9 - Obesidade x Exercício

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OBESIDADE
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 A obesidade pode ser definida, de forma resumida, como o grau de armazenamento de gordura no organismo associado a riscos para a saúde, devido a sua relação com várias complicações metabólicas .
 		(WORLD HEALTH ORGANIZATION, 2006). 
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HIPOCINESIA
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DOENÇAS ASSOCIADAS
HIPERCOLESTEROLEMIA 
ARTEROSCLEROSE
HIPERTENSÃO ARTERIAL
DIABETES
ARTROSE
CÂNCER (American Cancer Society) mostrou que a incidência de câncer intestinal (colo-retal) e de próstata, foi de 1,33 vezes maior em homens obesos e o câncer de endométrio, vesícula, colo de útero e mama, 1,55 vêzes maior em mulheres obesas. 
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OBESIDADE X SOBREPESO
Obesidade - Refere-se ao aumento na quantidade generalizada ou localizada de gordura em relação ao peso corporal.
Sobrepeso - Aumento do peso corporal total que pode acorrer em função de modificações em apenas um constituinte (gordura, músculo, ossos ou água) ou um conjunto desses fatores.
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TIPOS DE OBESIDADE
ENDÓGENA – proveniente de causas hormonais. Disfunção do metabolismo tireoidiano, gonadal, hipotálamico, hipófisiário, em função de alguns tumores e síndromes genéticas.
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EXÓGENA – gordura corporal armazenada em decorrência de ingesta calórica positiva,correspondendo DE 95 A 98% dos casos de obesidade.
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CLASSIFICAÇÃO ANATÔMICA
 OBESIDADE ANDRÓIDE OBESIDADE GINÓIDE
OBESIDADE ANDROGINÓIDE
OBESIDADE GINOANDRÓIDE
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DIFERENÇAS NA OBESIDADE GINÓIDE
Síndrome de Barraquer-Simmonds
Obesidade pelviana distrófica
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EVOLUÇÃO DA OBESIDADE
Obesidade hipertrófica – hipertrofia das células adiposas (adipócitos)
Obesidade hiperplásica – aumento na quantidade de células adiposas.
*Os períodos críticos para a obesidade hiperplásica são os último mês de gestação, os12 primeiros meses de vida, fase pré-escolar e puberdade.
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SÍNDROME METABÓLICA
Conjunto de alterações metabólicas que ocorrem em um indivíduo e que aumentam o risco de doenças cardiovasculares
Prevalência: 20-25% da população geral 
Presente em 42% dos indivíduos com mais de 60 anos
Aumenta 2-3 vezes o risco de morte por doença cardiovascular
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Diagnóstico de Síndrome Metabólica
Critérios
NCEP ATP III
Obesidade
Medida de Cintura
102 cm – Homens
88 cm – Mulheres
Glicemia jejum
110mg/dL
Pressão Arterial
130 x 85 mm Hg
Triglicérides
150mg/dL
HDL- Colesterol
< 40mg/dL – Homens
<50mg/dL - Mulheres
Critérios
3ou mais critérios
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HÁBITOS
SEDENTARISMO
	HÁBITOS ALIMENTARES
		DISTÚRBIOS PSICOLÓGIOS
			DISTÚRBIOS HORMONAIS
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Avaliação do obeso
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DEXA
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I.M.C.
(Índice de Massa Corporal)
Uma das formas mais usadas para determinação da obesidade é o I.M.C., ele foi desenvolvido na Europa e América do Norte (paises industrializados).
Um I.M.C. superior a 30 Kg/m² é aproximadamente:
30% de gordura corporal em média para homens de 20 anos;
40% de gordura corporal em média para homens de 60anos e mulheres de 20 anos;
50% de gordura corporal em média para mulheres de 60 anos. 
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I.M.C. = Massa(Kg)/(Estatura(m))²
I.M.C.
Classificação
Abaixode 18,5 Kg/m²
Abaixo doPeso
De 18,5 à 24,9 Kg/m²
Normal
De 25 à 29,9 Kg/m²
Sobrepeso
De 30 à 34,9 Kg/m²
Obesidade 1
De 35 à 39,9 Kg/m²
Obesidade2
Acima de 40 Kg/m²
ObesidadeMórbida
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CIRCUNFERÊNCIA CINTURA
O excesso de gordura abdominal, principalmente quando desproporcional à gordura corporal total, é um preditor independente de fatores de risco.
O valor de corte da circunferência cintura combinado com o IMC, permite identificar o aumento do risco de doenças, principalmente as síndromes metabólicas.
# Medida tomada no plano horizontal sobre a cicatriz umbilical.
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RELAÇÃO DO IMC E CIRCUNFERÊNCIA DA CINTURA COM O RISCO DE DOENÇAS
I.M.C.
Classificação
RISCOS ASSOCIADOS
HOMEM ≤ 102cmMULHER ≤ 88cm
HOMEM > 102cmMULHER > 88cm
Abaixo- 18,5 Kg/m²
Abaixo doPeso
-
-
18,5 à 24,9 Kg/m²
Normal
-
-
25,0 à 29,9 Kg/m²
Sobrepeso
↑
↑↑
30,0 à 34,9 Kg/m²
Obesidade 1
↑↑
↑↑↑
35,0 à 39,9 Kg/m²
Obesidade2
↑↑↑
↑↑↑
Acima - 40 Kg/m²
ObesidadeMórbida
↑↑↑↑
↑↑↑↑
*Doenças cardiovasculares e hipertensão (ACSM,2001)
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Relação Cintura/Quadril (RCQ)
Permite verificar o tipo de distribuição da gordura corporal(andróide ou ginóide).
É conveniente utilizar outras medidas de avaliação; em conjunto com a RCQ.
A avaliação da distribuição da gordura corporal, combinada com a estimativa da gordura corporal total, é um importante aspecto de avaliação do risco de doenças.
#Quadril – medida tomada no plano horizontal sobre os pontos trocantéricos.
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 IDADE BAIXO MODERADO ALTO MUITO ALTO
20 – 29 < 0.71 0.71-0.77 0.78-0.82 > 0.82
30 – 39 < 0.72 0.72-0.78 0.79-0.84 > 0.84
40 – 49 < 0.73 0.73-0.79 0.80-0.87 > 0.87
50 – 59 < 0.74 0.74-0.81 0.82-0.88 > 0.88
60 – 69 < 0.76 0.76-0.83 0.84-0.90 > 0.90
RCQ E RISCO DE DOENÇAS – MULHERES (ACSM,2001) 
 IDADE BAIXO MODERADO ALTO MUITO ALTO
20 – 29 < 0.83 0.83-0.88 0.89-0.94 > 0.94
30 – 39 < 0.84 0.84-0.91 0.92-0.96 > 0.96
40 – 49 < 0.88 0.88-0.95 0.96-1.00 > 1.00
50 – 59 < 0.90 0.90-0.96 0.97-1.02 > 1.02
60 – 69 < 0.91 0.91-0.98 0.99-1.03 > 1.03
RCQ E RISCO DE DOENÇAS – HOMENS (ACSM,2001) 
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Cálculo da Demanda Energética (WILLIANS, 1995)
Homens  
TMB = 66,5 + (13,7 X P) + (5 X A) - (6,8 X I) = Kcal/dia
Mulheres
TMB = 655,1 + (9,56 X P) + (1,85 X A) - (4,7 X I) = Kcal/dia
*Onde: P = peso em Kg;   A = altura em cm;   I = idade em anos.
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CUSTO ADICIONAL DE ACORDO COM A OCUPAÇÃO
Pessoas inativas - ocupação muito inativa. Assentado a maior parte do dia; não pratica esportes ou exercícios = 0
Pessoas moderadamente ativas - ocupação muito inativa; ocupação leve em casa; pratica esportes ou exercícios ocasionalmente = +20%
Pessoas Ativas - Ocupação ativa ou pratica exercícios vigorosos ou caminhada/ pedala diariamente = + 40%
Atletas de performance – treinamento com fins competitivos = + 60%
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DEMANDA ENERGÉTICA PARA CRIANÇAS
CRIANÇAS – Masculino
3 -9 anos = TMB = (22,7 x Peso) + 495
10 -17 anos = TMB = (17,47 x Peso) + 651
CRIANÇAS – Feminino
3 -9 anos = TMB = (22,5 x Peso) + 499
10 -17 anos = TMB = (12,2 x Peso) + 746
*Peso em kg.
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Intervenção no obeso
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Componentes da terapia comportamental para tratamento da obesidade
OBESITY
Wadden and Foster. Med Clin North Am 2000:84:441.
Auto Monitoramento
Resolução de Problemas
Gestão de contingência
Reestruturação cognitiva
Apoio Social
Gerenciamento do Estresse
Controle de estímulo
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Components of behavioral therapy for obesity
Behavioral therapy of obesity usually includes the following components:
Self-monitoring is the most important component of behavior therapy for obesity and involves keeping daily records of food intake and physical activity, and checking weight regularly. Self-monitoring records can provide information needed to identify links in the behavior chain that can be targeted for intervention. In addition, record keeping enhances compliance with dietary and physical activity interventions. 
Problem solving is a systematic method of analyzing problems and identifying possible solutions.
Contingency management involves developing methods to help recovery from episodes
of overeating or weight regain.
Stimulus control is the process of avoiding triggers that prompt eating.
Stress management is used to decrease the negative impact of stress on positive behavior patterns.
Social support from family members and friends is important for modifying lifestyle behaviors. 
Cognitive restructuring teaches patients to think in a positive manner and to correct thoughts that undermine weight management efforts. Cognitive techniques also help patients accept realistic, but less-than-desired, weight losses. Inappropriate feelings of failure after achieving modest but clinically-important weight loss can lead to relapse and weight regain.
