INTRODUCTION
Maybe you often ask to your sely "why you can be obese?". In this sesassion I will tell you why some one can be obese. Reading this article and givi information to another people. God Bless You...
The weight and body composition remain relatively constant in the adult for long periods of time, despite fluctuations in the daily intake and expenditure energético1. In this sense, it assumes the existence of regulatory processes, which conform precisely the nutrient fuels and energy demands to maintain a body mass estable2-4. This balance seems to include a series of highly integrated physiological mechanisms that contribute to the regulation of body weight and tissue deposits adipose.
In this context, the laws of conservation and energy conversion are implementing agencies vivos11 12. The control of appetite as well as the stability of body composition has been attributed, according to different hypothesis on the existence of a physiological levels set for the weight corporal13, 14, regulating appetite through processes glucostáticos or glucogenostáticos15-17, use of substrates energéticos18 homeostatic-20 system involvement nervioso21-23 and a adipostato mediated signals produced in the tissue adiposo24-27 or conductuales28 models. Furthermore, the description of mutations associated with obesity and the identification of transcription factor or nutrient, which regulates the function and differentiation of adipocytes or the expression of genes affecting lipid content, are new areas of research interest in this campo29, 30, among them the resistina, linking diabetes with obesidad31.
WEIGHT AND REGULATION OF ADIPOSE DEPOSITE
The accuracy of the regulation of body weight (often ± 1% for years) requires powerful feedback mechanisms that control the body mass grasa7, 32. However, a continued imbalance between intake and energy expenditure in daily life contributes to the development of obesidad33-35. Other factors such as the distribution of macronutrients in the diet, the involvement of different components of energy expenditure (basal metabolic rate, thermogenic effect of food and physical activity) and metabolism of nutrients específicos36-38 also influence the energy equation. In this context, we can hypothesize that the control of body weight and composition depends on a shaft with three closely interrelated components: 1) appetite, 2) nutrient metabolism and thermogenesis and 3) body fat deposits, of which there are complex feedback mechanisms between ellos7. However, it should be assumed that body weight is ultimately determined by the interplay of genetic, environmental (dietary habits and physical activity) and psychosocial working through different physiological mechanisms of appetite and metabolism energético39, 41.
Appetite
The appetite center, located in the central nervous system is sensitive to different sensory signals mediated by circadian rhythms or the relaxation or release of local hormones and nutritional signals, which modulate food intake through different mechanisms measured by specific neurotransmisores40, 42 -43, including monoamines (noradrenaline, dopamine, serotonin, etc..) amino acids (tryptophan, tyrosine, GABA, etc..) and neuropeptides (orexinas, melanocortinas, pancreatic polypeptides, hormone releasing factors, such as the gastrointestinal peptides colecistoquinina and neuropeptide Y, etc.).. All these factors generate neural and endocrine signals that trigger appropriate quantitative and qualitative adjustments not only on the intake of nutrients, but also on the metabolism energético18, 44. Theories glucostática, lipostática and aminostática appetite did not seem sufficient to explain these processes reguladores17, 45. Thus, the autonomic nervous system and various circulating hormones (insulin, cortisol, growth hormone, etc..) Are involved in the metabolic response to the intake of alimentos46-48.
Nutrient metabolism and thermogenesis
A second control circuit include the regulation of metabolic substrates and thermogenesis, which not only depend on the nutrient intake but also of the specific regulation of its use through processes nervous, endocrine and enzimáticos7, 49 and the existence of futiles50 cycles. In this regard, lipid oxidation is poorly regulated with respect to the oxidation of protein and carbohydrates after the ingesta51, 52. Furthermore, the thermogenic response of brown adipose tissue is the result of a balance between the influences of central nervous origin and sympathetic innervation of fat parda53. The result of this balance has a direct influence both on the accumulation of body fat on the apetito46, 48.
