Obesity and Cardiovascular Disease Risk Factors among the Indigenous and Immigrant Pakistani Population: A Systematic Review

AimThe aim of this study was to systematically describe the gender and ethnic differences regarding the prevalence of general/central obesity and cardiovascular disease (CVD) risk factors such as diabetes mellitus type 2, hypertension, and hypercholesterolemia among the indigenous and immigrant Pakistani communities.MethodsThe search engine used was PubMed, supplemented with regional data from the Medical Institutes of Pakistan. The focus was on the adult Pakistani population (18 years and older).ResultsWe found only 7 studies among the immigrant Pakistani community and 24 studies among the indigenous Pakistani community. The studies had limitations such as low participation rates and use of self-reported data. There is a higher prevalence of central obesity among women (42.2%) than among men (14.7%) (National Health Survey of Pakistan). Certain ethnicities such as Muhajir and Baluchis showed a higher prevalence of cardiovascular risk factors when compared to other ethnicities in the indigenous Pakistani population. The results also indicate that the prevalence of obesity is 10-20% higher among the immigrant Pakistanis than in the indigenous Pakistanis.ConclusionThe relatively high prevalence of obesity and associated CVD risk factors (especially in women) among both indigenous and immigrant Pakistani populations require the attention of the healthcare professionals and policy makers, both inside and outside Pakistan.Key Words: Cardiovascular diseases, Obesity, Diabetes, Hypertension, Hypercholesterolemia, Pakistanis     

Outcomes of group-based treatment program with parental involvement for the management of childhood and adolescent obesity

Objective

An uncontrolled study was conducted to evaluate the effects of a group-based program on weight control, metabolic profiles, and obesity-related complications in obese youth.

Methods

The program consisted of an initial in-patient session and five group sessions, one, two, three, six, and nine months into the study, providing participants and their parents with information about the consequences of obesity and lifestyle modifications. The severity of obesity and obesity-related complications were evaluated at baseline and 12 months after the intervention. The participants’ and their parents’ perceptions of the program were assessed.

Results

Of the obese youth recruited (n = 126), 115 completed the study. Their percentage weight for height and percentage body fat decreased significantly (both p < 0.001), and their insulin resistance, lipid profiles, and transaminases levels improved (all p < 0.01). The prevalence of prediabetes, dyslipidemia, and elevated transaminases decreased significantly (all p < 0.05). The participants and their parents perceived the program as valuable.

Conclusion

A group-based program is effective in managing childhood obesity, improving metabolic profiles, and alleviating certain obesity-related complications.

Practice implications

A group-based program that provides education and raises the awareness of obese children and their parents about the consequences of obesity is an effective model for treating childhood obesity.     

COVID-19 and Obesity: Overlapping of Two Pandemics

BackgroundThe coronavirus disease 2019 (COVID-19) pandemic has recently led to worldwide research efforts to identify subjects at greater risk of developing more severe illness: overall obesity displayed a strong correlation with critical illness and major severity of COVID-19 manifestations.SummaryObesity and metabolic disorders are closely linked to chronic systemic inflammation. The adipose tissue constitutes a source of cytokines, which configure a low-grade inflammation and a hypercoagulation status; in addition, diagnosis and care of obese patients are often complicated by excess weight and ventilation difficulties.Key MessagesThis review aims to examine the intersection between obesity and adverse outcomes of COVID-19, in order to investigate its preventive and/or therapeutic potential in the management of obesity-related COVID-19 complications.     

Obesity and aging: Molecular mechanisms and therapeutic approaches

The epidemic of obesity is a major challenge for health policymakers due to its far-reaching effects on population health and potentially overwhelming financial burden on healthcare systems. Obesity is associated with an increased risk of developing acute and chronic diseases, including hypertension, stroke, myocardial infarction, cardiovascular disease, diabetes, and cancer. Interestingly, the metabolic dysregulation associated with obesity is similar to that observed in normal aging, and substantial evidence suggests the potential of obesity to accelerate aging. Therefore, understanding the mechanism of fat tissue dysfunction in obesity could provide insights into the processes that contribute to the metabolic dysfunction associated with the aging process.Here, we review the molecular and cellular mechanisms underlying both obesity and aging, and how obesity and aging can predispose individuals to chronic health complications. The potential of lifestyle and pharmacological interventions to counter obesity and obesity-related pathologies, as well as aging, is also addressed.     

