<p>Fetman i Sverige har under de senaste två decennierna ökat kraftigt. Till följd av detta är hälsokostnaderna relaterat till fetma ansenliga och förväntas öka ytterligare om ingenting görs åt problemet. I denna studie studeras prevention och gastric bypass som alternativa behandlingsmetoder mot fetma sett ur ett samhällsekonomiskt perspektiv. Tre hypotetiska kohorter utvecklas; status quo, effektiv prevention i ungdomsåren samt individer som utvecklar svår fetma opereras med gastric bypass. Dessa kohorter följs under åldern 20-64 år där kostnader och effekter observeras med hjälp av en beslutsträdsmodell. Både gastric bypass och prevention påvisas vara kostnadseffektiva behandlingsmetoder mot fetma. Gastric Bypass visas vara mer effektiv än en studerad befolkningsinriktad preventionsåtgärd. Slutligen påvisas att effektiva högriskpreventioner kan bidra med en högre samhällsnytta än gastric bypass operationer.</p><p> </p><p>Nyckelord: Fetma, Gastric Bypass, Prevention</p><p> </p> / <p>The prevalence of obesity has increased rapidly the past two decades. As a consequence the health expenditures related to obesity are high and are expected to increase if nothing is done.</p><p>The objective of this thesis was to study whether prevention in early years or gastric bypass is the preference from a societal perspective as an intervention to obesity. I develop three hypothetical cohorts; status quo, effective prevention in early years and people whom develop obesity have gastric bypass surgery. The cohorts are followed from age 20 to age 64 where costs and effects are observed using a decision tree model. The results were that both gastric bypass and prevention in early years are found to be cost-effective treatments to obesity. Gastric bypass is found being more effective than a studied population-based prevention. Effective high-risk preventive methods can contribute to a higher benefit to society than a gastric bypass surgery.</p><p> </p><p>Keyword: Obesity, Gastric Bypass, Prevention</p><p> </p>

Fetman i Sverige har under de senaste två decennierna ökat kraftigt. Till följd av detta är hälsokostnaderna relaterat till fetma ansenliga och förväntas öka ytterligare om ingenting görs åt problemet. I denna studie studeras prevention och gastric bypass som alternativa behandlingsmetoder mot fetma sett ur ett samhällsekonomiskt perspektiv. Tre hypotetiska kohorter utvecklas; status quo, effektiv prevention i ungdomsåren samt individer som utvecklar svår fetma opereras med gastric bypass. Dessa kohorter följs under åldern 20-64 år där kostnader och effekter observeras med hjälp av en beslutsträdsmodell. Både gastric bypass och prevention påvisas vara kostnadseffektiva behandlingsmetoder mot fetma. Gastric Bypass visas vara mer effektiv än en studerad befolkningsinriktad preventionsåtgärd. Slutligen påvisas att effektiva högriskpreventioner kan bidra med en högre samhällsnytta än gastric bypass operationer.   Nyckelord: Fetma, Gastric Bypass, Prevention / The prevalence of obesity has increased rapidly the past two decades. As a consequence the health expenditures related to obesity are high and are expected to increase if nothing is done. The objective of this thesis was to study whether prevention in early years or gastric bypass is the preference from a societal perspective as an intervention to obesity. I develop three hypothetical cohorts; status quo, effective prevention in early years and people whom develop obesity have gastric bypass surgery. The cohorts are followed from age 20 to age 64 where costs and effects are observed using a decision tree model. The results were that both gastric bypass and prevention in early years are found to be cost-effective treatments to obesity. Gastric bypass is found being more effective than a studied population-based prevention. Effective high-risk preventive methods can contribute to a higher benefit to society than a gastric bypass surgery.   Keyword: Obesity, Gastric Bypass, Prevention