Adipose tissue
Maintaining the lipid balance in adipose tissue has received little scientific attention because the fatty deposits, do not seem to be adjusted on a relatively large imbalances in the daily intake calórica18. The hormone leptin could cover this third regulatory system,-lipostato, providing information about the actual deposits of fat in a central control24, which in turn modulates the accumulation of fat through neural or endocrine signals mediated by receptors adrenergic b354-55, and some hormones or peptides that affect the lipid metabolism such as growth hormone, insulin and esteroides18, 56. Body fat could affect nutrient utilization and selection of macronutrients directly or indirectly. The role of genes that affect adipocyte differentiation and fat accumulation are investigated recientes29, 57, as well as the efficiency mitocondrial58.
ETIOLOGY OF OBESITY
Obesity is defined as excess body fat due to a positive balance in the energy equation or by excessive intake or by a decrease in energy expenditure, or imbalances in both factores13. Obesity is associated with different pathophysiological conditions (diabetes, hypercholesterolemia ...), entails a high cost and has great significance in health pública34, 44.59. Moreover, the increasing rate of obesity in recent years suggests that social and cultural influences, may be involved in setting the energy equation along with genetic determinants and fisiopatológicos14, 60. Thus, it is estimated that between 40-70% of the variation in phenotypes related to obesity is hereditario61, while environmental influences may explain about 30% of obesidad62. The enormous increase in the prevalence of obesity in populations, whose genetic background has remained relatively stable, providing a confirmation that environmental agents may have an important considerable63, 64. The process of modernization and socio-economic restructuring in developed and developing countries has changed the patterns of activity and nutritional física65, 66. Supply systems have improved the availability of food of high energy density, while sedentary lifestyles are extending constantemente41, 67. Moreover, cross-sectional studies have shown a strong association between dietary habits and physical inactivity with overweight and situations obesidad68-69. In addition, prospective studies have provided additional evidence suggesting that physical exercise can help prevent situations of overweight and obesidad70-71.
Obesity rates in the range of 10-15% in Europa35, 72, justifies the efforts of the scientific community to understand the causes of obesity, including genetic components, together with endocrine and environmental factors (dietary habits and patterns physical activity).
Role of heredity in obesity
Genetic predisposition to obesity is linked with both the intake with the gasto73-74. In this context, some findings reported individual mutations with implications in obesity (leptin, leptin receptor, PPAR, POMC, etc..) Mendelian syndromes in which obesity is a manifestation (Prader-Willi, Wilson - Turner, Bordet-Bielke, etc..) of genetically obese animal models (transgenic animals, genetically obese animal testing or animal breeding), and through association studies, linkage, and case-control study to identify genes and searches for candidate markers in genoma75-76.
Genes can determine efferent and afferent signals and central mechanisms involved in regulating weight corporal77-78. The number of markers or genes involved in obesity may be more than 20,076.79. Several genes are involved in the control of food intake (neuropeptide, leptin, POMC, CCK, MCH, etc..) Or the regulation of thermogenesis (b2 and b3-adrenergic receptors, proteins, leptin, etc..), While the expression of some other genes influencing various signaling pathways, adipogénesis, etc.. that could affect the equation energética7 ,57,79-82. Other potential physiological mechanisms through which genetic susceptibility may act, are a low rate of basal metabolism, the decrease in the oxidation of nutrients, low in lean mass and other factors related to the use of micronutrients or hormonal profile, including sensitivity to insulina65, 75. The existence of genes or mutations responsible for the susceptibility of certain individuals or groups of individuals to gain weight in the presence of a high energy density diet or low levels of physical activity are being investigados83-85. The description of some additive effects of mutations as the b3 adrenergic receptor proteins, and 1 on the maintenance of body weight indicates possible interactions between genes86. Thus, individuals with a BMI of 40 kg/m2 with the Trp64Arg mutation for the b3 adrenergic receptor show less leptinemia that without such controls mutación81 obese. Other findings related to the role of genes in obesity resulting from experiments in which the gene has been transferred to the muscle of leptin in mice ob/ob87, which suggests the possible application of gene therapy in certain situations of obesity.
