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Relevant bibliographies by topics / And metabolically normal obese

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Academic literature on the topic 'And metabolically normal obese'

Author: Grafiati

Published: 5 June 2025

Last updated: 25 June 2025

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Journal articles on the topic "And metabolically normal obese"

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Kelishadi, Roya, Stephen R. Cook, Mohammad Esmaeil Motlagh, et al. "Metabolically Obese Normal Weight and Phenotypically Obese Metabolically Normal Youths: The CASPIAN Study." Journal of the American Dietetic Association 108, no. 1 (2008): 82–90. http://dx.doi.org/10.1016/j.jada.2007.10.013.

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Guerrero-Romero, Fernando. "Metabolically obese normal-weight children." World Journal of Clinical Pediatrics 1, no. 4 (2012): 37. http://dx.doi.org/10.5409/wjcp.v1.i4.37.

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Teixeira, T. F., R. D. Alves, A. P. B. Moreira, and M. d. C. G. Peluzio. "Main characteristics of metabolically obese normal weight and metabolically healthy obese phenotypes." Nutrition Reviews 73, no. 3 (2015): 175–90. http://dx.doi.org/10.1093/nutrit/nuu007.

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Wu, Shenghui, Susan P. Fisher-Hoch, Belinda Reninger, Kristina Vatcheva, and Joseph B. McCormick. "Metabolic Health Has Greater Impact on Diabetes than Simple Overweight/Obesity in Mexican Americans." Journal of Diabetes Research 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/4094876.

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Purpose. To compare the risk for diabetes in each of 4 categories of metabolic health and BMI.Methods. Participants were drawn from the Cameron County Hispanic Cohort, a randomly selected Mexican American cohort in Texas on the US-Mexico border. Subjects were divided into 4 phenotypes according to metabolic health and BMI: metabolically healthy normal weight, metabolically healthy overweight/obese, metabolically unhealthy normal weight, and metabolically unhealthy overweight/obese. Metabolic health was defined as having less than 2 metabolic abnormalities. Overweight/obese status was assessed by BMI higher than 25 kg/m2. Diabetes was defined by the 2010 ADA definition or by being on a diabetic medication.Results. The odds ratio for diabetes risk was 2.25 in the metabolically healthy overweight/obese phenotype (95% CI 1.34, 3.79), 3.78 (1.57, 9.09) in the metabolically unhealthy normal weight phenotype, and 5.39 (3.16, 9.20) in metabolically unhealthy overweight/obese phenotype after adjusting for confounding factors compared with the metabolically healthy normal weight phenotype.Conclusions. Metabolic health had a greater effect on the increased risk for diabetes than overweight/obesity. Greater focus on metabolic health might be a more effective target for prevention and control of diabetes than emphasis on weight loss alone.

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Kaur, Akaal, Desmond G. Johnston, and Ian F. Godsland. "Does metabolic health in overweight and obesity persist? – Individual variation and cardiovascular mortality over two decades." European Journal of Endocrinology 175, no. 2 (2016): 133–43. http://dx.doi.org/10.1530/eje-16-0095.