Obesity Status on associations between cancer-related beliefs and health behaviors in cancer survivors: Implications for patient-clinician communication

ObjectiveAssociations between cancer beliefs and health behavior engagement are largely unexplored in cancer survivors, particularly among those with overweight and obesity. We investigated belief-behavior associations for cancer survivors, and whether obesity altered these associations.MethodsCancer survivors were identified from the National Cancer Institute HINTS Survey 5 data and classified as having had an obesity-related cancer or not. Linear and multiple logistic regression analyses examined whether cancer risk beliefs and self-efficacy predicted dining out behaviors and physical activity (PA). Restricted analyses were conducted in those with overweight or obesity.ResultsLow self-efficacy to take care of one’s health was associated with longer sitting time in the overall sample (p = 0.04). In cancer survivors with overweight or obesity, engagement in healthier behaviors was associated with 1) feeling less overwhelmed by cancer risk recommendations and 2) believing that PA or obesity influences cancer development (both p < 0.05). Among those with overweight and obesity, associations between cancer beliefs and health behaviors were not significantly different by cancer type (obesity-related vs. not).ConclusionsObesity altered associations between cancer risk beliefs and health behavior engagement from the overall sample.Practice ImplicationsWeight status may be a useful tailoring factor when delivering health-promoting interventions for cancer survivors.     

Obesity: genetic, molecular, and environmental aspects

Obesity has emerged as one of the most serious public health concerns in the 21st century. Obese children tend to become obese adults. The dramatic rise in pediatric obesity closely parallels the rapid increase in the prevalence of adult obesity. As overweight children become adults they face the multitude of health problems associated with obesity at younger ages. The morbidity and mortality associated with obesity continue to increase. Obesity is one of the leading causes of preventable death. Complications of obesity include cardiovascular risks, hypertension, dyslipidemia, endothelial dysfunction, type 2 diabetes mellitus and impaired glucose tolerance, acanthosis nigricans, hepatic steatosis, premature puberty, hypogonadism and polycystic ovary syndrome, obstructive sleep disorder, orthopedic complications, cholelithiasis and pseudotumor cerebri. Genetic and molecular and environmental factors play an important role in the assessment and management of obesity.     

Hyperinsulinaemia, a key factor of the metabolic syndrome in postmenopausal women

The metabolic syndrome (MetS) is a complex disorder combining obesity, hypertension, atherogenic dyslipidaemia and insulin resistance, a clustering of factors which markedly enhance the risk of developing cardiovascular disease (CVD) and type 2 diabetes. Main features of the MetS, which are found in many postmenopausal women, are increasing prevalence of insulin resistance and obesity (particularly visceral adiposity). Accordingly, a majority of postmenopausal women comply with criteria defining the MetS, and CVD is the first cause of morbidity/mortality in women, occurring even more frequently than in men. Moreover, obesity-related type 2 diabetes approaches pandemic proportions. Simultaneous occurrence of insulin resistance and obesity are most detrimental for metabolic health, and are also associated with increased oxidative stress, inflammatory and prothrombotic processes as well as with postmenopausal alterations in adipocytokine production. Hormone replacement therapy, provided the selected progestin does not antagonize estrogen action, may improve fat mass and distribution, dyslipidaemia and insulin sensitivity in postmenopausal women.     