Moreover, obesity is a complex syndrome of multifactorial origin, which could be explained by monogenic mutations, although in most cases seems to result from polygenic interactions, which could in turn be affected by a number of factors ambientales79, 88.
Dietary factors and metabolic
The energy balance is determined by macronutrient intake, energy expenditure and oxidation of specific substrates energéticos69, 89. Thus, the intake of protein and carbohydrate spontaneously unleashes a powerful set of rules in the oxidation of proteins and carbohydrates, while the balance is regulated by lipid less acute and precisa15, 90.91. Moreover, most individuals reach a weight where the composition of oxidized energy substrates is in line with the distribution of macronutrients in dieta1, 77,92,93. Under conditions of rigorous study has found that subjects often have a high respiratory rate when they tend to burn more fat and less glucose, which seems to imply a greater risk of weight gain throughout the años90, 94.
The fact that oxidizes all the fat that is consumed appears to be a protective factor for obesity, which is corroborated by the fact that the adjustment of the oxidation of fat intake seems to be slower than in obese subjects delgados95 - 96.
Additionally, it appears that those individuals genetically predisposed to obesity could present an altered lipid oxidation in situations postobesidad96-98. Therefore, the adjustment between the individual composition of the mixture of substrates oxidized to the distribution of macronutrients in the diet could play a crucial role for the stability of the peso in the short and long plazo99-100.
Furthermore, weight gain may also depend on the distribution of energy substrates from the diet, as they may have a different impact on metabolism and appetite as well as the response of the sympathetic nervous system and therefore in the balance energy and weight corporal89, 101. Thus, feeding two different formulations of macronutrient composition, rich in carbohydrates or fat, healthy volunteers led to higher rates of glucose oxidation, a greater thermogenic effect and increase in heart rate as an indicator of sympathetic activity in those individuals receiving diet hiperglucídica in relation to diet hipergrasa50. However, when a similar dietary intervention was carried out in obese individuals, the results indicated that these subjects were less efficient to oxidize fat and had a rate of lipogenesis superior102. Moreover apart, a high respiratory rate may reflect a lower lipid oxidation, which could be a gain peso41, 91, although other investigadores103, have published that metabolic efficiency may play a minor role in the development of obesity .
The influence of dietary fat on the prevalence of obesity is the subject of controversia104. Thus, there are arguments against the involvement of dietary fat in obesity based on ecological and longitudinal studies, which suggest that the reduction in fat intake and frequent use of low-calorie products in some countries has been associated with a paradoxical increase in the prevalence of obesidad105-106.
Additionally, although hipolipídicas diets may be useful in reducing body fat or prevent gain peso107, current data suggest that a reduction of lipids in the diet should be used primarily as a means to reduce the density energética14, 108. Furthermore, experiments in animals that received fat-rich diets have consistently shown a gradual increase in the peso109. Excessive consumption of fat is common in individuals who consume diets high density energética28, 110, while populations with a very low fat levels typically do not show high prevalence of obesidad111. In addition, two meta-analysis of intervention studies have revealed a loss of weight when they reduce the consumption of lípidos64 112. Research on the role of the intake of carbohydrates or sugar in the prevalence of obesity, established through epidemiological and laboratory studies have reported that those groups who consume a high proportion of energy as carbohydrates have a less likely to be obese than those who consume low levels of sugar, which has been explained by reciprocal changes in intake grasa68, 89. Some of these results could be explained by consumption of modifying factors such as genetic predisposition, gender and physical activity 25112-116.
Physical Activity
Energy expenditure can influence the weight and composition corporal117-118, through changes in the rate of basal metabolism in the thermogenic effect of food and energy demand of the activity itself física113, 119120. Thus, the results suggest that a sedentary is a major factor of increase in the prevalence of obesity, although a lower thermogenic response to the intake and lower rates of basal metabolism may also have an impact on the gain peso41, 121,122 .