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Objective Overweight and obese individuals may be metabolically healthy, but attention needs to be given to long-term persistence of this trait and any associated variation in cardiovascular risk. Design Cross-sectional and longitudinal variation in metabolic health and associated cardiovascular mortality were analysed in 1099 white European-origin normal-weight and overweight or obese males followed for 20years. Methods Definitions of metabolic health were based on LDL and HDL cholesterol, triglycerides, blood pressure, fasting glucose and cardiovascular risk. Insulin resistance (e.g. HOMA-IR) and sub-clinical inflammation (ESR and white blood cell count) were explored. Cardiovascular mortality risks and persistence of metabolic health status were evaluated. Results There were 87 cardiovascular deaths. Insulin resistance was increased in metabolically healthy overweight or obese participants (median HOMA-IR 2.63, 95% CI: 1.79–3.65, P<0.001) relative to normal-weight participants (median HOMA-IR 1.67, 95% CI: 1.08–2.67, P<0.001) as was sub-clinical inflammation but metabolically healthy overweight or obese individuals were not at increased risk of cardiovascular mortality compared with the metabolically healthy normal-weight individuals (hazard ratio 1.13, 95% CI: 0.34–3.72, P=0.8). The proportions of initially metabolically healthy overweight or obese who remained metabolically healthy for visits 2, 3 and 4 were 54, 48 and 39% respectively, and for initially normal-weight individuals, 68, 51 and 41%. A lower proportion of metabolically healthy overweight or obese individuals remained metabolically healthy at visit 2 compared with normal-weight individuals (P=0.007), but proportions converged thereafter. Conclusions Despite being insulin resistant and having greater sub-clinical inflammation, and despite instability in metabolic health status, metabolically healthy overweight or obese individuals were at no greater risk of cardiovascular mortality than their normal-weight equivalents.

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Gómez-Zorita, Saioa, Maite Queralt, Maria Angeles Vicente, Marcela González, and María P. Portillo. "Metabolically healthy obesity and metabolically obese normal weight: a review." Journal of Physiology and Biochemistry 77, no. 1 (2021): 175–89. http://dx.doi.org/10.1007/s13105-020-00781-x.

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Naher, Sabikun, M. Mozammel Hoque, and Hasan Imam. "Obesity phenotypes and their adipocyte dysfunction among the attendants at outpatient department." Bangabandhu Sheikh Mujib Medical University Journal 11, no. 2 (2018): 112. http://dx.doi.org/10.3329/bsmmuj.v11i2.36507.

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<p>The present study was aimed to find out the frequency of obesity phenotypes and to correlate adipocyte dysfunction with different obesity phenotypes. A total of 1,507 apparently healthy adults attending the outpatient department were grouped into three based on body mass index which were then further categorized into six groups according to metabolically unhealthy or healthy phenotypes by the presence or absence of metabolic syndrome. Of them, metabolically obese normal weight, overweight, healthy obese and unhealthy obese groups were included as obesity phenotypes. Then by purposive sampling, leptin and adiponectin concentration of 184 subjects with different phenotypes were measured to find out the adipocyte dysfunction. Metabolically obese overweight followed by metabolically unhealthy obese were more prevalent i,e., 24.9% and 19.5%. All obesity phenotypes except metabolically obese normal weight were significantly documented with adipocyte dysfunction (p&lt;0.05).</p>

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Ruderman, N., D. Chisholm, X. Pi-Sunyer, and S. Schneider. "The metabolically obese, normal-weight individual revisited." Diabetes 47, no. 5 (1998): 699–713. http://dx.doi.org/10.2337/diabetes.47.5.699.

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Succurro, Elena, Maria A. Marini, Simona Frontoni, et al. "Insulin Secretion in Metabolically Obese, but Normal Weight, and in Metabolically Healthy but Obese Individuals." Obesity 16, no. 8 (2008): 1881–86. http://dx.doi.org/10.1038/oby.2008.308.

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BEDDAR, Lamia, Abdelmadjid CHAA, and Akila ZENATI. "Prevalence of metabolically obese normal weight population in adolescent." Nutrition & Santé 04, no. 02 (2015): 62–68. http://dx.doi.org/10.30952/ns.4.2.4.

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Dissertations / Theses on the topic "And metabolically normal obese"

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Hayes, Louise. "Why are some obese individuals metabolically normal?" Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445545.

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Hinnouho, Guy-Marino. "Phénotype « obésité à profil cardiométabolique normal » et risque de pathologies chroniques dans les cohortes Whitehall II et GAZEL." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T060/document.