 
Wadden TA, Foster GD. Behavioral treatment of obesity. Med Clin North Am 2000;84:441-461.
Keywords: problem solving, contingency management, stimulus control, stress management, social support, cognitive restructuring, self-monitoring
Obesity Is Caused by Long-Term Positive Energy Balance
Fat
Stores
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A obesidade é causada pelo balanço energético positivo a longo prazo
A obesidade é causada pela ingestão de mais energia do que é se tem de gasto por um longo período de tempo. O excesso de calorias consumidas leva a um acúmulo de gordura corporal, que serão armazenadas como gordura ou impedem a mobilização e a oxidação da gordura endógena. Em geral, a ingestão de 3.500 kcal (mais ou menos) do que se gasta vai levar a um ganho (ou perda) de aproximadamente 1 kg de gordura. Os fatores genéticos podem influenciar a quantidade de peso ganho com a superalimentação. 
Em um estudo realizado com 12 pares de gêmeos monozigóticos ingerindo 1.000 kcal / d a mais que a demanda energética, o ganho de peso variou muito entre os 12. No entanto, os ganhos de peso foram semelhantes em cada membro de um par de gêmeos. Em outro estudo, o ganho de gordura, após 8 semanas de superalimentação também variou entre os sujeitos do estudo, mas foi inversamente relacionada com a evolução das despesas de energia não-volitiva, tais como inquietação, que pode ser determinada geneticamente [2].
Bouchard C, A Tremblay, JP Despres, et al. A resposta a superalimentação de longo prazo em gêmeos idênticos. N Engl J Med 1990; 322:1477-1482.
Levine JA, NL Eberhardt, Jensen MD. Papel da termogênese sem exercício de atividade na resistência ao ganho de gordura em seres humanos. Science 1999; 282:212-214.
OBJETIVOS DIETÉTICOS
Reduzir a ingestão de calorias, principalmente as gorduras;
Manter uma ingestão adequada de carboidrato, mínimo 60%;
Ingestão de proteínas de aproximadamente 1,4 a 1,7 g/kg/peso corporal por dia é necessária para manter a massa muscular e as proteínas corporais durante a perda de peso
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RECOMENDAÇÕES DO A.C.S.M. PARA PROGRAMAS DE PERDAS DE PESO
A restrição dietética deve ser moderada (500 a 1000 kcal/dia abaixo do gasto real total).
A dieta deve ser compatível ao gosto e hábito alimentar do indivíduo e de fácil preparo.
A ingestão de calorias não deve ser inferior a 1200 kcal/dia (adultos normais).
Inclusão de técnicas de modificação de comportamento para identificar e modificar hábitos que contribuem com a nutrição imprópria.
Programa de exercício que envolva grandes grupos musculares que promova um dispêndio calórico diário de 300 ou mais kcal.
A perda de gordura não deve ultrapassar 1 kg/semana.
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REDUÇÃO DE CARBOIDRATOS NA DIETA
Letargia
Diminuição das reservas de glicogênio
Alto índice de Fadiga
Intensidade de treinamento reduzida e baixo desempenho
Aumento de apetite
Diminuição da síntese de proteína (músculo) e perda de massa muscular
Estado Mental Negativo
*Nunca consumir menos calorias que sua TMB (taxa metabólica basal) - Bean ,1999.
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DIETAS DE BAIXAS CALORIAS E ESTRESSE
Uma dieta de baixas calorias pode levar a um aumento da produção do hormônio do estresse, Cortisol. 
Combinados com exercícios intensos, o Cortisol pode aumentar a perda de massa muscular estimulando a oxidação de proteínas. 
O Cortisol também estimula a redução de testosterona, dando sinal ao corpo para reduzir o processo anabólico e armazenar gordura.
Portanto, para minimizar a perda do tecido magro é importante evitar a redução drástica de calorias.
*Fonte: Anita Bean, O guia completo do treinamento de força, 1999. 
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Prescrição dos exercícios
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CÁLCULO DA GASTO CALÓRICO
Segundo o ACSM, para haver uma perturbação significativa para perda de peso, um indivíduo de 70 Kg deve ter um gasto mínimo de 300Cal. com o exercício, Logo:
 70Kg-------------------300cal.
Peso(Kg)---------------- X cal.
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ORGANIZAÇÃO DO PROGRAMA 
Objetivo = perda de peso 
Peso extra = Calorias acumuladas (gorduras)
Calorias = quantidade de calor necessária para aquecer em 1º, 1 grama de água.
Logo = quanto mais calor o indivíduo liberar maior é o gasto energético.
Sendo assim, o exercício intermitente ou com pausa ativa se torna mais adequado do que o exercício de pausa passiva.
Intensidade – pesquisas relatam que exercícios de baixa intensidade e longa duração tem um melhor efeito no controle do peso corporal (Guedes, 2006).
Em contrapartida e sabido que, uma maior massa muscular tem um gasto energético basal maior. 
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CONSIDERAÇÕES PARA A PRESCRIÇÃO
Estudos mostram que um aumento de 1,3Kg de músculo é capaz de aumentar a demanda energética em 7-15%.
Em repouso, 453 g de músculo queimam de 30-50 kcal por dia apenas para manter a sua massa.
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QUAL O MELHOR TIPO DE TREINAMENTO?
Misto.
Musculação e exercícios aeróbios, sendo que a musculação deve ter uma freqüência semanal de até 3 sessões enquanto os exercícios aeróbios podem ser praticados diariamente.
A musculação deve ser feita com intervalos ativos já que a recuperação se torna mais eficiente e o aluno está em movimento ou seja produzindo calor.
Não existe consenso com relação a colocação do exercício aeróbio(antes ou depois do treino da musculação), provavelmente por este ser um fator que tenha uma adaptação diferente para cada indivíduo.
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ESTIMATIVA DE TEMPO NECESSÁRIO PARA SE ATINGIR O OBJETIVO
Variáveis necessárias:
Sobra de Gordura em Cal.
1Kg de gordura ~ 7.000 Cal.
Sobra de gordura(Cal.) \ Perda prevista por treino
*O resultado obtido equivale ao nº de sessões de treinamento para alcançar o objetivo. 
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Energia armazenada (homem – 70kg)
Adipose tissue triglyceride = 
120,000 kcal
Muscle triglyceride =
3000 kcal
Liver triglyceride = 450 kcal
Liver glycogen = 400 kcal
Muscle glycogen =
2500 kcal
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A energia armazenada no corpo de um homem de 70 kg magro
A energia é armazenada no organismo na forma de triglicérides e glicogênio no tecido adiposo, fígado e músculo esquelético. Triglicérides presentes no tecido adiposo de reserva de combustível do corpo principal. Um adulto magro possui cerca de 35.000 milhões adipócitos, e cada adipócito contém cerca de 0,4 a 0,6 g de triglicérides. Um adulto extremamente obesos pode ter 4 vezes mais adipócitos muitos, cada uma contendo até duas vezes mais lipídios . O glicogênio e triglicérides intramuscular constituem uma importante fonte de combustível para trabalhar os músculos durante o exercício.
Os triglicerídeos são um combustível cinco vezes mais potentes em relação ao glicogênio, pois são armazenadas de forma compacta como um óleo dentro dos adipócitos e liberaram 9,3 kcal / g, quando oxidados, enquanto que o glicogênio é armazenado intracelularmente na forma de um gel, contendo 2 g de água para cada 1 g de glicogênio, e libera 4,1 kcal / g quando oxidado.
Hirsch J, JL Knittle. Celularidade de obesos e não obesos tecido adiposo humano. Fed Proc 1970; 29:1516-1521.
Components of Daily Energy Expenditure
Segal KR et al. Am J Clin Nutr. 1984;40:995-1000.
Thermic effect 
of feeding
Energy expenditure of physical activity
Resting energy expenditure
Sedentary Person 
(1800 kcal/d)
Physically Active Person 
(2200 kcal/d)
8%
17%
75%
8%
60%
32%
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Componentes do gasto energético básico 
O gasto energético diário total (GET) é composto de três componentes: gasto energético de repouso, o efeito térmico da alimentação e gasto energético da atividade física. Gasto energético de repouso refere-se a energia gasta para a função celular normal e órgão durante condições de repouso, o que representa a aproximadamente 65% -75%. O efeito térmico da alimentação refere-se ao gasto energético associado com a digestão, absorção e aumento da atividade do sistema nervoso simpático, depois de uma refeição. Este componente tem cerca de 5% a 10%. A energia gasta na atividade física é o resultado de um trabalho mecânico volitivo, tal como o exercício e as atividades diárias, tais como inquietação, contrações musculares espontâneas, e manter a postura, o que representa entre 15% -30%. A energia gasta pela atividade física depende da intensidade e duração das atividades e é o componente mais variável do gasto energético. Durante a alta intensidade de exercício aeróbio, como correr ou andar de bicicleta vigorosa, a energia consumida por trabalhar os músculos podem aumentar mais de 50 vezes, causando um aumento de 15 vezes no gasto energético total. Os indivíduos obesos requerem a mesma quantidade de energia para desempenhar a mesma quantidade de trabalho quando o peso do corpo é suportado como os indivíduos de peso normal. Na verdade, pessoas obesas gastam mais energia para o mesmo nível de intensidade pelo maior peso. 
KR Segal et al. Thermic efeito dos alimentos durante o exercício físico progressivo no peso normal e obesos. Am J Clin Nutr. 1984; 40:995-1000. 
Metabolismo energético em indivíduos magros e obesos
Energy Expenditure (k/cal/d)
Resting Energy Expenditure
*P<0.05 vs lean subjects
Ravussin et al. Am J Clin Nutr 1982;35:566.