Besides cross found any association between physical activity in leisure time (reverse) or the time spent sitting (directly) with the Body Mass Index (BMI) 66. Thus a low participation in sports, a lack of interest in participating in physical activity and a high number of hours spent sitting at work are significant predictors of obesidad69. Furthermore, an analysis of questionnaires that time and budgets for the physical labor has decreased in recent decades, which is accompanied by a weak, but significant increase in BMI in men but not in mujeres123.
In this context, estimates related to the development of social activities and use of electrical equipment between 1950 and 1990 indicate that men and women are now much less generación65 a year ago. Thus, "play" requires approximately 9000 Kcal/4h and "watching television" only 310 Kcal/3h, "buy the market" requires 2500 kcal / week and "buy in a supermarket with a cart" requires less than 100 Kcal / week "make a fire for cooking requires 11,300 kcal / week and" electric light a fire "only a few Kcal, washing clothes by hand" requires 1500 kcal / day while the "automatic washing machine with a" needs only 270 Kcal/2h etc..
In fact, few jobs would be classified as very active in relation to several tens of years atrás65. These data, however, does not offer an explanation for a causal relationship between the inverse association of BMI and physical activity, making it difficult to know if the obese are less active because of their obesity or sedentary if their causes obesidad124-126. Some information on trends in the energy levels show that the growing prevalence of obesity is due to reduction models of physical activity and increased sedentary behavior in various poblaciones65, 70. Thus, the first U.S. national health survey taken between 1971 and 1974 in which 8300 individuals showed that low levels of physical activity in the previous 10 years were associated with weight gain, whereas leisure activities were inversely correlated sports with weight corporal127. Moreover, in a 5200 Finnish study, regression analysis showed that men and women who are not engaged in exercise had a weekly gain of body mass clinically significant in relation to groups activos128. Other studies using questionnaires and indirect indicators of physical activity and hours spent watching TV115, 129, number of cars hogar68 and number of hours seated during ocio66, 69, indicate that the reduction of energy expenditure could be determining the most of the obesity epidemic actual130-133.
Finally the interactions between genetic inheritance and sedentary twins have been valued at and it was concluded that genetic predisposition may modify the effect of physical activity on weight changes varones133 and mujeres84 and lifestyle could have a specific effect on obesity of genetic predisposition depended 62134-139.
CONCLUSIONS
The high precision of the regulation of body weight is reached with a set of integrated systems, which adjust the energy balance (intake and expenditure). The physiological consequences of this complex homeostatic machinery is to minimize weight gain or loss, which is an advantage for human evolution during periods of starvation, survival and abundance. In this context, three factors seem specifically involved in maintaining the constancy of body weight: the metabolic utilization of nutrients, dietary habits and physical activity. Genes, in turn, can influence the energy expenditure, substrate metabolism and appetite. Rising rates of obesity should not be attributed directly to changes in the genetic component, although genetic variants that remained "silent" can now demonstrate the high availability of energy in diets hipergrasas and the increasing sedentary nature of modern societies.
Interactions between genotype and environment are evident when the response of a phenotype (fat) to environmental changes depends on the genotype of the individual. Although it is well known that there are interindividual differences in response to various dietary interactions few attempts have been carried out to establish whether these differences are dependent on genotype. Moreover, genotype-environment interactions, energy expenditure and body fat accumulation induced by the consumption of diets rich in fat can affect body weight, which supports the fact that genetic traits can increase the risk of obesity through the regulation of macronutrient oxidation.
In this context, flows on the current epidemiological trends in obesity rates indicate that a major cause of the obesity problem lies in the dietary patterns and physical activity, whereas metabolic and genetic studies reveal that individuals are more likely to win weight than others. The prevention and treatment of obesity requires an integrated vision. Consideration of factors such as genetics and lifestyle factors as predictors of obesity contribute to the development of preventive actions.