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L’obésité est devenue un véritable problème de santé publique. Elle est fréquemment associée à plusieurs anomalies cardiométaboliques telles que l’hypertension artérielle, l’insulinorésistance et les dyslipidémies qui font le lit du diabète de type 2 et des maladies cardiovasculaires. Cependant la fréquence de ces anomalies varie considérablement parmi les sujets obèses faisant de cette maladie chronique une situation clinique très hétérogène. A ce titre un nouveau concept a émergé, impliquant une population de patients sans facteurs de risque apparents, appelé « obèse métaboliquement sain » ou « metabolically healthy obese » (MHO). Des efforts sont en cours pour comprendre les mécanismes sous-jacents à ce phénotype et ses conséquences à long terme. L’objectif principal de cette thèse était d’étudier le lien entre le phénotype MHO et diverses pathologies chroniques connues pour être associées à l’obésité. Les données provenant des cohortes Whitehall II et GAZEL ont été utilisées pour examiner les associations entre le phénotype MHO et la mortalité, les maladies cardiovasculaires, le diabète de type 2 et la dépression. En comparaison aux sujets de poids normal métaboliquement sains, les individus MHO ont un risque accru de mortalité globale et cardiovasculaire, de diabète de type 2 et de maladies cardiovasculaires mais pas de dépression. Comparés aux sujets obèses avec anomalies métaboliques, les individus MHO ont un risque similaire de mortalité et de maladies cardiovasculaires, mais un moindre risque de diabète de type 2 et dépression. Nos résultats suggèrent que l’obésité à profil cardiométabolique normal n’est pas une condition bénigne. Une meilleure compréhension de ce phénotype contribuera à améliorer la décision thérapeutique et aidera peut-être à identifier des cibles thérapeutiques nouvelles<br>Obesity has become a major public health concern. It is frequently associated with several cardiometabolic abnormalities such as hypertension, insulin resistance and dyslipidemia leading to type 2 diabetes and cardiovascular disease. However, the frequency of these abnormalities varies widely among obese subjects, making this chronic condition a very heterogeneous clinical situation. As such a new concept has emerged, involving a population of patients without metabolic risk, called "metabolically healthy obese" (MHO). Intense interest surrounds the MHO phenotype with on-going efforts to understand the mechanisms underlying this phenotype and its long-term consequences. The main objective of this thesis was to study the relationship between the MHO phenotype and various chronic diseases known to be associated with obesity. Data from the Whitehall II and GAZEL cohorts were used to examine associations between this phenotype and mortality, cardiovascular diseases, type 2 diabetes, and depression. Compared to metabolically healthy normal weight subjects, MHO individuals have an increased risk of overall and cardiovascular mortality, type 2 diabetes and cardiovascular diseases, but not depression. Compared to metabolically unhealthy obese subjects, MHO individuals have a similar risk of mortality and cardiovascular disease, but a lower risk of type 2 diabetes, and depression. Our results suggest that obesity with normal cardiometabolic profile is not a benign condition. A better understanding of this phenotype will enhance therapeutic decision making and possibly help to identify new therapeutic targets

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Earl, Nathan R. "Microvascular Function in Metabolically Healthy Groups Differing in BMI and Waist Circumference." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4337.

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BACKGROUND: Microvascular dysfunction (MD: impaired performance of blood flow, tissue perfusion, blood pressure, etc.) is one of the earliest stages in the progression of various chronic diseases. OBJECTIVE: The aim of this study was to determine if a difference in microvascular function existed between two metabolically healthy groups that differed in BMI and waist circumference. DESIGN: This study employed a causal comparative design, with two groups: I) normal weight (n =14, BMI 28 kg/m2). METHODS: Microvascular function was assessed by measuring skin blood flow (SkBF) using laser Doppler flowmetry during postocclusive reactive hyperemia (PORH). The area under the SkBF time curve during the 60-second PORH response was used to quantify the magnitude of the microvascular response. RESULTS: Group I (control) had a significantly higher average area under the SkBF time curve (3240 ± 879) than Group II (1948 ± 808) (Z= -3.0094, p = 0.0026). CONCLUSIONS: The overweight/obese subjects exhibited a diminished skin blood flow response to occlusion compared to their normal-weight counterparts. This supports the hypothesis that overweight/obese subjects who are otherwise metabolically healthy exhibit a biological change that is linked to chronic disease.