Total Energy Expenditure
Lean (BMI=21 kg/m2)
Obese (BMI=38 kg/m2)
*
*
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Metabolismo energético em indivíduos obesos e magros
A maioria das pessoas obesas não têm uma redução anormal do metabolismo energético. Tanto o gasto energético total e gasto energético de repouso são geralmente maiores nos obesos do que pessoas magras que são da mesma altura e sexo por causa da maior massa celular corporal (gordura e sem gordura nas massas celulares) em pessoas obesas. Portanto, as pessoas obesas devem consumir mais calorias do que pessoas magras para manter seu tamanho de corpo maior.
Ravussin E, Burnand B, Y Schutz, Jequier E. gasto energético de vinte e quatro horas por dia e taxa metabólica de repouso em obesos, moderadamente obeso, e assuntos do controle. Am J Clin Nutr 1982; 35:566-573.
melhora da sensibilidade à insulina, com perda de peso em pacientes com Diabetes Tipo 2
Insulin (pmol/L)
Before
Weight Loss at 1 Year (%)
Wing et al. Arch Intern Med 1987;147:1749.
*P<0.01 vs before.
*
*
*
0-2.4
2.5-6.9
7.0-14.0
>15
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A melhora da sensibilidade à insulina, com perda de peso em pacientes com diabetes tipo 2
Em pacientes obesos com diabetes tipo 2, a perda de peso modesta melhora a sensibilidade à insulina e controle glicêmico. Este valor representa dados de um ensaio realizado em 114 pacientes com diabetes tipo 2 que estavam sendo tratados com hipoglicemiantes orais e que completaram um programa de controle de peso de 1 ano. Concentração plasmática de insulina de jejum, que prevê um índice de sensibilidade à insulina, a diminuição de forma progressiva, com diminuição do peso corporal. Mesmo uma perda de peso tão pequena quanto de 2,5% foi associada com uma diminuição significativa na concentração de insulina plasmática. Reduções na hemoglobina glicosilada, glicemia de jejum, e os requisitos de medicação dos diabéticos também foram diretamente associados com a perda de peso. A necessidade de medicação hipoglicemiante foi diminuído em todos os indivíduos que perderam 15% ou mais do seu peso corporal.
Wing RR, R Koeske, LH Epstein, et al. Os efeitos a longo prazo da perda de peso modesta em pacientes diabéticos tipo II. Arch Intern Med 1987; 147:1749-1753.
Total
Cholesterol
LDL-C
TG
HDL-C
(weight
stable)
HDL-C
(actively
losing)
Plasma Lipids Improve with Weight Loss Meta-analysis of 70 Clinical Trials
 mmol/L kg of Weight Loss
LDL-C=low density lipoprotein cholesterol; HDL-C=high-density lipoprotein cholesterol; TG=triglycerides
Dattilo et al. Am J Clin Nutr 1992;56:320.
*P<0.05.
 mg/dL per kg of Weight Loss
*
*
*
*
*
0.5
0.0
-0.5
-1.0
-1.5
-2.0
-2.5
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Os lipídios plasmáticos melhoraram com a perda de peso: metanálise de 70 ensaios clínicos
Os ensaios clínicos têm demonstrado os efeitos das variáveis de perda de peso sobre os níveis séricos de colesterol total, LDL-colesterol, triglicérides e HDL-colesterol. Os dados deste slide são tomadas a partir de uma meta-análise de 70 estudos e demonstrar uma relação direta entre a perda de peso e melhoras na concentração sérica de lipídios. Durante a perda de peso, o HDL-colesterol, diminuiu a concentração, mas depois aumentou uma vez que a perda de peso foi estabilizada. As grandes melhorias nas concentrações séricas de lipídios tendem a ocorrer nas primeiras 4 a 8 semanas de perda de peso. O grau de melhora na concentração de triglicerídeos e colesterol está relacionada com a quantidade de peso perdido e ao recuperar o peso à reincidência nos níveis de lipídios no soro. Aos 2 anos, de uma perda de peso sustentável de 5% é suficiente para manter a redução das concentrações séricas de triglicérides, enquanto a concentração sérica total e LDL-colesterol basal pode ser revertida a menos que haja uma perda de peso de 10% mantida.
National Institutes of Health, National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res 1998; 6(suppl 2):51S-209S. 
Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr 1992;56:320-328. 
Wadden TA, Anderson DA, Foster GD. Two-year changes in lipids and lipoproteins associated with the maintenance of a 5% to 10% reduction in initial weight: some findings and some questions. Obes Res 1999;7:170-178.
Rössner S, Sjöström L, Noack R, et al. Weight loss, weight maintenance, and improved cardiovascular risk factors after 2 years treatment with orlistat for obesity. Obes Res 2000;8:49-61
Rössner S, Bjorvell H. Early and late effects of weight loss on lipoprotein metabolism in severe obesity. Atherosclerosis 1987;64:125-130.
Ryttig KR, Flaten H, Rossner S. Long-term effects of a very low calorie diet (Nutrilett) in obesity treatment. A prospective, randomized, comparison between VLCD and a hypocaloric diet+behavior modification and their combination. Int J Obes Relat Metab Disord 1997;21:574-579.
Relação entre a mudança no peso e pressão arterial: Trials of Hypertension Prevention II
Change in Blood
Pressure (mm Hg)
Stevens et al. Ann Intern Med 2001;134:1.
1
2
3
4
5
Change in Weight (kg)
Quintile of Weight Change
1
2
3
4
5
Diastolic
Systolic
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Relação entre mudanças de peso e pressão arterial: Estudos para a prevenção da hipertensão
A perda de peso diminui a pressão arterial sistólica e diastólica. Estudos para a prevenção da hipertensão, com cerca de 1.200 indivíduos com sobrepeso e obesos foram randomizados para um programa de 3 anos e a perda de peso, envolvendo dieta e atividade física, ou cuidado habitual. Os resultados, mostrados na figura, demonstrar uma relação linear entre a perda de peso e pressão arterial. Uma perda de peso média de 8,8 kg, foi associado com uma redução de 7 mm Hg na pressão arterial diastólica (PAD) e de 5 mmHg na pressão arterial sistólica (PAS). Uma perda de 2,6 kg causou reduções de 4,5 mm Hg na PAD e 2,5 mm Hg na PAS. Uma perda de 0,1 kg foi associado com reduções de 2,0 mm Hg na PAD, sem uma mudança no PAS. Os participantes que recuperaram a maioria ou a totalidade do seu peso perdido experimentaram um aumento da pressão
arterial para valores próximos aos do inicio do estudo. 
Em pacientes extremamente obesos com hipertensão arterial, a perda de peso induzida pela cirurgia gástrica melhora ou resolve completamente hipertensão em cerca de dois terços dos pacientes. No entanto, dados recentes de estudos suecos concluem que o efeito benéfico da perda de peso sobre a pressão arterial observada em um e dois anos após a cirurgia gástrica desaparecido por três anos, tanto sistólica quanto diastólica, a pressão arterial continua a aumentar gradualmente para os próximos cinco anos. Mais dados são necessários para avaliar plenamente os efeitos a longo prazo da perda de peso por cirurgia sobre a pressão arterial. 
Stevens VJ, Obarzanek E, NR Cook, et al. perda de peso a longo prazo e mudanças na pressão arterial: resultados dos ensaios de prevenção da hipertensão, Fase II. Ann Intern Med. 2001; 134:1-11. 
Foley EF, PN Benotti, BC Borlase, et al. Impacto da cirurgia gástrica restritiva sobre a hipertensão nos obesos mórbidos. Am J Surg 1992; 163:294-297. 
Carson JL, Ruddy ME, AE Duff, et al. O efeito da cirurgia de bypass gástrico na hipertensão em pacientes obesos mórbidos. Arch Intern Med 1994; 154:193-200. 
Sjostrom CD, Peltonen M, H Wedel, efeitos Sjostrom L. diferenciadas de longo prazo da perda de peso intencional sobre diabetes e hipertensão. Hypertension 2000; 36:20-25. 
Impact of Weight Loss on Risk Factors
~5%
Weight Loss
5%-10%
Weight Loss
HbA1c
Blood Pressure
Total Cholesterol
HDL Cholesterol
Triglycerides
1. Wing RR et al. Arch Intern Med. 1987;147:1749-1753.
2. Mertens IL, Van Gaal LF. Obes Res. 2000;8:270-278.
3. Blackburn G. Obes Res. 1995;3 (Suppl 2):211S-216S.
4. Ditschunheit HH et al. Eur J Clin Nutr. 2002;56:264-270.
1
2
3
3
1
2
3
3
4
59
O impacto da perda de peso nos fatores de risco 
As perdas de peso de 5% a 10% demonstraram ter um impacto significativo sobre vários aspectos da síndrome metabólica, incluindo fatores de risco bem conhecidos para doença cardiovascular e diabetes. Por exemplo: 
Wing e seus colegas da Universidade Brown, avaliarm o efeito da perda de peso modesta em 114 pacientes com diabetes tipo 2. Aqueles que perderam 5% ou mais do seu peso inicial mostrou uma diminuição estatisticamente significativa nos níveis séricos de HbA1c. 
O Julgamento de anti-hipertensivos intervenções e Estudo de Gestão constatou que as perdas de peso de 5% ou mais, produziu reduções na pressão diastólica, que foram equivalentes aos produzidos por uma única dose da medicação anti-hipertensiva. 
Numerosos estudos têm mostrado que as perdas de peso de 5% -10% melhoraram o colesterol total, LDL razão para a HDL, e a proporção de colesterol total para HDL . Em um estudo de redução de peso, de apenas 5,8% foi associada uma redução de 16% no colesterol total, um aumento de 18% no colesterol HDL e uma diminuição de 12% nos níveis de colesterol LDL. Mais recentemente, Ditschunheit e colegas documentaram reduções significativas nos níveis de colesterol total, triglicérides e VLDL em pacientes obesos com hiperlipidemia, sendo que tiveram uma perda de peso de 7,6%. 