Familial Non-Medullary Thyroid Carcinoma: An Update

Familial thyroid cancer can arise from follicular cells (familial non-medullary thyroid carcinoma (FNMTC)) or from the calcitonin-producing C-cell (familial medullary thyroid carcinoma). This is usually a component of multiple endocrine neoplasias (MEN) IIA or IIB, or as pure familial medullary thyroid carcinoma syndrome. The genetic events in the familial C-cell-derived tumors are known and genotype–phenotype correlations are well established. In contrast, the case for a familial predisposition of non-medullary thyroid carcinoma is only now beginning to emerge. Although the majority of papillary (PTC) and follicular thyroid carcinomas (FTC) are sporadic, familial tumors account for over 5% of cases. The presence of multifocal papillary carcinoma is a common feature of FNMTC. The familial follicular cell-derived tumors or non-medullary thyroid carcinomas encompass a heterogeneous group of diseases, including diverse syndromic-associated tumors and non-syndromic tumors. Based on clinico-pathologic findings, FNMTC is divided into two groups. The first includes familial syndromes characterized by a predominance of non-thyroidal tumors, such as familial adenomatous polyposis (FAP), PTEN hamartoma tumor syndrome (PHTS), Carney complex type 1, and Werner syndrome. The second group includes familial syndromes characterized by a predominance of NMTC, such as pure familial (f) PTC with or without oxyphilia, fPTC with papillary renal cell carcinoma, and fPTC with multinodular goiter. Some characteristic morphologic findings should alert the pathologist of a possible familial cancer syndrome, which may lead to further molecular genetic evaluation.     

Novel risk factors for cardiovascular disease in rheumatoid arthritis

Since cardiovascular disease (CVD) is the most common cause of mortality in patients with rheumatoid arthritis (RA), we aimed to determine factors associated with such a complication in a large series of Colombian patients. This was a cross-sectional analytical study in which 800 consecutive Colombian patients with RA were assessed for variables associated with CVD. Furthermore, a systematic literature review was performed to address the state of the art about non-traditional risk factors for CVD in RA. The preferred reporting items for systematic reviews and meta-analyses guidelines were followed in data extraction, analysis, and reporting of articles selected. Hypercholesterolemia, type 2 diabetes mellitus, abnormal body mass index, abdominal obesity, and current smoking were all traditional risk factors significantly associated with CVD in Colombians. As non-traditional risk factors, familial autoimmunity, more than 10 years of duration of the disease, patients working on household duties, use of systemic steroids, and low education level were associated with CVD in the studied population. Out of a total of 9,812 articles identified in PubMed and Scopus databases, 140 fulfilled the eligibility criteria and were included. Through this systematic review, several factors and outcomes related to CVD were confirmed and identified. These were categorized into genetics, RA-related, and others. Traditional risk factors do not completely explain the high rates of CVD in patients with RA; thus, novel risk factors related to autoimmunity are now recognized predicting the presence of CVD as strong as traditional risk factors. Our results may assist health professionals and policymakers in making decisions about CVD in patients with RA.     

Epidemiological Influences and Requirements of Global Childhood Obesity Research

IntroductionObesity is classified as a global epidemic and judged to be the greatest public health threat in Western countries. The tremendously increasing prevalence rates in children lead to morbidity and mortality in adults. In many countries, prevalence has doubled since the 1980s. Other countries show a continuous increase or stagnate at a very high level. Given these regional differences, this study aims to draw a global world map of childhood obesity research, including regional epidemiological characteristics, to comprehensively assess research influences and needs.MethodsIn addition to established bibliometric parameters, this study uses epidemiological data to interpret metadata on childhood obesity research from the Web of Science in combination with state-of-the-art visualization methods, such as density equalizing map projections.ResultsIt was not until the 1990s that belated recognition of the dangerous effects of childhood obesity led to an increase in the number of publications worldwide. In addition, our findings show that countries'' study output does not correlate with epidemiologic rates of childhood obesity. In contrast, the primary driver of the research efforts on childhood obesity appears to be largely driven government funding structures.Discussion/ConclusionThe geographical differences in the epidemiological background of childhood obesity complicate the implementation of transnational research projects and cross-border prevention programs. Effective realization requires a sound scientific basis, which is facilitated by globally valid approaches. Hence, there is a need for information exchange between researchers, policy makers, and private initiatives worldwide.     