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莊硯琦 and Yin-kei Doris Chong. "Anaerobic recovery and physical activity in normal and obese children." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31257173.

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Chong, Yin-kei Doris. "Anaerobic recovery and physical activity in normal and obese children /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23435872.

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BIGIONI, MARIO. "Ruolo dei polimorfismi genetici nella definizione della sindrome Normal-weight obese." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/845.

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Come hanno rivelato numerosi studi, l’espressione, la produzione e il rilascio di un gran numero di citochine proinfiammatorie è aumentata nel tessuto adiposo dei soggetti obesi. Recentemente è stata identificata una nuova sindrome, denominata sindrome Normal Weight Obese (NWO) caratterizzata da peso ed indici antropometrici normali, ma da un’aumentata massa grassa >30%. I soggetti NWO pur non manifestando alterazioni metaboliche conclamate, rappresentano un sottogruppo dal profilo “vulnerabile”, che le rende suscettibili di sviluppare le complicanze tipiche dell’obesità. Gli obiettivi di questo studio sono stati sostanzialmente due: a) lo studio dell’associazione tra il fenotipo NWO e alcuni polimorfismi a carico di citochine proinfiammatorie; b) individuare eventuali markers genetici di rischio nei soggetti NWO. In una popolazione selezionata di soggetti caratterizzati da questa sindrome sono stati considerati i seguenti polimorfismi: il polimorfismo del gene del recettore per Interleuchina-1; il polimorfismo -174G/C a livello del promotore genico di Interleuchina-6; il polimorfismo del gene del recettore alpha di Interleuchina-15. I risultati ottenuti suggeriscono la natura multifattoriale della sindrome NWO e indicano che i soggetti affetti, presentano un profilo in termini di citochine infiammatorie che fa presupporre uno stato infiammatorio alterato. Inoltre sono stati individuati markers precoci di malattia utilizzabili al fine di evitare l’instaurarsi della sindrome o almeno di ritardarne la comparsa e progressione.<br>In obese subjects, the adipose mass may represents an important source of proinflammatory cytokines. Recently it was identified a new syndrome - the normal-weight obese (NWO) syndrome – in subjects with normal weight and body mass index but whose fat mass is >30% of their total body weight and whose risk of developing obesity-related diseases is likely increased. Main objectives of the present study were: a) to tested the hypothesis that the polymorphism in a panel of three selected cytokines might be associated with NWO syndrome; b) to identified a risk genetic marker of the syndrome. The polymorphism of intron 2 in the interleukin-1 receptor antagonist gene, -174G/C IL-6 promoter gene polymorphism and polymorphisms of IL-15Rα receptor gene were evaluated in a selected population affected by NWO syndrome. As a whole our results indicated that the NWO syndrome is a multifactorial desease, and suggest that the study of proinflammatory cytokines could be regarded as significant indicators of the risk of obesity, CVD, and the metabolic syndrome in NWO subject. In particular the study of their polymorphism permitted to identified, time in advance, “vulnerable” individuals at risk of age and obesity related diseases.

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Siegfried, Lisa A. "Attentional and Approach Biases for Food Cues in Normal Weight, Overweight, and Obese Individuals." Marietta College / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=marietta1272660402.

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Kerrigan, Angela Mary. "Care of obese women during labour : the development of a midwifery intervention to promote normal birth." Thesis, University of Stirling, 2017. http://hdl.handle.net/1893/27479.