Blackburn Ob G. Res 1995; 3 (Suppl2): 211S-216S. 
Ditschunheit HH, et al. Lipoproteína respostas perda de peso e manutenção do peso em indivíduos obesos de alto risco. Eur J Clin Nutr 2002; 56:264-270. 
Mertens IL, Van Gaal LF. Sobrepeso, obesidade e pressão arterial: os efeitos da redução de peso modesta. Ob Res 2000; 8 (3) :270-278. 
Wing RR, et al. Os efeitos a longo prazo da perda de peso modesta em pacientes diabéticos tipo 2. Arch Intern Med 1987; 147:1749-1753. 
TCHAU....
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Bariatric Surgery for the Treatment of Obesity
Samuel Klein, MD, MS, and Harvey Sugerman, MD
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61
Bariatric Surgery for the Treatment of Obesity
Bariatric Surgery
Indications
BMI >40 kg/m2 or 
	BMI 35–39.9 kg/m2 and 
	life-threatening cardiopulmonary 
	disease, severe diabetes, or
	lifestyle impairment
Failure to achieve adequate weight loss with nonsurgical treatment 
Contraindications
History of noncompliance with medical care
Certain psychiatric illnesses: personality disorder, uncontrolled depression, suicidal ideation, substance abuse
Unlikely to survive surgery
NIH Consensus Development Panel. Ann Intern Med 1991;115:956.
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62
Bariatric surgery
Bariatric surgery is the most effective available weight loss therapy for obesity. In 1991, a National Institutes of Health Consensus Conference established guidelines for the surgical treatment of obesity.1 This panel concluded that patients with Class III obesity (BMI 40 kg/m2) or those with Class II obesity (BMI 35.0–39.9 kg/m2) and one or more severe obesity-related medical complications such as hypertension, type 2 diabetes, heart failure, and sleep apnea are eligible for surgery. These criteria were supported with the Medicare National Coverage Determination (NCD) in February, 2006.2 Moreover, potential candidates should be patients who are unable to lose weight or maintain weight loss with nonsurgical therapy, are able to comply with long-term treatment and follow-up, and have an acceptable operative risk. Patients with a history of noncompliance with medical care and psychiatric illnesses that may hinder compliance with the postoperative regimen are not suitable for surgery. Active substance abuse is an absolute contraindication.
The photograph in this slide was taken during a laparoscopic gastric bypass procedure. This section will review the risks and benefits of the bariatric surgical procedures used to treat obese patients.
References:
NIH conference. Gastrointestinal surgery for severe obesity. NIH Consensus Development Conference Panel. Ann Intern Med. 1991 Dec 15;115(12):956-961.
Decision Memo for Bariatric Surgery for the Treatment of Morbid Obesity (CAG-00250R). U.S. Dept. of Health and Human Services, Centers for Medicare and Medicaid Services. February 21, 2006.
Current Bariatric Surgical Procedures
Classification
Gastric restriction
Primarily restrictive and partially malabsorptive
Primarily malabsorptive and partially restrictive
Procedure
Adjustable Gastric Banding
Roux-en-Y Gastric Bypass
Biliopancreatic diversion with duodenal switch
Biliopancreatic diversion 
Distal gastric bypass
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63
Current bariatric surgical procedures
Bariatric surgical procedures can be divided into two general categories—those that primarily restrict gastric volume and those that primarily cause malabsorption. The gastric bypass procedure is the most commonly performed operation and accounts for more than 90% of the bariatric surgery procedures currently being performed in the United States.
The jejunoileal bypass (also known as small bowel bypass) procedure was first reported in 19691 but is no longer being performed because of excessive serious medical complications.2
References:
Payne JH, DeWind LT. Surgical treatment of obesity. Am J Surg. 1969;118:141-147.
Hocking MP, Duerson MC, O'Leary JP, Woodward ER. Jejunoileal bypass for morbid obesity. Late follow-up in 100 cases. N Engl J Med. 1983;308:995-999.
Complications of Bariatric Surgery
All procedures: 
Atelectasis and pneumonia 
Deep vein thrombosis
Pulmonary embolism
Wound infection
Gastrointestinal bleeding
Gallstones
Failure to lose weight
Intractable vomiting/kwashiorkor (B1)
Mortality (0.1%–2%)
Gastric bypass:
Anastomotic leak with peritonitis
Stomal stenosis 
Marginal ulcers 
Staple line disruption
Nutrient deficiencies (iron, calcium, folic acid, vitamin B12)
Dumping syndrome
Small bowel obstruction
Internal hernia
Adhesions
Gastric banding procedure:
Band slippage 
Band erosion 
Esophageal dilatation
Band or port infections
Port disconnection
Port displacement
Biliopancreatic diversion:
Anastomotic leak with peritonitis 
Protein-calorie malnutrition
Calcium, iron, folic acid, fat soluble vitamin (A,D,E,K) deficiencies
Dehydration
Steatorrhea
Small bowel obstruction
Internal
hernia
Adhesions
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Complications of bariatric surgery
The complications associated with bariatric surgical procedures are shown in this table. Perioperative mortality is usually less than 1.5%,1,2 with approximately three-quarters of the deaths due to anastomotic leaks and peritonitis and one-quarter due to pulmonary embolism. Anastomotic leak with peritonitis is a serious complication that can be difficult to diagnose because patients rarely develop peritoneal signs. The leak rate after open gastric bypass is approximately 2.5%, and the mortality risk from this complication is approximately 0.3%.1,3 The risk of pulmonary embolism after surgery is increased in extremely obese patients. In one series, the risk of a fatal pulmonary embolism was 0.2% and increased to 4% in patients with severe venous stasis disease.4 Gallstones occur in approximately one-third of patients within six months after a gastric restrictive procedure and can be even more common following a malabsorptive procedure. The incidence of gallstone formation is decreased markedly with prophylactic ursodeoxycholic acid therapy.5 The risks for incisional hernia6 and wound infections also are markedly increased following abdominal surgery in severely obese patients compared with lean patients.
Inadequate weight loss (failure to lose >40% of excess body weight) occurs in approximately 15% of patients after gastric bypass surgery1,3 and in more patients after gastroplasty.7 This failure to lose weight is usually due to frequent ingestion of high-fat snacks, fried foods, and high-calorie soft foods and liquids. Increased food intake also occurs with staple line disruption in patients who have had a stapled gastroplasty or gastric bypass.
References: 
Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222:339-350.
MacLean LD, Rhode BM, Sampalis J, Forse RA. Results of the surgical treatment of obesity. Am J Surg. 1993;165:155-162. 
Sugerman HJ, Kellum JM, Engle KM, et al. Gastric bypass for treating severe obesity. Am J Clin Nutr. 1992;55:560S-566S. 
Sugerman HJ, Sugerman EL, Wolfe L, et al. Risks and benefits of gastric bypass in morbidly obese patients with severe venous stasis disease. Ann Surg. 2001;234:41-46. 
Sugerman HJ, Brewer WH, Shiffman ML, et al. A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss. Am J Surg. 1995;169:91-97. 
Sugerman HJ, Kellum JM Jr, Reines HD, et al. Greater risk of incisional hernia with morbidly obese than steroid-dependent patients and low recurrence with prefascial polypropylene mesh. Am J Surg. 1996;171:80-84.
Balsiger BM, Poggio JL, Mai J, Kelly KA, Sarr MG. Ten and more years after vertical banded gastroplasty as primary operation for morbid obesity. J Gastrointest Surg. 2000;4(6):598-605.
0
25
50
75
100
Patents with 
Type 2 Diabetes
Patients with 
IGT
Patients with Normal Fasting 
Blood Glucose and HbA1c After Surgery (%)
Gastric Bypass Surgery Improves Glycemic Control in Impaired Glucose Tolerance or Type 2 Diabetes 
Pories et al. Ann Surg 1995;222:339.
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65
Gastric bypass surgery improves glycemic control in impaired glucose tolerance or type 2 diabetes
Gastric bypass surgery has a considerable beneficial effect on glycemic control in patients with impaired glucose tolerance (IGT) or type 2 diabetes. Eighty-three percent of 146 patients with type 2 diabetes and 99% of 152 patients with impaired glucose tolerance normalized their fasting blood glucose and glycosylated hemoglobin concentrations for as long as 14 years after surgery. The normalization of glucose metabolism often occurred very rapidly and before there was significant weight loss, which underscores the early beneficial effects of negative energy balance on insulin sensitivity with respect to glucose metabolism. This improvement in diabetes control persists for at least 10 years after bariatric surgery.
Reference:
Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult onset diabetes mellitus. Ann Surg. 1995;222:339-352.
4.7
18.5
0.0
3.6
0.0
4.0
8.0
12.0
16.0
20.0
2
8
Follow-up After Surgery (y)
Incidence of Type 2 Diabetes
(% Patients)
 Control
 Bariatric surgery
Prevention of Type 2 Diabetes at 8 Years 
After Bariatric Surgery (94% Restrictive)
Sjostrom et al. Hypertension 2000;36:20.
			Control 	Surgery 
Initial BMI (kg/m2)		 41  5 	 41  4
Weight change at year 8: 1  11% 	-16  12% 
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Prevention of type 2 diabetes at 8 Years After Bariatric Surgery (94% Restrictive)
Long-term surgically induced weight loss can prevent the development of diabetes in obese patients. This slide shows data from the Swedish Obese Subjects (SOS) Study, which is a prospective intervention study comparing clinical outcomes in obese patients treated with gastric surgery with matched obese control subjects. At eight years, no significant weight change occurred in 346 control subjects (1% ± 11%), whereas the 346 subjects who had gastric surgery (vertical banded gastroplasty, gastric banding, or gastric bypass) lost 16% ± 12% of their initial weight. The two-year incidence of diabetes among control subjects was 4.7% compared with 0% among surgically treated patients (P=0.0012); the eight-year incidence of diabetes among control subjects was 18.5% compared with 3.6% among surgically treated patients (P<0.0001).