Orientador: Lício Augusto Velloso / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-25T13:42:33Z (GMT). No. of bitstreams: 1 Nascimento_LucasFranciscoRibeirodo_D.pdf: 2796257 bytes, checksum: 15ca1e9976cd62582cd7aac7715e861c (MD5) Previous issue date: 2014 / Resumo: Em modelos experimentais de obesidade induzida por dieta rica em gordura há desenvolvimento de resistência hipotalâmica à leptina decorrente da ativação de uma resposta inflamatória específica no hipotálamo. Estudos recentes revelaram que além da indução da inflamação, a dieta rica em gordura ativa também vias de sinalização apoptóticas que culminam com a morte de neurônios em regiões hipotalâmicas envolvidas com o controle da fome e do gasto energético. Acredita-se que a perda de sub-populações específicas de neurônios no hipotálamo acarrete em dano dos mecanismos de controle do balanço entre consumo calórico e gasto energético, resultando no desenvolvimento ou perpetuação da obesidade. A composição de ácidos graxos da dieta tem papel central na resposta inflamatória hipotalâmica, sendo os ácidos graxos saturados de cadeia longa os mais lesivos. Por outro lado, em outras regiões do cérebro, alguns ácidos graxos insaturados podem desempenhar papel anti-inflamatório e induzir reparo funcional através da neurogênese. Neste trabalho, nós avaliamos os efeitos dos ácidos graxos poliinsaturados ?-linolênico (ALA C18:3-n3), e docosaexaenoico (DHA 22:6-n3) sobre a indução de neurogênese no hipotálamo de animais com obesidade induzida por dieta rica em gordura (HFD). Nossos resultados mostram que ácidos graxos ômega-3 administrados tanto na dieta ou diretamente no cérebro, são capazes de modular a neurogênese no hipotálamo de camundongos obesos, favorecendo a proliferação de neurônios anorexigênicos POMC, mas sem redução da ingestão alimentar. Embora esses animais não comam menos, eles se movimentam mais e exibem um discreto aumento do gasto energético. A suplementação com ômega-3 em HFD reduz a inflamação e a apoptose no hipotálamo, além de melhorar o metabolismo glicêmico e proteger os animais do ganho de peso. Aparentemente, os neurônios recém-formados surgem a partir da proliferação de células com características de células progenitoras, presentes na parede do terceiro ventrículo. Nesse processo, o receptor de ácidos graxos livres, GPR40, e o fator neurotrófico derivado do cérebro, BDNF, desempenham papel fundamental, mas a participação dessas proteínas em tais eventos parece ser dependente do estado nutricional e metabólico do animal / Abstract: In experimental models of high-fat diet (HFD)-induced obesity there is a development of hypothalamic leptin resistance due to the activation of a specific inflammatory responsein the hypothalamus. Recent studies have revealed that besides the induction of inflammation, a fat-rich diet can also activate apoptotic signaling pathways that culminate in neuronal death in hypothalamic areas responsible for the control of feeding and energy expenditure. It is believed that the loss of specific hypothalamic neuronal subpopulations deteriorates mechanisms involved in the control of caloric intake and energy expenditure, resulting in the development and perpetuation of obesity. The fatty acid composition of diet, particularly the saturated fatty acid content, can modulate immune activity in the hypothalamus, inducing an inflammatory response. However, in other regions of the brain, some unsaturated fatty acids can acts as anti-inflammatory agents and induce functional repair through neurogenesis. In this study we evaluated the effects of polyunsaturated fatty acids ?-linolenic (ALA C18:3-n3) and docosahexaenoic (DHA 22:6-n3) on the induction of hypothalamic neurogenesis in HFD-induced obese animals. Our results show that omega-3 fatty acids administered either in the diet or directly into the brain are able to modulate neurogenesis in the hypothalamus of obese mice, leading to the proliferation of anorexigenic POMC neurons. This effect is not accompanied by changes in food intake, but increase unstimulated physical activity resulting in a discrete increase in energy expenditure. In addition, omega-3 supplemented HFD reduces inflammation and apoptosis in the hypothalamus, improve glucose metabolism and protect the mice against body mass gain. Apparently, these newly formed neurons arise from progenitor cell proliferation present in the wall of the third ventricle. In this process, free fatty acid receptor, GPR40, and brain-derived neurotrophic factor, BDNF, play a key role; however, the involvement of these proteins in such events appears to be dependent on the nutritional and metabolic status of the animal / Doutorado / Biologia Estrutural, Celular, Molecular e do Desenvolvimento / Doutor em Ciências