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Normal birth, defined as birth without induction of labour, anaesthetic, instruments or caesarean section conveys significant maternal and neonatal benefits. Currently one-fifth of women in the United Kingdom are obese. There is increasing evidence of the detrimental effects obesity has on intrapartum outcomes. There is a lack of research on how to minimise the associated risks of obesity through non-medicalised interventions and how to support obese women to maximise their opportunity for normal birth. This thesis aims to provide evidence to address this gap and develop an evidence-based intervention to promote normal birth. Using a methodological approach aligned with pragmatism, this research was conducted in four parts and underpinned by the Medical Research Council framework for the development of complex interventions. Part one was a national survey involving 24 maternity units. Part two was a qualitative study of the experiences of 24 health professionals and part three involved 8 obese women. The final part was a multi-disciplinary workshop that used consensus decision-making to design the intervention. Collectively, the findings suggest that intrapartum care of obese women is medicalised. Health professionals face challenges when caring for obese women but many strive to optimise the potential for normal birth by challenging practice and utilising ‘interventions’ to promote normality. The findings also demonstrate that obese women have an intrinsic fear of pregnancy and birth, have a desire for normal birth and ‘obese pregnancy’ presents a window of opportunity for change. The intervention consists of three component parts; an educational aspect (e-learning package), a clinical aspect (intrapartum care pathway) and a leadership aspect (ward champions). Whilst acknowledging the importance of safety, increasing intervention during labour for obese women may further increase the risk of complications, with detrimental effects. Addressing intrapartum management of obese women through non-medicalised interventions is of paramount importance in order to promote normality, maximise the opportunity for normal birth and reduce the associated morbidities.

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Romney, Lora Light. "The Relationship between Sleep Deprivation, Food Motivation, and Energy Intake in Normal-Weight and Obese Females." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/8823.

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Objective: Sleep deprivation has been proposed as a potential correlate of obesity, particularly influencing energy intake. Therefore, the purpose of this study was to compare neural indices of attention related to food motivation and energy intake in normal-weight and obese women under two separate sleep conditions: 1) sleep-restricted (<5 hours) and 2) recommended sleep (~8 hours). This study used a combined cross-over and ex post facto design with condition order counter-balanced. Methods: Twenty-two normal-weight (age=30.9±9.5y, BMI=22.0±1.6 kg/m2) and 18 obese (age=29.7±10.7 y, BMI=36.4±5.3 kg/m2) women completed both sleep conditions. To confirm sleep levels, participants recorded sleep quality and quantity via sleep logs and wore a wrist actigraph. Following each condition, participants reported to the laboratory under the same fed state (energy shake ~10% of total daily needs) to verify they followed the sleep protocol. Subsequently, motivation for food was tested using electroencephalogram (EEG); participants completed a computerized passive-viewing task of food and flowers, while event-related brain potentials (ERPs) were recorded. After EEG testing, participants continued their normal routine but recorded all energy intake using weighed food scales. There were no instructions or limitations on dietary intake. Analyses included P300 and LPP amplitudes in response to picture type, total next day energy intake, and energy intake by several periods of the day. Results: Participants averaged 4.7±0.4 hours of sleep during the sleep-restricted condition and 7.7±0.3 hours during the recommended sleep condition (F=1057.02; P<0.0001). There was no group*condition interaction for next day food motivation (P300: F<2.896, P>0.09; LPP: F<2.967, P>0.093). Next day total energy intake also did not differ by group*condition (F=1.81; P=0.187). When participants were pooled, there was no difference in energy intake by sleep condition (F=0.00; P=0.953). However, when participants’ energy intake was analyzed during the lunch period (following testing to 1:30pm) there was a significant group*condition interaction (F=6.12; P=0.018). The obese women ate significantly more (~300 kcal) during the sleep-deprived condition compared to the recommended condition, whereas the normal-weight women did not. Conclusion: Compared to suggested levels of sleep, sleep restriction and obesity do not influence next day food motivation or total next day energy intake. However, sleep restriction and obesity may influence feeding during certain portions of the day.