Reference
Sjöström CD, Peltonen M, Wedel H, Sjöström L. Differentiated long-term effects of intentional weight loss on diabetes and hypertension. Hypertension. 2000;36:20-25.
Effect of Bariatric Surgery on Obesity-related Metabolic Complications
Sjöström: N Engl J Med 2004;351:2683.
Ratio of Recovery (% of subjects)
21
72
Diabetes
Hypertension
Hypertriglyceridemia
13
36
21
34
11
19
22
62
24
46
Control
Surgery
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67
Effect of bariatric surgery on obesity-related metabolic complications
The improvement in diabetes was significant at 10 years when compared to a matched cohort group in the Swedish Obese Subjects (SOS) trial.1 There were also significant improvements in hypertriglyceridemia, hyperuricemia and high molecular weight cholesterol at 10 years. However, the significant improvement in hypertension seen at 2 years was no longer present at 10 years. But in another SOS report, in the 6% of patients who underwent a gastric bypass who had a significantly greater weight loss than purely restrictive procedures, there was a significant improvement in both systolic and diastolic blood pressure at eight years.2
References:
Sjöström L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Eng J Med. 2004;351:2683-93.
Sjöström CD, Peltonen M, Sjöström L. Blood pressure and pulse pressure during long-term weight loss in the obese: the Swedish Obese Subjects (SOS) Intervention Study. Obes Res. 2001;9:188-95.
0
1
2
3
Steatosis
Histology score 
(Brunt et al. system)
Before GBS
 1 Yr after GBS
Inflammation
Fibrosis
Effect of Gastric Bypass Surgery-induced Weight Loss on Liver Histology
Klein S. et al. Gastroenterology 130:1564, 2006
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68
Effect of gastric bypass surgery-induced weight loss on liver histology
Weight loss is usually recommended as therapy for obese patients with NAFLD. Moderate diet-induced weight loss (~10% body weight) decreases liver fat content and improves liver biochemistries.1 Marked weight loss, induced by bariatric surgery, decreases steatosis.2-8 but has also been reported to increase hepatic inflammation and fibrosis.2,3 It has been hypothesized that rapid weight loss associated with bariatric surgery has adverse
effects on the liver because increased liver inflammation and fibrosis also occur after fasting9 and very-low-calorie diet therapy.10 This figure shows data from a longitudinal study that obtained liver tissues samples during gastric bypass surgery and one-year surgery when subjects had lost about 25% of their initial body weight. These data demonstrate that surgery-induced weight loss causes a decrease in hepatic steatosis without worsening hepatic inflammation or fibrosis.11 
References:
Palmer M, Schaffner F. Effect of weight reduction on hepatic abnormalities in overweight patients. Gastroenterology. 1990;99:1408-13.
Luyckx FH, Desaive C, Thiry A, et al. Liver abnormalities in severely obese subjects: effect of drastic weight loss after gastroplasty. Int J Obes Relat Metab Disord. 1998;22:222-6.
Kral JG, Thung SN, Biron S, et al. Effects of surgical treatment of the metabolic syndrome on liver fibrosis and cirrhosis. Surgery. 2004;135:48-58.
Dixon JB, Bhathal PS, Hughes NR, O'Brien PE. Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss. Hepatology. 2004;39:1647-54.
Silverman EM, Sapala JA, Appelman HD. Regression of hepatic steatosis in morbidly obese persons after gastric bypass. Am J Clin Pathol. 1995;104:23-31.
Ranlov I, Hardt F. Regression of liver steatosis following gastroplasty or gastric bypass for morbid obesity. Digestion. 1990;47:208-14.
Halverson JD, Zuckerman GR, Koehler RE, Gentry K, Michael HE, DeSchryver-Kecskemeti K. Gastric bypass for morbid obesity: a medical-surgical assessment. Ann Surg. 1981;194:152-60.
Clark JM, Alkhuraishi AR, Solga SF, Alli P, Diehl AM, Magnuson TH. Roux-en-Y gastric bypass improves liver histology in patients with non-alcoholic fatty liver disease. Obes Res. 2005;13:1180-6.
Capron JP, Delamarre J, Dupas JL, Braillon A, Degott C, Quenum C. Fasting in obesity: another cause of liver injury with alcoholic hyaline? Dig Dis Sci. 1982;27:265-8.
Andersen T, Gluud C, Franzmann MB, Christoffersen P. Hepatic effects of dietary weight loss in morbidly obese subjects. J Hepatol. 1991;12:224-9.
Klein S, Mittendorfer B, Eagon JC, et al. Gastric bypass surgery improves metabolic and hepatic abnormalities associated with nonalcoholic fatty liver disease. Gastroenterology. 2006;130:1564-72.
Long-term Survival: Canada
Rel. Risk = 0.11 (.04-.27)
89% reduction in risk of
death over 5 years
Christou et al. Ann Surg 2004;240:416-424
% Mortality
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69
Long-term survival: Canada
In addition to this study by Christou et al.,1 there have been a number of other published studies or abstracts documenting a decreased mortality after bariatric surgery when compared to matched cohorts.2-7 Most of the improvement is due to decreased diabetes, myocardial infarction, and cancer-related deaths.
References:
Christou NV, Sampalis JS, Liberman M, et al. Surgery decreases long-term mortality, morbidity, and health care use in morbidly obese patients. Ann Surg. 2004;240:416-23.
MacDonald KG Jr, Long SD, Swanson MS, et al. The gastric bypass operation reduces the progression and mortality of non-insulin-dependent diabetes mellitus. J Gastrointest Surg. 1997;1:213-20.
Flum DR, Dellinger EP. Impact of gastric bypass operation on survival: a population-based analysis. J Am Coll Surg. 2004;199:543-51. 
Sjostrom L. Soft and hard endpoints over 5 to 18 years in the intervention trial Swedish obese subjects (abstract). Obesity Reviews. 2006;7 S2:27.
Peeters A, O'Brien P, Laurie C, et al. Does weight loss improve survival? Comparison of a bariatric surgical cohort with a community based control group (abstract). Obesity Reviews. 2006;7 S2:95.
 Adams T, Gress R, Smith S, et al. Long-term mortality following gastric bypass surgery (abstract). Obesity Reviews. 2006;7 S2:94.
 Busetto L, Mazza M, Miribelli D, et al. Total mortality in morbid obese patients treated with laparoscopic adjustable gastric banding: A case-control study (abstract). Obesity Reviews. 2006;7 S2:95.
Basic Principles of Obesity Therapy
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Obesity Therapy
Adipose 
tissue
Energy 
Intake
Energy 
Expenditure
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Obesity therapy
The cornerstone of obesity treatment involves consuming less calories that are expended to mobilize and oxidize endogenous triglycerides as fuel. Approximately 75%–85% of weight that is lost by dieting is composed of fat, and 15%–25% is fat-free mass [1]. Most, if not all, of the loss of fat is due to a decrease in adipocyte triglyceride content [2]. It is also possible that long-term weight loss can decrease the number of fat cells [3] by stimulating apoptosis (programmed cell death) or morphologic reversion of mature adipocytes to preadipocytes. However, these possibilities have not been evaluated in obese subjects. This section provides an overview of the the key therapeutic principles involved in obesity management.
Ballor DL, Poehlman ET. Exercise-training enhances fat-free mass preservation during diet-induced weight loss: a meta-analytical finding. Int J Obes Relat Metab Disord 1994;18:35-40.
Knittle JL, Ginsberg-Fellner F. Effect of weight reduction on in vitro adipose tissue lipolysis and cellularity in obese adolescents and adults. Diabetes 1972;21:754-761. 
Naslund I, Hallgren P, Sjostrom L. Fat cell weight and number before and after gastric surgery for morbid obesity in women. Int J Obes 1988;12:191-197.
Short-term Obesity Therapy Does Not Result in Long-term Weight Loss
Change in Weight (kg)
Wadden et al. Int J Obes 1989;13 (Suppl 2):39.
5-year
Follow-up
1-year
Follow-up
End of
Treatment
Baseline
Diet alone
Behavior therapy
Combined therapy
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Short-term obesity therapy does not result in long-term weight loss
Obesity is a chronic disease that requires long-term therapy for successful long-term weight management. Often, patients who are able to lose weight with obesity therapy regain their lost weight after therapy is discontinued. This figure represents data from 76 obese women (mean body mass index 39.4 kg/m2) who were were randomly assigned to one of three treatment groups: 4 months of a very-low-calorie diet (VLCD) of 400–500 kcal/d, 6 months of behavior therapy and a 1000–1200 kcal/d balanced deficit diet, or 6 months of a combination of a VLCD and behavior therapy. Each treatment program was effective in achieving short-term weight loss. However, most subjects regained a considerable amount of weight by 1 year and had returned to their pretreatment weight at 5 years.
Wadden TA, Sternberg JA, Letizia KA, et al. Treatment of obesity by very low calorie diet, behavior therapy, and their combination: a five-year perspective. Int J Obes 1989;13 (suppl 2):39-46.
Long-term Weight Loss is Improved with Long-term Maintenance Therapy
Weight Loss (%)
Perri et al. J Consult Clin Psychol 1988;56:529.
0
1
2
3
4
5
6
7
8
9
10
11
12
Time (mo)
13
14
15
16
17
P <0.05
No maintenance tx
Maintenance tx
Diet and
behavior
modification
therapy
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Long-term weight loss is improved with long-term maintenance therapy
Maintenance therapy is important for long-term weight management success after initial weight loss is achieved by diet and behavior therapy. In this study, Perri and colleagues [1] randomized obese subjects who lost weight after 5 months of diet and behavior modification therapy to “no maintenance” or a “maintenance program” that involved biweekly contact. At 1 year after initial weight loss was achieved, participants who received maintenance therapy maintained long-term weight loss, whereas those who did not receive maintenance therapy regained half of their lost weight. 