Clinical and laboratory assessment of cardiovascular risk in children: Guidelines for screening, evaluation, and treatment

The early lesions of atherosclerosis begin in childhood and are related to antecedent cardiovascular disease (CVD) risk factors. Environmental and genetic factors (eg, diet, obesity, exercise, and certain inherited dyslipidemias) influence progression of such lesions. Identification of youth at risk for atherosclerosis includes an integrated assessment of these predisposing factors. Treatment starts with a diet low in total and saturated fat and cholesterol, use of water-soluble fiber, plant stanols and plant sterols, weight control, and exercise. Drug therapy, for example, with inhibitors of hydroxymethylglutaryl-CoA reductase, bile acid sequestrants, and cholesterol absorption inhibitors, can be considered in those with a positive family history of premature CVD and low-density lipoprotein cholesterol >160 mg/dL after dietary and hygienic measures. Candidates for drug therapy often include those with familial hypercholesterolemia, familial combined hyperlipidemia, the metabolic syndrome, polycystic ovarian syndrome, type 1 diabetes, and the nephrotic syndrome. Such dietary and drug therapy appears safe and efficacious. Early identification and treatment of youth with CVD risk factors and dyslipidemia are likely to retard the atherosclerotic process. Optimal detection and treatment of high-risk children either from the general population or from families with premature CVD will require a comprehensive universal screening and evaluation program.     

Gene discovery in familial cancer syndromes by exome sequencing: prospects for the elucidation of familial colorectal cancer type X

Recent advances in genotyping and sequencing technologies have provided powerful tools with which to explore the genetic basis of both Mendelian (monogenic) and sporadic (polygenic) diseases. Several hundred genome-wide association studies have so far been performed to explore the genetics of various polygenic or complex diseases including those cancers with a genetic predisposition. Exome sequencing has also proven very successful in elucidating the etiology of a range of hitherto poorly understood Mendelian disorders caused by high-penetrance mutations. Despite such progress, the genetic etiology of several familial cancers, such as familial colorectal cancer type X, has remained elusive. Familial colorectal cancer type X and Lynch syndrome are similar in terms of their fulfilling certain clinical criteria, but the former group is not characterized by germline mutations in DNA mismatch-repair genes. On the other hand, the genetics of sporadic colorectal cancer have been investigated by genome-wide association studies, leading to the identification of multiple new susceptibility loci. In addition, there is increasing evidence to suggest that familial and sporadic cancers exhibit similarities in terms of their genetic etiologies. In this review, we have summarized our current knowledge of familial colorectal cancer type X, discussed current approaches to probing its genetic etiology through the application of new sequencing technologies and the recruitment of the results of colorectal cancer genome-wide association studies, and explore the challenges that remain to be overcome given the uncertainty of the current genetic model (ie, monogenic vs polygenic) of familial colorectal cancer type X.     

Newly identified set of obesity-related genotypes and abdominal fat influence the risk of insulin resistance in a Korean population

We aimed to identify obesity-related single-nucleotide polymorphism (SNP) loci in a Korean population and construct an obesity genetic risk score (GRS) to examine the association of the genetic predisposition to obesity with insulin resistance (IR). In total, 9675 subjects were included, and 7666 of these subjects were used for replication. A GRS was constructed using the SNP loci that overlapped in both cohort sets. The subjects showed a trend toward an increase in body mass index, waist circumference, systolic/diastolic blood pressure, homeostatic model assessment (HOMA)-IR, HOMA-B, and levels of insulin, triglyceride, and alanine aminotransferase across the tertiles of obesity GRS, while the adiponectin level showed a trend toward a decrease with increasing GRS. The associations between the obesity GRS and the measures of fasting insulin, HOMA-IR, and adiponectin were significant after adjusting for confounding factors. Moreover, a significant association between obesity GRS and HOMA-IR was observed in subjects with abdominal obesity. The present results indicate that a predisposition to obesity may affect IR in the Korean population and that abdominal fat may alter or modify the genetic effects. Furthermore, the set of obesity-related genotypes and abdominal fat may play interactive roles in determining the risk of IR.     

The MEN1 gene and associated diseases: An update

Heterozygous germline mutations of the tumor suppressor gene MEN1 are responsible for multiple endocrine neoplasia type 1 (MEN1), a dominantly inherited familial cancer syndrome characterized by the combined occurrence of pituitary, parathyroid, and enteropancreatic tumors. Various types of mutations likely causing loss of the gene function have been identified throughout the entire gene region in patients with MEN1 and related disorders including a small fraction of familial isolated hyperparathyroidism (FIHP). Neither mutation hot spot nor phenotype-genotype correlation has been established in classical MEN1, although some missense mutations may be specifically associated with a phenotype of FIHP. Familial isolated pituitary tumor and atypical familial MEN1 consisting of only pituitary tumor and hyperparathyroidism usually lack germline MEN1 mutations, suggesting that these familial endocrine tumor syndromes are genetic entities distinct from MEN1. DNA test for MEN1 germline mutations is a robust tool for diagnosis of predisposition to MEN1, and will be useful for the counseling and management of patients and their families. In this review, we will summarize the most recent findings on the MEN1 gene, focusing primarily on germline mutations and associated diseases.     