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Petro, Carrie A. "Eye Tracking Food Cues in Subjects who are Overweight/Obese, Weight Loss Maintainers, and Normal Weight." DigitalCommons@CalPoly, 2016. https://digitalcommons.calpoly.edu/theses/1698.

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Adult obesity is associated with increased morbidity and mortality. Increasing success in weight loss maintenance will decrease the prevalence of overweight and obesity, and therefore help control the adverse health effects of excess weight. Much is known about the behavioral characteristics of successful long-term weight loss maintenance, but less is known about the cognitive processes behind weight loss maintenance. The purposes of this study were to (1) identify differences in visual attention to high-energy dense foods between individuals who are normal weight, weight loss maintainers, and overweight/obese in a high-risk (food-buffet) situation; (2) to evaluate differences in food choices from a food buffet between weight status groups; (3) to analyze correlations between food attention and food choice across weight status groups. No significant differences were found between groups with respect to food attention or food choice. Overall, findings from this study may have been limited by methodology, technology, and sample size. Future research is needed to better understand the interaction of cognitive processes and weight loss maintenance.

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Books on the topic "And metabolically normal obese"

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Corbett, Lauren. Secretory immunity in overweight and obese versus normal-weight early-and late-pubertal females. Brock University, Faculty of Applied Health Sciences, 2008.

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Haroun, Dalia. Fat-free mass hydration values differ between obese and normal children matched for age and sex. University of Surrey Roehampton, 2003.

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Weinbroum, Avi A. Peri-Hospital Advantageousness of Ketamine for All Individuals : : OBESE AND NORMAL-WEIGHT PATIENTS, ADULTS AND CHILDREN. GlobeEdit, 2019.

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The effect of exercise intensity on excess post-exercise oxygen consumption (EPOC) in normal fat and obese women. 1993.

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The effect of exercise intensity on excess post-exercise oxygen consumption (EPOC) in normal fat and obese women. 1993.

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The effect of exercise intensity on excess post-exercise oxygen consumption (EPOC) in normal fat and obese women. 1993.

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Diabetes Code for People with Normal Weight: The Complete Guide to Prevent and Reverse Diabetes Naturally for the Underweight, Slim, and People Who Are Not Obese. Independently Published, 2022.

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Wordsworth, B. P. Skeletal dysplasias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0150.

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Bone is metabolically active throughout life and metabolic disturbances may have wide-ranging consequences that are not restricted to altering its mechanics. The study of some genetic bone diseases has already provided remarkable insights into the normal regulation of bone metabolism. Skeletal dysplasias are developmental disorders of the chondro-osseous tissues commonly resulting in short stature, which is often disproportionate. The underlying mutations are often in the structural genes encoding components of the matrix but may also involve growth factors or cell signalling. In contrast, the dysostoses tend to affect single bones or groups of bones, reflecting the transient nature of the many different signalling factors to which they are responsive during development. Abnormalities of bone density (high or low) may be due to primary deficiency of bone matrix synthesis (e.g. osteogenesis imperfecta and hypophosphatasia) but may also reflect an imbalance between bone formation and resorption. This may be caused by abnormalities of bone formation (e.g. hyperostosis/sclerosteosis and osteoporosis pseudoglioma syndrome) or bone resorption (e.g. classic osteopetrosis and fibrous dysplasia).

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Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.

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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.

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Lal, Mira. Women’s psychosomatic health promotion and the biopsychosociocultural nexus. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749547.003.0008.