The weight and body composition remain relatively constant in the adult for long periods of time, despite fluctuations in the daily intake and expenditure energético1. In this sense, it assumes the existence of regulatory processes, which conform precisely the nutrient fuels and energy demands to maintain a body mass estable2-4. This balance seems to include a series of highly integrated physiological mechanisms that contribute to the regulation of body weight and tissue deposits adipose.
In this context, the laws of conservation and energy conversion are implementing agencies vivos11 12. The control of appetite as well as the stability of body composition has been attributed, according to different hypothesis on the existence of a physiological levels set for the weight corporal13, 14, regulating appetite through processes glucostáticos or glucogenostáticos15-17, use of substrates energéticos18 homeostatic-20 system involvement nervioso21-23 and a adipostato mediated signals produced in the tissue adiposo24-27 or conductuales28 models. Furthermore, the description of mutations associated with obesity and the identification of transcription factor or nutrient, which regulates the function and differentiation of adipocytes or the expression of genes affecting lipid content, are new areas of research interest in this campo29, 30, among them the resistina, linking diabetes with obesidad31.
WEIGHT AND REGULATION OF ADIPOSE DEPOSITE
The accuracy of the regulation of body weight (often ± 1% for years) requires powerful feedback mechanisms that control the body mass grasa7, 32. However, a continued imbalance between intake and energy expenditure in daily life contributes to the development of obesidad33-35. Other factors such as the distribution of macronutrients in the diet, the involvement of different components of energy expenditure (basal metabolic rate, thermogenic effect of food and physical activity) and metabolism of nutrients específicos36-38 also influence the energy equation. In this context, we can hypothesize that the control of body weight and composition depends on a shaft with three closely interrelated components: 1) appetite, 2) nutrient metabolism and thermogenesis and 3) body fat deposits, of which there are complex feedback mechanisms between ellos7. However, it should be assumed that body weight is ultimately determined by the interplay of genetic, environmental (dietary habits and physical activity) and psychosocial working through different physiological mechanisms of appetite and metabolism energético39, 41.
Appetite
The appetite center, located in the central nervous system is sensitive to different sensory signals mediated by circadian rhythms or the relaxation or release of local hormones and nutritional signals, which modulate food intake through different mechanisms measured by specific neurotransmisores40, 42 -43, including monoamines (noradrenaline, dopamine, serotonin, etc..) amino acids (tryptophan, tyrosine, GABA, etc..) and neuropeptides (orexinas, melanocortinas, pancreatic polypeptides, hormone releasing factors, such as the gastrointestinal peptides colecistoquinina and neuropeptide Y, etc.).. All these factors generate neural and endocrine signals that trigger appropriate quantitative and qualitative adjustments not only on the intake of nutrients, but also on the metabolism energético18, 44. Theories glucostática, lipostática and aminostática appetite did not seem sufficient to explain these processes reguladores17, 45. Thus, the autonomic nervous system and various circulating hormones (insulin, cortisol, growth hormone, etc..) Are involved in the metabolic response to the intake of alimentos46-48.
Nutrient metabolism and thermogenesis
A second control circuit include the regulation of metabolic substrates and thermogenesis, which not only depend on the nutrient intake but also of the specific regulation of its use through processes nervous, endocrine and enzimáticos7, 49 and the existence of futiles50 cycles. In this regard, lipid oxidation is poorly regulated with respect to the oxidation of protein and carbohydrates after the ingesta51, 52. Furthermore, the thermogenic response of brown adipose tissue is the result of a balance between the influences of central nervous origin and sympathetic innervation of fat parda53. The result of this balance has a direct influence both on the accumulation of body fat on the apetito46, 48.