Familial partial lipodystrophy: two types of an X linked dominant syndrome, lethal in the hemizygous state.

Familial lipodystrophy (referred to in publications as the Köbberling-Dunnigan syndrome) comprises at least two clinical phenotypes which are consistent within each pedigree. In type 1 familial lipodystrophy, loss of subcutaneous fat is confined to the limbs, sparing the face and trunk. In type 2 familial lipodystrophy, the trunk is also affected with the exception of the vulva, giving an appearance of labial hypertrophy. Diabetes mellitus, hyperlipoproteinaemia, and acanthosis nigricans are present to a variable degree in some but not all patients with familial lipodystrophy, and the abnormal distribution of subcutaneous fat is the essential hallmark of the syndrome. In addition to a survey of published reports, new cases with the syndrome are described. Both types of partial lipodystrophy, occurring either as familial disease or as sporadic cases, have only been observed in female patients. Study of the pedigrees of five families with familial lipodystrophy (two Scottish and three German) suggests an X linked dominant mode of transmission, lethal in the hemizygous (XY) state. The two clinical phenotypes with their variably expressive metabolic abnormalities are consistent either with different mutants of the same allele or with two genes on adjacent loci. Other clinical phenotypes of familial lipodystrophy may exist due to further mutations of the same allele or of genes on adjacent loci. The nature of the disorder in patients with familial lipodystrophy usually escapes recognition for many years and the syndrome is almost certainly much commoner than the few families described to date suggest.     

Identification of novel SDHD mutations in patients with phaeochromocytoma and/or paraganglioma

Familial paraganglioma is a dominantly inherited disorder characterised by the development of highly vascular tumours in the head and neck. Recently, a relationship between hereditary tumours derived from the autonomic nervous system and germline mutations in the gene encoding succinate dehydrogenase complex subunit D (SDHD) is increasingly a subject of study. Familial paraganglioma syndrome is embryologically related to phaeochromocytoma, another neuroendocrine tumour that shows great aetiological and genetic heterogeneity. Some hereditary phaeochromocytomas may be associated with germline mutations in VHL, RET and NF1 genes in genetic disorders such as von Hippel-Lindau disease (VHL), multiple endocrine neoplasia type 2 (MEN 2) and neurofibromatosis type 1 (NF 1), respectively. However, there are many cases that cannot be explained by mutations in these genes. In this report, we describe two previously unreported mutations in two patients from 25 unrelated kindreds with phaeochromocytoma and/or paraganglioma disorders and with or without familial antecedents: a mutation featuring the change of tryptophan to a termination codon in exon 2, and a 4-bp deletion in exon 4 that results in a truncated protein. We also describe one missense substitution of uncertain significance. The patients had previously tested negative for germline mutations in VHL and RET genes and had not been previously selected. The involvement of SDHD mutations in familial phaeochromocytoma and/or paraganglioma predisposition is of considerable interest since other studies have shown these alterations to be associated with highly expressed angiogenic factors.     

Relationship between Sarcopenic Obesity and Cardiovascular Disease Risk as Estimated by the Framingham Risk Score

This study was conducted to assess the association between sarcopenic obesity and cardiovascular disease (CVD) risk in Korean adults (n=3,320; ≥40 yr) who participated in the 5th Korean National Health and Nutrition Examination Survey in 2010. The appendicular skeletal muscle mass divided by body weight was calculated for each participant; participants with values <1 standard deviation below the mean reference value (i.e., aged 20-39 yr) were considered sarcopenic. Subjects were further classified into 4 groups according to their obesity (i.e., body mass index ≥25 kg/m²) and sarcopenic status. Individuals'' 10-yr CVD risk was determined using the Framingham risk model. The sarcopenic obese group had more participants (43.8% men, 14.6% women) with a high risk of CVD (≥20%). The sarcopenic obese group was associated with an increased 10-yr CVD risk than the non-sarcopenic, non-obese group (odds ratio [OR], 2.49; 95% confidence interval [CI], 1.53-4.06, P<0.001 in men; OR, 1.87; 95% CI, 1.02-3.41, P=0.041 in women). Sarcopenic non-obese and non-sarcopenic obese subjects were not associated with an increased 10-yr CVD risk. Sarcopenic obesity, but not non-sarcopenic obesity, was closely associated with an increased CVD risk in Korean adults.