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Chapter 8 discusses the promotion of women's psychosomatic health by prevention or early treatment of cancer and obesity. Health providers have to consider the biological, psychological, social, and cultural factors that alter psychosomatic interactions to generate these health conditions. Primary/secondary prevention need more emphasis than tertiary prevention or treatment. The transition of normal cervical epithelium to cervical-intraepithelial neoplasia (CIN), and the progression of CIN 2/3 to cancer is preventable. Two-thirds of patients with CIN have HPV infection. Cervical screening allows astute clinical decision-making as CIN could revert back to normal epithelium. Colposcopically-directed early treatment of CIN 2/3 is a secondary preventive measure. Cervical screening has reduced cervical cancer in the West but organised screening is unavailable in low-middle income countries where cervical cancer is common. Sociocultural practices promote unsafe sex, such as when minors in these countries acquire HPV infection through marriage to an older infected male or when women/adolescents are war victims. Inebriated party-goers may acquire HPV infection through unsafe sex. HPV vaccines protect against 70% of carcinogenic HPV strains only. Serious adverse effects after vaccination are uncommon. Barrier contraception prevents HPV, and other sexually transmitted diseases. Obesity increases the risk of endometrial cancer. Type-1 endometrial cancer relates to obesity and starts at a younger age, unlike type-2. Obesity also affects fertility. Transgenerational changes in the fetus of the obese gravida can promote obese offspring. Bariatric surgery for obesity is however expensive, with a potential for complications. WHO directives thus advise on prevention of obesity, and the overweight habitus. Primary prevention of obesity through lifestyle changes should start in childhood.

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Book chapters on the topic "And metabolically normal obese"

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Ronshaugen, Natalie, and Kody Moffatt. "Case of an Obese Adolescent with Back Pain: Studies Normal." In Back Pain in the Young Child and Adolescent. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50758-9_29.

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Mazlan, M. H., N. A. Abu Osman, and W. A. B. Wan Abas. "Hip 3D Joint Mechanics Analysis of Normal and Obese Individuals’ Gait." In IFMBE Proceedings. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21729-6_43.

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Alger, Sharon A., Michael J. Schwalberg, Jean M. Bigaouette, Lyn J. Howard, and Larry D. Reid. "Using Drugs to Manage Binge-Eating Among Obese and Normal Weight Patients." In Opioids, Bulimia, and Alcohol Abuse & Alcoholism. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4613-9000-8_8.

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Ondrak, Kristin S., and Anthony C. Hackney. "Body Composition Differences in Normal Weight, Obese-Overweight and Anorexic Adolescents: Role of Adipocytokines." In Cytokines, Growth Mediators and Physical Activity in Children during Puberty. KARGER, 2010. http://dx.doi.org/10.1159/000321970.

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Vettor, Roberto, Claudio Pagano, Marco Rossato, and Giovanni Federspil. "Cardiac and Vascular Effects of Adipocytokines in Normal and Obese Individuals: The Concept of Cardiometabolic Risk." In Nutritional and Metabolic Bases of Cardiovascular Disease. Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444318456.ch12.

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Le, Jennifer. "Do I Dose Medications the Same for an Obese Child as for a Normal Weight Child?" In Curbside Consultation in Pediatric Obesity. CRC Press, 2024. http://dx.doi.org/10.1201/9781003523666-47.

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Loche, Sandro, Paola Cambiaso, Maria Rosaria Casini, et al. "Effects of Hexarelin on Growth Hormone Secretion in Short Normal Children, in Obese Children, and in Subjects with Growth Hormone Deficiency." In Growth Hormone Secretagogues. Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2396-2_22.

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Tejaswi, Sooraj. "A 38-Year-Old Mildly Obese Female Presented With Gerd Symptoms And Was Found To Have A Persistently Elevated Amylase Level Around 250 Iu/L (Normal < 125) But Normal Lipase. How Should I Manage This Patient?" In Curbside Consultation in Endoscopy, 2nd ed. CRC Press, 2024. http://dx.doi.org/10.1201/9781003523505-13.

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Makkar, Brij, Manisha Taneja, and Mohd Furqan. "Metabolically Healthy Obese: A Myth or Reality?" In RSSDI Diabetes Update 2016. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13026_67.