Adipose tissue
Maintaining the lipid balance in adipose tissue has received little scientific attention because the fatty deposits, do not seem to be adjusted on a relatively large imbalances in the daily intake calórica18. The hormone leptin could cover this third regulatory system,-lipostato, providing information about the actual deposits of fat in a central control24, which in turn modulates the accumulation of fat through neural or endocrine signals mediated by receptors adrenergic b354-55, and some hormones or peptides that affect the lipid metabolism such as growth hormone, insulin and esteroides18, 56. Body fat could affect nutrient utilization and selection of macronutrients directly or indirectly. The role of genes that affect adipocyte differentiation and fat accumulation are investigated recientes29, 57, as well as the efficiency mitocondrial58.
ETIOLOGY OF OBESITY
Obesity is defined as excess body fat due to a positive balance in the energy equation or by excessive intake or by a decrease in energy expenditure, or imbalances in both factores13. Obesity is associated with different pathophysiological conditions (diabetes, hypercholesterolemia ...), entails a high cost and has great significance in health pública34, 44.59. Moreover, the increasing rate of obesity in recent years suggests that social and cultural influences, may be involved in setting the energy equation along with genetic determinants and fisiopatológicos14, 60. Thus, it is estimated that between 40-70% of the variation in phenotypes related to obesity is hereditario61, while environmental influences may explain about 30% of obesidad62. The enormous increase in the prevalence of obesity in populations, whose genetic background has remained relatively stable, providing a confirmation that environmental agents may have an important considerable63, 64. The process of modernization and socio-economic restructuring in developed and developing countries has changed the patterns of activity and nutritional física65, 66. Supply systems have improved the availability of food of high energy density, while sedentary lifestyles are extending constantemente41, 67. Moreover, cross-sectional studies have shown a strong association between dietary habits and physical inactivity with overweight and situations obesidad68-69. In addition, prospective studies have provided additional evidence suggesting that physical exercise can help prevent situations of overweight and obesidad70-71.
Obesity rates in the range of 10-15% in Europa35, 72, justifies the efforts of the scientific community to understand the causes of obesity, including genetic components, together with endocrine and environmental factors (dietary habits and patterns physical activity).
Role of heredity in obesity
Genetic predisposition to obesity is linked with both the intake with the gasto73-74. In this context, some findings reported individual mutations with implications in obesity (leptin, leptin receptor, PPAR, POMC, etc..) Mendelian syndromes in which obesity is a manifestation (Prader-Willi, Wilson - Turner, Bordet-Bielke, etc..) of genetically obese animal models (transgenic animals, genetically obese animal testing or animal breeding), and through association studies, linkage, and case-control study to identify genes and searches for candidate markers in genoma75-76.
Genes can determine efferent and afferent signals and central mechanisms involved in regulating weight corporal77-78. The number of markers or genes involved in obesity may be more than 20,076.79. Several genes are involved in the control of food intake (neuropeptide, leptin, POMC, CCK, MCH, etc..) Or the regulation of thermogenesis (b2 and b3-adrenergic receptors, proteins, leptin, etc..), While the expression of some other genes influencing various signaling pathways, adipogénesis, etc.. that could affect the equation energética7 ,57,79-82. Other potential physiological mechanisms through which genetic susceptibility may act, are a low rate of basal metabolism, the decrease in the oxidation of nutrients, low in lean mass and other factors related to the use of micronutrients or hormonal profile, including sensitivity to insulina65, 75. The existence of genes or mutations responsible for the susceptibility of certain individuals or groups of individuals to gain weight in the presence of a high energy density diet or low levels of physical activity are being investigados83-85. The description of some additive effects of mutations as the b3 adrenergic receptor proteins, and 1 on the maintenance of body weight indicates possible interactions between genes86. Thus, individuals with a BMI of 40 kg/m2 with the Trp64Arg mutation for the b3 adrenergic receptor show less leptinemia that without such controls mutación81 obese. Other findings related to the role of genes in obesity resulting from experiments in which the gene has been transferred to the muscle of leptin in mice ob/ob87, which suggests the possible application of gene therapy in certain situations of obesity.