Perri MG, McAllister DA, Gange JJ, et al. Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol 1988;56:529-534.
Obesity Treatment Pyramid
Diet
Physical Activity
Lifestyle Modification
Pharmacotherapy
Surgery
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Obesity treatment pyramid
The clinical approach to obesity can
be viewed as a pyramid consisting of several levels of therapeutic options. All patients should be involved in an effort to change their lifestyle behaviors to decrease energy intake and increase physical activity. Lifestyle modification also should be a component of all other levels of therapy. Pharmacotherapy can be a useful adjunctive measure for properly selected patients. Bariatric surgery is an option for patients with severe obesity, who have not responded to less-intensive interventions. The number of obese patients who require a specific level of treatment decreases as one moves up the pyramid.
Obesity Treatment Guidelines
The Practical Guide
can be found at:
NHLBI web site:
www.nhlbi.nih.gov
NAASO web site:
www.naaso.org
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Obesity treatment guidelines
The National Institutes of Health in conjunction with the National Heart, Lung, and Blood Institute (NHLBI) and the North American Association for the Study of Obesity have developed a Practical Guide for the identification, evaluation, and treatment of overweight and obesity in adults [1]. The Practical Guide is based on the clinical guidelines that were developed by the NHLBI’s Obesity Education Initiative, in cooperation with the National Institute of Diabetes and Digestive and Kidney Diseases, in June 1998. The Practical Guide contains useful information on diet therapy, physical activity, and behavior therapy and also provides guidance on the appropriate use of pharmacotherapy and surgery for healthcare practitioners.
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub No 00-4084.
Guide for Selecting Obesity Treatment
Treatment
25-26.9
27-29.9
30-34.9
35-39.9
>40
Diet, Exercise, Behavior Tx
+
+
+
+
+
Pharmaco-therapy
With co-
morbidities
+
+
+
Surgery
With co-
morbidities
+
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub. No.00-4084
BMI Category (kg/m2)
76
Guide for selecting obesity treatment
This table summarizes the guidelines for selecting treatment options for obesity [1]. Any effective treatment plan must consider the patient’s willingness to undergo therapy, his/her ability to comply with specific treatment approaches, access to skilled caregivers, and financial considerations. Lifestyle modification, which involves a program of appropriate diet, physical activity, and behavior therapy, should be considered for all patients with a body mass index (BMI) 25 kg/m2. Long-term pharmacotherapy should be considered in appropriate patients who were unable to achieve adequate weight loss after 6 months of lifestyle therapy and who have a BMI 30 kg/m2, or 27 kg/m2 with concomitant obesity-related disease. Bariatric surgery may be necessary in patients with severe obesity who failed to lose weight with non-surgical therapy. Eligible surgical candidates should have a BMI 40 kg/m2 or a BMI 35 kg/m2 and a concomitant serious obesity-related disease. 
The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. October 2000, NIH Pub No 00-4084.
 
Major Obesity-related Comorbidities That Have Been Improved by Bariatric Surgery
Type 2 diabetes
Hypertension
Obstructive sleep apnea
Obesity hypoventilation
GERD
NALD, NASH
Pseudotumor cerebri
Depression
Dyslipidemias
Coronary artery disease
Cardiac dysfunction
Venous stasis disease
Polycystic ovary syndrome
Infertility
Cancers
Degenerative joint disease
Quality of life
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77
Major obesity-related comorbidities that have been improved by bariatric surgery
Numerous comorbidities as listed above have been shown to resolve or markedly improve.
Reference:
Sugerman HJ, Kral JG. Evidence-based medicine reports on obesity surgery: a critique. Int J Obes (Lond). 2005;29:735-45.
Obesity and Dietary Therapy
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Obesity and dietary therapy
Ad Libitum Low-Fat Diets Decrease Daily Energy Intake
Lee-Han, 1988
Boyd, 1990
Sheppard, 1991
Kasim, 1993
Pritchard, 1996
Siggaard, 1996
Simon, 1997
Weststate, 1998
Stefanick (M), 1998
Stefanick (F), 1998
Saris SCHO, 2000
Saris CCHO, 2000
Weighted sum
Astrup et al. Int J Obes Relat Metab Disord 2000;24:1545. 
Copyright 2002 McMillan Publishers Ltd. Reprinted with permission.
Meta-analysis of 12 Intervention Trials
Change in Energy Intake on Low-fat Diet (kJ/d) 
2000
0
-2000
-4000
-6000
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79
Ad libitum low-fat diets decrease daily energy intake
Dietary fat is composed primarily of triglycerides, which increase food palatability and energy-density. Therefore, low-fat diets often are prescribed for obese patients because these diets facilitate energy restriction. This figure shows the individual and combined results from 12 controlled trials, involving a total of 1910 subjects, that evaluated the effect of an ad libitum low-fat diet on daily energy intake [1]. At baseline, all subjects consumed a diet that contained approximately 38% of total calories as fat. Initiating an ad libitum low-fat diet resulted in a weighted overall 10.8% decrease in the percent of total calories consumed as fat and a 1138 kJ/d (272 kcal/d) decrease in energy intake, as compared with the control group (P=0.002). 
Astrup A, Grunwald GK, Melanson EL, et al. The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies. Int J Obes Relat Metab Disord 2000;24:1545-1552.
Decreasing Dietary Fat is Associated with a Decrease in Body Weight
Analysis of 37 Diet Intervention Studies
Change in Body Weight (kg)
Change in Dietary Fat (% of Energy Intake)
Yu-Poth et al. Am J Clin Nutr 1999;69:632. 
© American Society for Clinical Nutrition. Reproduced with permission.
-30
-25
-20
-15
-10
-5
0
5
10
r = 0.46.
9:32 
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Decreasing dietary fat is associated with a decrease in body weight
This figure shows the results of a meta-analysis of 37 diet intervention studies, conducted in a total of 9276 subjects who were given the National Cholesterol Education Program’s Step I or Step II reduced-fat diets (30% of total energy intake from fat) [1]. The data show that decreasing dietary fat was directly associated with a decrease in body weight. Changes in percent dietary fat were also highly correlated with changes in energy intake. For every 1% decrease in energy from fat there was a corresponding 0.28 kg weight loss. The broken line illustrates that a 10% decrease in the percent of calories from fat was associated with a 3-kg decrease in body weight. 
Yu-Poth S, Zhao G, Etherton T, et al. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-646.
Relationship Between Dietary Macronutrient Composition and Body Weight
Time (months)
Body Weight (% change)
Control:
35% Fat
45% CHO
Saris WHM et al.,Int J Obes 24:1310,2000
0
2
4
6
25% Fat
55% simple CHO
28% Fat
52% complex CHO
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Relationship between dietary macronutrient composition and body weight
This figure shows the results of a clinical trial that randomized subjects to a low fat diet with either simple or complex carbohydrates (CHO), or to a standard diet containing 35% calories from fat [1]. The data indicate that decreasing dietary fat intake (to 25-30% of total calories) results in decreased total energy intake and modest weight loss. 
Saris WH, Astrup A, Prentice AM, Zunft HJ, Formiguera X, Verboeket-van de Venne WP, Raben A, Poppitt SD, Seppelt B, Johnston S, Vasilaras TH, Keogh GF: Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates on body weight and blood lipids: the CARMEN study. The Carbohydrate Ratio Management in European National diets. Int J Obes Relat Metab Disord. 24:1310-1318, 2000.
Fat Content of Selected Foods
Grams/unit
Adapted from Alpers et al. Manual of Nutritional Therapeutics (4th ed); 
Lippincott: Philadelphia, 2002.
 Whole milk (1 cup)
 Skim milk (1 cup)
 Butter (1 tbs)
 Margarine (1 tbs)
 American cheese (1 oz)
 Ice cream (1 cup)
 Boiled shrimp
 Fried shrimp 
 Flatfish fillet
 Salmon fillet
Chicken: White, no skin
 Dark, no skin
 Dark, fried
Ground beef
 Ground beef, lean
Sirloin steak
 Sirloin steak, trimmed
 Sponge cake (1 slice)
 Chocolate cake (1 slice)
Baked potato (3 oz)
 French fries (3 oz)
 Potato chip (1 oz)
Dairy products
Meat products
(3 oz servings)
Other products
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Fat content of selected foods
This figure depicts the fat content of selected dairy products, meat products, and other foods. The data illustrate the differences in fat content between popular foods, and the effect of food preparation on fat content. For example, untrimmed sirloin steak has approximately 19 g of fat per 3 oz serving, the highest fat content of all meat products shown; whereas, sirloin steak with the fat trimmed away has only 3 g of fat per 3 oz serving. Moreover, trimmed sirloin steak contains less fat than dark meat chicken. Frying food has a marked affect on fat content. Boiled shrimp has much less fat per serving than does fried shrimp, and french fries and potato chips have substantially more fat than does a baked potato.
Alpers et al. Manual of Nutritional Therapeutics (4th ed); Lippincott: Philadelphia, 2002.
Energy Density of Selected Foods
Energy Density (kcal/g)
Lettuce
Vegetable soup
Skim milk
Apple
Black beans
White fish
Yogurt
Vegetable lasagna
Roast chicken
White bread
Pretzels
Cheddar cheese
Salad dressing
Potato chips
Bacon
Butter
Reprinted from Klein S, et al. Gastroenterology. 2002: 123:882-932 
with permission from Elsevier.
