypolipidemic and antioxidant efficacy for the diabetic rats and protects the liver function avoiding alloxan induced damage.
The antioxidant ability of OA might be the main mechanism of hypoglycemic and hypolipidemic effects.
Sample preparation and characterizationThe extraction of Ligustrum lucidum Ait was based on the multi-crystal method (Gao et al., 2007), and the white powder was obtained. The mass spectrometric analysis results were in agreement with the molecular characteristics of OA. Preparation of alloxan-induced diabetic ratsWistar rats weighing 180-200 g were purchased and house as previous condition. Eight rats were randomly picked up as normal control (NC), and the rest were fed on high-fat diet.
After injection 72 h, the fasting blood glucose level of the rats was determined according to glucose oxidase method (Trinder, 1969) using a Glucose Analyzer.
Determination hypolipidemic effect of OAThe rats of DC, DM + OA LD and DM + OA HD groups were fasted overnight with free access to water, blood glucose level of each animal was determined as zero-time blood glucose. The animals of DC group were received 0.5% carboxymethylcellulose (CMC) solution by gavage. Blood samples of all the rats were taken at 0.5, 1, 2, 4 and 6 hour intervals following the administration and blood plasma glucose levels at various time points were measured.
On day 0, 10, 20, 30 and 40, blood samples were collected from a tail vein, following overnight fasting, and measured.The supplement of OA improved the acute blood glucose levels in the rats (Figure 6).
They were consistently staying at similar levels within the time course of 0 to 40 days in NC group and DC group.
Determination of blood lipid parametersOn the day 41, the rats were fasted overnight, and blood samples were collected from eyepit of all rats under ether anaesthesia.

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