Moreover, obesity is a complex syndrome of multifactorial origin, which could be explained by monogenic mutations, although in most cases seems to result from polygenic interactions, which could in turn be affected by a number of factors ambientales79, 88.
Dietary factors and metabolic
The energy balance is determined by macronutrient intake, energy expenditure and oxidation of specific substrates energéticos69, 89. Thus, the intake of protein and carbohydrate spontaneously unleashes a powerful set of rules in the oxidation of proteins and carbohydrates, while the balance is regulated by lipid less acute and precisa15, 90.91. Moreover, most individuals reach a weight where the composition of oxidized energy substrates is in line with the distribution of macronutrients in dieta1, 77,92,93. Under conditions of rigorous study has found that subjects often have a high respiratory rate when they tend to burn more fat and less glucose, which seems to imply a greater risk of weight gain throughout the años90, 94.
The fact that oxidizes all the fat that is consumed appears to be a protective factor for obesity, which is corroborated by the fact that the adjustment of the oxidation of fat intake seems to be slower than in obese subjects delgados95 - 96.
Additionally, it appears that those individuals genetically predisposed to obesity could present an altered lipid oxidation in situations postobesidad96-98. Therefore, the adjustment between the individual composition of the mixture of substrates oxidized to the distribution of macronutrients in the diet could play a crucial role for the stability of the peso in the short and long plazo99-100.
Furthermore, weight gain may also depend on the distribution of energy substrates from the diet, as they may have a different impact on metabolism and appetite as well as the response of the sympathetic nervous system and therefore in the balance energy and weight corporal89, 101. Thus, feeding two different formulations of macronutrient composition, rich in carbohydrates or fat, healthy volunteers led to higher rates of glucose oxidation, a greater thermogenic effect and increase in heart rate as an indicator of sympathetic activity in those individuals receiving diet hiperglucídica in relation to diet hipergrasa50. However, when a similar dietary intervention was carried out in obese individuals, the results indicated that these subjects were less efficient to oxidize fat and had a rate of lipogenesis superior102. Moreover apart, a high respiratory rate may reflect a lower lipid oxidation, which could be a gain peso41, 91, although other investigadores103, have published that metabolic efficiency may play a minor role in the development of obesity .
The influence of dietary fat on the prevalence of obesity is the subject of controversia104. Thus, there are arguments against the involvement of dietary fat in obesity based on ecological and longitudinal studies, which suggest that the reduction in fat intake and frequent use of low-calorie products in some countries has been associated with a paradoxical increase in the prevalence of obesidad105-106.
Additionally, although hipolipídicas diets may be useful in reducing body fat or prevent gain peso107, current data suggest that a reduction of lipids in the diet should be used primarily as a means to reduce the density energética14, 108. Furthermore, experiments in animals that received fat-rich diets have consistently shown a gradual increase in the peso109. Excessive consumption of fat is common in individuals who consume diets high density energética28, 110, while populations with a very low fat levels typically do not show high prevalence of obesidad111. In addition, two meta-analysis of intervention studies have revealed a loss of weight when they reduce the consumption of lípidos64 112. Research on the role of the intake of carbohydrates or sugar in the prevalence of obesity, established through epidemiological and laboratory studies have reported that those groups who consume a high proportion of energy as carbohydrates have a less likely to be obese than those who consume low levels of sugar, which has been explained by reciprocal changes in intake grasa68, 89. Some of these results could be explained by consumption of modifying factors such as genetic predisposition, gender and physical activity 25112-116.
Physical Activity
Energy expenditure can influence the weight and composition corporal117-118, through changes in the rate of basal metabolism in the thermogenic effect of food and energy demand of the activity itself física113, 119120. Thus, the results suggest that a sedentary is a major factor of increase in the prevalence of obesity, although a lower thermogenic response to the intake and lower rates of basal metabolism may also have an impact on the gain peso41, 121,122 .