83
Energy density of selected foods
This slide depicts the energy density of selected popular foods. Foods shown in yellow are low in energy density (1.0 kcal/g), and include fruits, vegetables and low-fat foods. Foods shown in orange are of medium energy density (1.1 to 4.0 kcal/g), and include many meats, cheeses, and desserts. Foods shown in blue are high in energy density (>4.0 kcal/g), and include high-fat and dry foods. The average energy density of a typical diet is around 1.8 kcal/g, not including beverages. Adding low-energy-density foods (e.g., vegetables) to specific dishes (e.g., soups, casseroles, and stews) lowers their overall energy density. Choosing low-energy-density foods allows dieters to eat larger portions while reducing calories.
Weight Loss at 6-Months in RCTs of Low-fat vs Low-Carbohydrate Diets
Weight Loss (kg)
Difference
Study
n
Low-fat
Low-carb
(kg)
Samaha
(2003)
132
-1.9
-5.8
3.9
Brehm
(2003)
42
-3.9
-8.5
4.6
Foster
(2003)
63
-5.3
-9.6
4.3
Yancy
(2004)
120
-6.5
-12.0
5.5
84
Weight loss at 6-months in RCTs of low-fat vs low-carbohydrate diets
Recently, there has been increased interest in the use of low-carbohydrate diets as potential therapy for obesity. The results of five RCTs in adults [1-5] found that subjects randomized to a low-carbohydrate, high protein/high fat diet (approximately 25-40% carbohydrate) achieved greater short-term (6 months) [1-4], but not long-term (12 months) [3, 5], weight loss than those randomized to a low-fat diet (approximately 25-30% fat, 55-60% carbohydrate). A consistent difference in weight loss at 6 months was observed between groups across studies; subjects randomized to the low-carbohydrate diet lost 4-5 kg more weight than those randomized to the low-fat diet. The data from these studies also found greater improvements in serum triglyceride and HDL-cholesterol concentrations, but not in serum LDL-cholesterol concentration, in the low-carbohydrate group than in the low-fat group. In addition, glycemic control was better with low-carbohydrate than a low-fat diet therapy in subjects who had type 2 diabetes [1, 5]. 
Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L: A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 348:2074-2081, 2003.
Brehm BJ, Seeley RJ, Daniels SR, D'Alessio DA: A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol.Metab 88:1617-1623, 2003
Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S: A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 348:2082-2090, 2003.
Yancy WS, Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia. Ann Intern Med 2004;140:769-777. 
Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow up of a randomized trial. Ann Intern Med 2004;140:778-785.
Effect of Sucrose-Sweetened Drinks on Total Energy Intake
Energy Intake (kcal)
Rolls et al. Physiol Behav 1990;48:19.
*P<0.01 vs other groups.
16 oz Drink
w/Sucrose
16 oz
Water
No Drink
*
Food Drink
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Effect of sucrose-sweetened drinks on total energy intake
The consumption of sucrose-sweetened drinks can lead to excessive energy intake. This figure shows the results from a study conducted in young adult men who received test meals on three different occasions [1]. At each meal, they were allowed to eat as much food as they chose and were given either 16 oz of sucrose-sweetened lemonade (166 kcal), an equal volume of water, or no drink at all. Total energy intake was greater when sucrose-sweetened lemonade was consumed than when water or no fluid was provided. In addition, sugar-sweetened drinks were not as effective as water in reducing thirst. The use of an intense artificial sweetener, aspartame, rather than sucrose prevented the increase in energy consumption associated with sugar-sweetened beverages. These data demonstrate that consumption of sucrose-sweetened beverages does not result in a compensatory decrease in energy consumed as food. Therefore, drinking water, or other low-calorie beverages, instead of sugar-sweetened drinks may be a useful weight management tool.
Sugar-sweetened drinks are a particular concern in children because children often consume large amounts of soft drinks. A recent prospective, observational analysis showed a significant relationship between the consumption of sugar-sweetened drinks and the prevalence of obesity in children [2].
Rolls BJ, Kim S, Fedoroff IC. Effects of drinks sweetened with sucrose or aspartame on hunger, thirst and food intake in men. Physiol Behav 1990;48:19-26.
Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001;357:505-508.
Blood Glucose Concentrations After Ingesting High and Low Glycemic Index Foods
Adapted from: Anderson et al. Modern Nutrition
in Health and Disease; 2001:1269.
*containing 50 g glucose
Blood Glucose (mg/dL)
Time (min)
0
30
60
90
120
New potatoes*
Kidney beans*
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Blood glucose concentrations after ingesting high and low glycemic index foods
Glycemic index refers to the increase in blood glucose that occurs after consumption of a food containing a standard amount of carbohydrate. The index represents the comparison of a tested food to a standard amount (50 g) of glucose. This figure illustrates the differences in blood glucose concentrations that are achieved after ingesting a food that has a high glycemic index (new potatoes) and a food that has a low glycemic index (kidney beans). The index number is the area under the blood glucose concentration curve during the 2 hours after food ingestion and represents the rate of digestion
and absorption of the carbohydrate present in the food being evaluated. Glucose has the highest glycemic index and is rated at 100. Low-glycemic-index foods have a glycemic index less than 55. Most refined grain products and potatoes have a high glycemic index, whereas most fruits, legumes, and non-starchy vegetables have a low glycemic index. However, the “true” glycemic index of a specific food that is ingested as part of a meal can be altered by several factors, such as the method of preparation and the effect of concomitantly ingested foods on intestinal motility. For example, a high-glycemic index food may cause a mild increase in blood glucose concentration if gastric emptying is slowed by simultaneous fat ingestion.
A low-glycemic-index diet has been proposed as a treatment for obesity because it may affect hunger by specific effects on postprandial pancreatic hormone secretion [3]. The results of one randomized controlled trial, conducted in 14 overweight adolescents, found a reduced glycemic index diet caused weight loss, while a low fat diet caused weight gain (2). However, additional randomized controlled trials conducted in a larger number of subjects are needed to evaluate the potential efficacy of a low-glycemic diet as a therapy for obesity.
Jenkins DJ, Wolever TM, Jenkins AL. Starchy foods and glycemic index. Diabetes care 1988;11:149-159.
Anderson JW, Geil PB. Nutritional management of diabetes. In: Shils ME, Olson JA, Shike M, eds. Modern Nutrition in Health and Disease. 8th ed. Philadelphia, PA: Lea & Febiger; 1994:1259-1286.
Ludwig DS, Majzoub JA, Al-Zahrani A, et al. High glycemic index foods, overeating, and obesity. Pediatrics 1999;103:261-266.
Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS: A reduced-glycemic load diet in the treatment of adolescent obesity. Arch Pediatr Adolesc.Med 2003;157:773-779.
Spieth LE, Harnish JD, Lenders CM, et al. A low-glycemic index diet in the treatment of pediatric obesity. Arch Pediatr Adolesc Med 2000;154:947-951.
Effect of Portion Size on Energy Intake
500
Amount Consumed (g)
Amount of Macaroni and Cheese Served (g)
Rolls et al. Am J Clin Nutr. 2000 Dec;76(6):1207-13.
625
750
1000
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Effect of portion size on energy intake
Food portion size affects energy intake. In this study, young adult men and women were served four different portions of macaroni and cheese for lunch on different days, and were allowed to consume as much food as they liked [1]. The data demonstrate a linear relationship between portion size served and intake: increasing the amount of macaroni and cheese served increased the amount that was consumed. 
Rolls BJ, Morris EL, Roe LS. Portion size of food affects energy intake in normal-weight and overweight men and women. Am J Clin Nutr 2002 Dec;76(6):1207-13.
VLCDs Do Not Produce Greater Long-term Weight Loss Than LCDs
Wadden et al. J Consult Clin Psychol 1994;62:165. Copyright 1994 by the American Psychological Association. Reprinted with permission.
Weight Loss (kg)
Time (wk)
0
26
52
78
Biweekly 
behavior therapy
Weekly 
behavior therapy
Very-low-calorie diet (420 kcal/d)
Low-calorie diet (1200 kcal/d)
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VLCDs do not produce greater long-term weight loss than LCDs
Very-low-calorie diets (VLCDs) usually provide 400–800 kcal/d and produce an average weight loss of approximately 20 kg over 12 to 16 weeks [1]. However, these diets may not result in greater long-term weight loss than standard low-calorie diets (LCD), which provide 1200–1500 kcal/d, because of greater regain of lost weight. This figure illustrates the data from a randomized, prospective study conducted in 49 obese women that compared the effect of a VLCD with a LCD on short-term and long-term weight loss [2]. Subjects were randomized to behavior therapy combined with either a LCD (1200 kcal/d) throughout treatment or with short-term use of a VLCD (420 kcal/d) for 16 wks followed by a 1200 kcal/d diet thereafter. All subjects attended weekly group behavior therapy sessions for 52 weeks, and then biweekly sessions for an additional 26 weeks. Initial weight loss was more rapid and of greater magnitude in those randomized to a VLCD than a LCD; at week 26, the VLCD group had lost significantly more weight than the LCD group (21.5 kg vs 11.9 kg). However, the VLCD group regained weight rapidly, so total weight loss was similar in both groups by 78 weeks. The use of a VLCD requires more medical supervision than does the use of a LCD, because rapid weight loss associated with VLCDs increases the risk of gallstone formation, dehydration, and electrolyte abnormalities.
Wadden TA, Van Itallie TB, Blackburn GL. Responsible and irresponsible use of very-low-calorie diets in the treatment of obesity. JAMA 1990;263:83-85.
Wadden TA, Foster GD, Letizia KA. One-year behavioral treatment of obesity: comparison of moderate and severe caloric restriction and the effects of weight maintenance therapy. J Consult Clin Psychol 1994;62:165-171.