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Neligan, Patrick J. "Metabolic syndrome." In Oxford Textbook of Anaesthesia for the Obese Patient, edited by Ashish C. Sinha. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198757146.003.0008.

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Abstract:

Obesity is a metabolic disease that arises from excessive energy consumption. The development of non-alcoholic fatty liver disease appears to be an early indicator of escalating endocrine and metabolic dysfunction. Fatty liver results in insulin resistance. This is a precursor to type 2 diabetes, metabolic syndrome, steatohepatitis, and cirrhosis. Obesity increases the risk for cardiovascular, cerebrovascular, and neoplastic disease. This probably results from a combination of dyslipidaemia, dysregulation of glycaemic control, and ongoing inflammation associated with adipocytokines. Central obesity, characterized by a large reservoir of metabolically active visceral fat, closely correlates with cardiovascular risk, and is the key component of a constellation of symptoms known as the metabolic syndrome. There is little or no epidemiological data available regarding the diagnosis of metabolic syndrome and perioperative risk. No guidelines are available. Risk reduction associated with modulation of the specific components of this syndrome, cardiovascular disease, dyslipidaemia, and hyperglycaemia, are currently in a state of flux.

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Conference papers on the topic "And metabolically normal obese"

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Kandori, Ayumu, Masato Takahashi, Chawan Koopipat, and Norimichi Tsumura. "Proteus effect in vertical jumping wearing a head-mounted display." In 3D Image Acquisition and Display: Technology, Perception and Applications. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/3d.2024.jth2a.10.

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Bai, Chuanmin, Rong Huang, Juan Zhao, Glen M. Borchert, Jingshan Huang, and Bin Wu. "Differential Expression of Adipocyte Transcripts in SAT and VAT between Normal Weight and Obese/Overweight Individuals." In 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10822168.

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Aljaber, Mashael Jamal, Nelson Orie, Mohamed Elrayess, et al. "Comparison of Cardiometabolic Risk Factors in Metabolically Healthy and Pathologically Obese Arabs and Caucasians." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2662.

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CHI, LUQI, Christopher Kim, Nicholas Jackson, Greg Maislin, and Richard Schwab. "Comparison Of Upper Airway Anatomic Structures Between Obese Normal Subjects And Obese Apneic Subjects." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3670.

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Almuraikhy, Shamma Abdulla, Mohamed Elrayess, and Wael Kafienah. "Combined metformin and insulin treatment reverses metabolically impaired omental adipogenesis and accumulation of 4hydroxynonenal in obese diabetic patients." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2018. http://dx.doi.org/10.5339/qfarc.2018.hbpd960.

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Gemicioglu, Bilun, Benan Musellim, Berk Degirmenci, et al. "Clinical differences of normal weight, over weight and obese asthma patients." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2716.

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Chen, Richard, Daniel Nemeth, Jason Mora, Mohan Muvvala, Derek Wu, and Yuri Griko. "Changes in Differential Expression of Genes in Normal and Metabolically Suppressed Mice in Response to Radiation." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513624.

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Huang, Jingtao, Swaroop J. Pinto, Eliot S. Katz, et al. "Upper Airway Collapsibility And Genioglossus Activity In Obese Adolescents With OSAS And Obese And Normal Weight Controls During Sleep." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5390.

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Manoliu, Vasile, and Cristina Maria Stanescu. "Assessment of the ventricular-arterial coupling in obese patients with normal ejection fraction." In 2013 8th International Symposium on Advanced Topics in Electrical Engineering (ATEE). IEEE, 2013. http://dx.doi.org/10.1109/atee.2013.6563432.

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Yi, Jae-Sik, Ji Hun Han, Min Jeong Kim, and Youn-Sik Hong. "Distinguish Between Obese and Normal Body Types Through Gait Analysis Using Classification Models." In 2024 International Conference on Artificial Intelligence in Information and Communication (ICAIIC). IEEE, 2024. http://dx.doi.org/10.1109/icaiic60209.2024.10463491.

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