Besides cross found any association between physical activity in leisure time (reverse) or the time spent sitting (directly) with the Body Mass Index (BMI) 66. Thus a low participation in sports, a lack of interest in participating in physical activity and a high number of hours spent sitting at work are significant predictors of obesidad69. Furthermore, an analysis of questionnaires that time and budgets for the physical labor has decreased in recent decades, which is accompanied by a weak, but significant increase in BMI in men but not in mujeres123.
In this context, estimates related to the development of social activities and use of electrical equipment between 1950 and 1990 indicate that men and women are now much less generación65 a year ago. Thus, "play" requires approximately 9000 Kcal/4h and "watching television" only 310 Kcal/3h, "buy the market" requires 2500 kcal / week and "buy in a supermarket with a cart" requires less than 100 Kcal / week "make a fire for cooking requires 11,300 kcal / week and" electric light a fire "only a few Kcal, washing clothes by hand" requires 1500 kcal / day while the "automatic washing machine with a" needs only 270 Kcal/2h etc..
In fact, few jobs would be classified as very active in relation to several tens of years atrás65. These data, however, does not offer an explanation for a causal relationship between the inverse association of BMI and physical activity, making it difficult to know if the obese are less active because of their obesity or sedentary if their causes obesidad124-126. Some information on trends in the energy levels show that the growing prevalence of obesity is due to reduction models of physical activity and increased sedentary behavior in various poblaciones65, 70. Thus, the first U.S. national health survey taken between 1971 and 1974 in which 8300 individuals showed that low levels of physical activity in the previous 10 years were associated with weight gain, whereas leisure activities were inversely correlated sports with weight corporal127. Moreover, in a 5200 Finnish study, regression analysis showed that men and women who are not engaged in exercise had a weekly gain of body mass clinically significant in relation to groups activos128. Other studies using questionnaires and indirect indicators of physical activity and hours spent watching TV115, 129, number of cars hogar68 and number of hours seated during ocio66, 69, indicate that the reduction of energy expenditure could be determining the most of the obesity epidemic actual130-133.
Finally the interactions between genetic inheritance and sedentary twins have been valued at and it was concluded that genetic predisposition may modify the effect of physical activity on weight changes varones133 and mujeres84 and lifestyle could have a specific effect on obesity of genetic predisposition depended 62134-139.
CONCLUSIONS
The high precision of the regulation of body weight is reached with a set of integrated systems, which adjust the energy balance (intake and expenditure). The physiological consequences of this complex homeostatic machinery is to minimize weight gain or loss, which is an advantage for human evolution during periods of starvation, survival and abundance. In this context, three factors seem specifically involved in maintaining the constancy of body weight: the metabolic utilization of nutrients, dietary habits and physical activity. Genes, in turn, can influence the energy expenditure, substrate metabolism and appetite. Rising rates of obesity should not be attributed directly to changes in the genetic component, although genetic variants that remained "silent" can now demonstrate the high availability of energy in diets hipergrasas and the increasing sedentary nature of modern societies.
Interactions between genotype and environment are evident when the response of a phenotype (fat) to environmental changes depends on the genotype of the individual. Although it is well known that there are interindividual differences in response to various dietary interactions few attempts have been carried out to establish whether these differences are dependent on genotype. Moreover, genotype-environment interactions, energy expenditure and body fat accumulation induced by the consumption of diets rich in fat can affect body weight, which supports the fact that genetic traits can increase the risk of obesity through the regulation of macronutrient oxidation.
In this context, flows on the current epidemiological trends in obesity rates indicate that a major cause of the obesity problem lies in the dietary patterns and physical activity, whereas metabolic and genetic studies reveal that individuals are more likely to win weight than others. The prevention and treatment of obesity requires an integrated vision. Consideration of factors such as genetics and lifestyle factors as predictors of obesity contribute to the development of preventive actions.
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