Energy Content of Alcoholic Beverages
Alcohol contains 7 kcal/g
Beer
12 oz
160 calories
Wine
5 oz
100 calories
Margarita
8 oz
270 calories
Gin and Tonic
8 oz (contains
1.7 oz gin)
190 calories
1 shot of liquor
2 oz
128 calories
89
Energy content of alcoholic beverages
Alcohol intake can increase total energy intake because it provides 7 kcal per gram and often stimulates appetite. Alcohol consumption increases the number of calories in a diet and has been associated with obesity in both epidemiologic and experimental studies [1]. Therefore, ingestion of alcoholic beverages should be limited in patients trying to lose weight or maintain weight loss. The energy content of selected alcoholic beverages is shown on this slide. The total energy content (in kcal) of an alcoholic beverage can also be estimated by using the following formula: 0.83 x proof of beverage x ounces of beverage. 
National Institutes of Health, National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report. Obes Res 1998;6(suppl. 2):51S-209S.
<15%
Saturated fatty
acids
Polyunsaturated
fatty acids
Monounsaturated
fatty acids
8%-10%
<10%
Recommended Nutrient Content of a Weight-Reducing Diet
Carbohydrate
>55%
Protein
15%
Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults– The Evidence Report. Obes Res. 1998;6 (suppl 2).
Fat
<30%
Calories: 500-1000 kcal/d reduction
Cholesterol: <300 mg/d
Fiber: 20-30 g/d
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90
Recommended nutrient content of a weight-reducing diet
Dietary guidelines proposed by the National Institutes of Health [1] recommend a 500 kcal/d deficit for overweight persons (BMI 25.0-29.9 kg/m2) who have obesity-related complications, and for persons with class I obesity (BMI 30-34.9 kg/m2). This energy deficit will result in approximately a 1-lb (0.45 kg) weight loss per week and about a 10% weight reduction at 6 months. A 500-1000 kcal/d deficit is recommended for those with class II (BMI 35.0-39.9 kg/m2) or class III (BMI 40 kg/m2) obesity, which will produce about a 1- to 2-lb weight loss per week and a 10% weight loss at 6 months. The recommended macronutrient composition for a low-calorie weight loss diet is shown in this figure and includes 55% or more of daily calories from carbohydrates, 15% from protein, and 30% or less from fat. In addition, specific recommendations are made regarding the composition of fat ingestion: total energy intake should be comprised of 8%-10% calories from saturated fat, 10% or less calories from polyunsaturated fats, and 15% or less calories from monounsaturated fats. Daily cholesterol intake should not exceed 300 mg/d, and daily fiber intake should be between 20-30 g/d.
National Institutes of Health, National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation,
and Treatment of Overweight and Obesity in Adults – The Evidence Report. Obes Res. 1998;6(suppl 2):51S-209S.
Obesity Treatment
The Role of Physical Activity
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Obesity treatment: the role of physical activity
Benefits of Regular Physical Activity in Obese Persons
Decreases loss of fat-free mass associated with weight loss
Improves maintenance of weight loss
Improves cardiovascular and metabolic health, independent of weight loss
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Benefits of regular physical activity in obese persons
Regular physical activity is an important component of any weight loss program because it is associated with long-term weight maintenance and has beneficial health effects, such as decreasing coronary heart disease and diabetes, that are independent of weight loss itself. The important physiological and clinical issues regarding the use of physical activity as part of obesity therapy will be reviewed in this section.
Keywords: physical activity, cardiovascular health, metabolic health, coronary heart disease, type 2 diabetes mellitus
Physical Activity Helps Preserve Fat-Free Mass During Weight Loss
Diet Only
Loss of Fat-Free Mass
(% Total Weight Loss)
Diet Plus
Physical Activity
Men
Women
*P<0.05
Reprinted with permission from Int J Obes Relat Metab Disord, Ballor 
and Poehlman;18:35. Copyright 1994 Macmillan Publishers Ltd. 
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Physical activity helps preserve fat-free mass during weight loss
Approximately 75% of weight that is lost by dieting is composed of fat and 25% is fat-free mass (FFM) [1]. Adding a physical activity program to dietary therapy can affect the composition of weight loss. Two meta-analyses that pooled data from 46 [1] and 28 [2] published trials found that exercise can attenuate the loss of FFM. In subjects with a mean weight loss of 10 kg, regular exercise decreased the percentage of weight lost as FFM by half, from approximately 28% to 13% in men and from 24% to 11% in women (P<0.05). However, this large difference in percentage of weight lost as FFM represented only a small (approximately 1 kg) difference in the absolute amount of FFM lost between groups. Moreover, conservation of FFM does not necessarily represent conservation of muscle protein; the greater retention of FFM associated with exercise may be related to increased retention of body water and muscle glycogen. It is not known whether performing resistance exercise while dieting leads to greater conservation of FFM than performing endurance exercise because of limited and conflicting data [3,4]. 
Ballor DL, Poehlman ET. Exercise-training enhances fat-free mass preservation during diet-induced weight loss: a meta-analytical finding. Int J Obes Relat Metab Disord 1994;18:35-40.
Garrow JS, Summerbell CD. Meta-analysis: effect of exercise, with or without dieting, on the body composition of overweight subjects. Eur J Clin Nutr 1995;49:1-10. 
Wadden TA, Vogt RA, Anderson RE, et al. Exercise in the treatment of obesity: effects of four interventions on body composition, resting energy expenditure, appetite and mood. J Consult Clin Psychol 1997;65:269-277.
Geliebter A, Maher MM, Gerace L, et al. Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr 1997;66:557-563. 
Keywords: physical activity, fat-free mass, FFM, weight loss
Physical Activity Alone Results in Minimal Weight Loss
Wing. Med Sci Sports Exerc 1999;31(suppl):S547.
*P<0.05 vs control group
Duration of each study ranged from 4 to 12 months.
Stefanick 1998
Stefanick 1998a
Anderssen 1995
Hammer 1989
Verity 1989
Rönnemaa 1988
Wood 1988
Wood 1983
Weight loss (kg)
Control Group
Exercise Group
*
*
*
*
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Physical activity alone results in minimal weight loss
Exercise alone, without concomitant dietary therapy, produces minimal weight loss. The results from most studies have demonstrated that participating in regular endurance exercise activities (eg, brisk walking for 45–60 min, 4 times weekly) for up to a year without an energy-restricted diet, usually results in minimal weight loss (an average 2-kg decrease in body weight compared with a control group) [1-8]. Moreover, it is not known whether weight loss was due to exercise alone or whether the participants also altered their dietary intake because they were enrolled in an exercise program. In addition, these data may not represent the effect of exercise in obese persons because most subjects enrolled in these studies were slightly overweight men. Vigorous exercise training causes much greater losses in body weight when energy intake is held constant [9].
Wing RR. Physical activity in the treatment of the adulthood overweight and obesity: current evidence and research issues. Med Sci Sports Exerc 1999;31(suppl)S547-S552.
Anderssen S, Holme I, Urdal P, Hjermann I. Diet and exercise intervention have favourable effects on blood pressure in mild hypertensives: the Oslo Diet and Exercise Study (ODES). Blood Press 1995;4:343-349.
Hammer RL, Barrier CA, Roundy ES, et al. Calorie-restricted low-fat diet and exercise in obese women. Am J Clin Nutr 1989;49:77-85.
Rönnemaa T, Marniemi J, Puukka P, Kuusi T. Effects of long-term physical exercise on serum lipids, lipoproteins, and lipid metabolizing enzymes in type 2 (non-insulin-dependent) diabetic patients. Diabetes Res 1988;7:79-84.
Stefanick ML, Mackey S, Sheehan M, et al. Effects of the NCEP Step 2 diet and exercise on lipoprotein in postmenopausal women and men with low high density lipoprotein (HDL)-cholesterol and high low density lipoprotein (LDL)-cholesterol. N Engl J Med 1998;329:12-20. 
Verity LS, Ismail AH. Effects of exercise on cardiovascular disease risk in women with NIDDM. Diabetes Res Clin Pract 1989;6:27-35.
Wood PD, Haskell WL, Blair SN, et al. Increased exercise level and plasma lipoprotein concentrations: a one-year, randomized, controlled study in sedentary, middle-aged men. Metabolism 1983;32:31-37. 
Wood PD, Stefanick ML, Dreon DM, et al. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med 1988;319:1173-1179. 
Bouchard C, Tremblay AJ, Nadeau A, et al. Long-term exercise training with constant energy intake: effect on body composition and selected metabolic variables. Int J Obes 1990;14:57-73. 
Keywords: physical activity, energy intake, exercise training
Effect of 16-month Supervised Aerobic Exercise on Body Weight in Overweight and Obese Young Adults
Donnelly et al.Arch Intern Med 2003;163:1343
*p<0.05 vs control
Weight Change (kg)
Men
Women
*
Control
Exercise
*
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Effect of 16-month supervised aerobic exercise on body weight in overweight and obese young adults
An carefully supervised aggressive exercise program may have greater effects on body weight than less rigorous exercise. This figure shows the results of a 16-month study that randomized 131 sedentary young adult men and women (average age 23 years old; range 17-35 years old) who were overweight and obese (average BMI 29 kg/m2; range 25.0-34.9 kg/m2) to either a control or exercise group [1]. The exercise group participated in supervised aerobic exercise performed at moderate intensity (55%-70% of their maximal oxygen consumption) during 45 minute sessions, 5 days/week for 16 months. The data are from those subjects who completed the entire 16-month study, representing 75% of the control group and 47% of the exercise group. Men and women randomized to exercise who completed the study, completed approximately 90% of the exercise sessions. By the end of the study, men were expending about 3300 kcal/wk and women about 2200 kcal/wk from supervised exercise. Exercise did not change total energy intake or dietary macronutrient composition [2]. These data demonstrate that 16 months of moderate intensity aerobic exercise for 45 min/day, 5 days/wk causes weight loss in young men and prevents weight