Graphical Abstract

相似文献   

Eating behaviors of children in the context of their family environment

Both a family history of obesity and early childhood obesity have been identified as strong predictors of adult obesity risk. The finding that parental obesity, maternal obesity in particular, increases a child's risk for developing obesity suggests that either shared genes, or environment, or likely a combination of both may promote overeating and excessive weight gain in children. Parents not only create food environments for children's early experiences with food and eating, but they also influence their children's eating by modeling their own eating behaviors, taste preferences, and food choices. Thus, it is important to identify intermediary behavioral eating traits which promote overeating and obesity in children and to determine the extent to which associations between eating traits and excessive weight gain in children may be influenced by genetic factors, environmental factors, or both. Behavioral genetic methods can be used to help partition genetic and environmental sources of variability in behavioral traits. The focus of this paper is to review and discuss findings from both short-term experimental and prospective cohort studies on eating behaviors of children at various stages in their lives. Select child eating traits and parent-child resemblances in eating will be further examined in the context of children's home environment and their familial predisposition to obesity.The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.     

Familial T-cell non-Hodgkin lymphoma caused by biallelic MSH2 mutations

Familial non-Hodgkin lymphoma (NHL) is rare and in most cases, no underlying cause is identifiable. We report homozygous truncating mutations in the mismatch repair gene MSH2 (226C-->T; Q76X) in three siblings who each developed T-cell NHL in early childhood. All three children had hyperpigmented and hypopigmented skin lesions. Constitutional biallelic MSH2 mutations have previously been reported in five individuals, all of whom developed malignancy in childhood. Familial lymphoma has not been reported in this context or in association with biallelic mutations in the other mismatch repair genes MLH1, MSH6 or PMS2. In addition, hypopigmented skin lesions have not previously been reported in biallelic MSH2 carriers. Our findings therefore expand the spectrum of phenotypes associated with biallelic MSH2 mutations and identify a new cause of familial lymphoma. Moreover, the diagnosis has important management implications as it allows the avoidance of chemotherapeutic agents likely to be ineffective and mutagenic in the proband, and the provision of cascade genetic testing and tumour screening for relatives.     

Prevention of cardiovascular disease in diabetes mellitus: by stressing the CARDS study

Recently, diabetes mellitus has become a global epidemic disease. There is a study indicating that type 2 diabetes mellitus (DM) is frequently found in children and teenager. Furthermore, in some countries, it is more frequent than type 1 diabetes mellitus.1 WHO stated that in the year of 2000, there were 177 million diabetes mellitus patient in the world and it is predicted that in the year of 2030, it will be increased to 366 million.2 This is very problematical for some countries such as India, People's Republic of China and Indonesia where the prevention and treatment facilities are still inadequate. To date, Indonesia has occupied the 4th rank, with predicted number of diabetes mellitus patient about 8.4 million and this number will be increased to 21.3 million in the year of 2030. There is no data about the number of patient with metabolic syndrome (MS) and insulin resistance syndrome (IR), but it should be higher than the number of diabetic patient. As we all have known, these conditions are the high-risk condition of diabetes mellitus development.2 One of reasons concerning why prevalence and pre-diabetic condition are increased (including the increased MS) is rising obesity frequency. In the United States, over 60% of recent adult population are overweight, which is defined as "body mass index" (BMI) 25; and about 30% of them have obesity, which is defined as BMI 30%.3 If diabetes mellitus occurred, cardiovascular disease (CVD) including coronary heart disease (CHD) also may occur. It is important to prevent the diabetes mellitus as well as to prevent the complication risk of CVD in diabetic patient.