Is it the fat? Is it the sugar? Is it the calories? Is it the lack of movement? The ultra processed food? The poverty, stress? Maybe genes or family history? Or everything combined.
I will go through a few of the theories and the pros and cons for each. The responses below were generated by chatGPT and shortened and edited by myself. The summary section is written by me.
Energy imbalance
This theory suggests that obesity results from an energy imbalance between calorie intake and calorie expenditure. When the energy intake from food exceeds the energy expenditure through physical activity and metabolic processes, it can lead to weight gain and obesity
Arguments in favour:
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Basic Physics: The energy imbalance theory is rooted in the laws of thermodynamics. It suggests that weight gain occurs when there is a positive energy balance, where more energy is consumed than expended. From a purely physiological standpoint, if the energy intake consistently exceeds energy expenditure, the excess energy will be stored as fat, leading to weight gain.
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Evidence of Caloric Intake: Studies have shown that the increase in obesity rates coincides with a rise in calorie consumption. The theory argues that the availability of calorie-dense foods, larger portion sizes, and the consumption of high-calorie beverages contribute to increased energy intake, which can lead to weight gain and obesity.
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Energy Storage Mechanisms: The energy imbalance theory aligns with our understanding of how the body stores and utilizes energy. When excess calories are consumed, the body stores the surplus energy as fat in adipose tissue for future use. This mechanism is an evolutionary adaptation to periods of scarcity, but in an environment of abundant food, it can contribute to weight gain.
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Weight Loss through Caloric Deficit: The energy imbalance theory finds support in weight loss interventions that focus on creating a caloric deficit. When individuals consume fewer calories than they expend, weight loss typically occurs. This is observed in various diet plans that restrict caloric intake or increase energy expenditure through increased physical activity.
Contraarguments:
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Individual Variations: The energy imbalance theory assumes a simplistic one-size-fits-all approach, suggesting that obesity is solely a result of excess calorie intake and inadequate physical activity. However, individual variations in metabolism, genetics, hormones, gut microbiota, and other factors can significantly influence weight regulation. Some individuals may be more prone to weight gain or have a harder time losing weight even when their caloric intake and expenditure are seemingly balanced.
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Quality of Calories: Critics argue that the quality of calories consumed, rather than just the quantity, plays a crucial role in obesity. Not all calories are metabolized and utilized in the same way by the body. Different types of foods can have varying effects on satiety, hormone regulation, metabolism, and overall health. For instance, highly processed foods high in added sugars and unhealthy fats can disrupt appetite regulation and metabolic processes, contributing to weight gain.
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Hormonal Regulation: Hormonal regulation of metabolism and fat storage is a complex process that extends beyond the simplistic energy balance equation. Hormones such as insulin, leptin, ghrelin, and others play critical roles in appetite regulation, fat storage, and energy expenditure. Disruptions in hormonal signaling, such as insulin resistance or leptin resistance, can influence weight regulation independent of calorie intake and expenditure.
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Set-Point Theory: The set-point theory suggests that the body has a predetermined weight range that it strives to maintain through various mechanisms. It argues that the body’s physiology and metabolism can adapt to changes in calorie intake and expenditure, making it challenging to sustain weight loss in the long term. This theory implies that weight regulation is not solely dependent on energy balance but is influenced by biological mechanisms that defend against significant changes in weight.
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Environmental Factors: Critics of the energy imbalance theory argue that the focus on individual responsibility overlooks the impact of environmental factors on obesity. Socioeconomic factors, food availability, cultural influences, marketing practices, built environments, and social norms can all contribute to obesogenic environments that make it difficult for individuals to maintain a healthy weight, regardless of their calorie intake and physical activity levels.
It’s important to note that these counter arguments do not invalidate the energy imbalance theory but rather highlight the need for a more comprehensive and nuanced understanding of obesity that considers the interplay of multiple factors beyond just energy balance. Obesity is a complex condition influenced by a combination of genetic, environmental, metabolic, and behavioral factors.
Genetics
Genetic factors play a role in determining a person’s susceptibility to obesity. Certain genes are associated with appetite regulation, metabolism, and fat storage, which can influence an individual’s tendency to gain weight. However, genetics alone cannot account for the sharp increase in obesity rates over the past few decades, suggesting that environmental factors also play a significant role.
Arguments in favour
Genetic Predisposition: Genetic factors can contribute to an individual’s susceptibility to obesity. Studies have shown that the heritability of body weight and body mass index (BMI) is estimated to be around 40-70%. This means that a portion of the variation in body weight and BMI can be attributed to genetic factors.
Single Gene Mutations: In rare cases, mutations in specific genes can lead to severe obesity. These mutations can affect various aspects of metabolism, appetite regulation, and fat storage. For example, mutations in the leptin gene or the melanocortin-4 receptor (MC4R) gene have been associated with rare forms of monogenic obesity.
Polygenic Obesity: The majority of obesity cases are influenced by multiple genetic variants, each contributing a small effect. These genetic variants are referred to as single nucleotide polymorphisms (SNPs) and are spread across various genes involved in appetite regulation, metabolism, and fat storage. Collectively, these genetic variants contribute to polygenic obesity, where the interaction of multiple genes determines an individual’s susceptibility to weight gain.
Appetite and Satiety Regulation: Genetic factors can influence appetite and satiety regulation, affecting an individual’s eating behaviors. Genes involved in the regulation of appetite hormones (e.g., leptin, ghrelin) and brain pathways controlling hunger and satiety signals can impact an individual’s tendency to overeat or feel satisfied after a meal.
Metabolism and Energy Expenditure: Genetic factors can influence an individual’s metabolic rate and energy expenditure. Variations in genes involved in energy expenditure, thermogenesis, and fat oxidation can affect how efficiently the body processes and utilizes energy. Some individuals may have a naturally higher or lower metabolic rate, which can impact weight regulation.
Some nuance
Gene-Environment Interactions: Genetic factors do not work in isolation but interact with environmental factors to influence obesity risk. The interplay between genetic susceptibility and lifestyle factors such as diet, physical activity, and socioeconomic conditions can determine the manifestation of obesity. For instance, individuals with a genetic predisposition to obesity may be more susceptible to weight gain in an environment with easy access to high-calorie foods and limited opportunities for physical activity.
It’s important to note that while genetic factors contribute to obesity risk, they do not dictate a person’s destiny. Environmental factors and lifestyle choices also play a crucial role in weight regulation. Understanding the genetic factors associated with obesity can help identify individuals at higher risk and guide personalized prevention and treatment strategies.
Counter arguments
Environmental Influence: Critics argue that the rising obesity rates over the past few decades cannot be solely attributed to genetic changes. Instead, they suggest that the drastic increase in obesity prevalence is more likely driven by changes in the environment, such as the availability of highly processed foods, sedentary lifestyles, and socioeconomic factors. These environmental factors may play a more significant role in the obesity epidemic than genetic factors alone.
Epigenetic Factors: Epigenetics refers to changes in gene expression that do not involve alterations in the underlying DNA sequence. Critics argue that epigenetic factors, influenced by environmental exposures and lifestyle choices, can modify gene expression and potentially override the impact of genetic predisposition. This suggests that environmental factors can influence obesity risk even in individuals with a genetic susceptibility.
Individual Agency and Lifestyle Choices: Critics argue that focusing solely on genetic factors may undermine the importance of personal agency and lifestyle choices in obesity prevention and management. While genetics can influence an individual’s susceptibility to obesity, lifestyle factors such as diet, physical activity, and overall behavior play a crucial role in weight regulation. Making positive lifestyle choices can mitigate the genetic risk and promote better health outcomes.
Incomplete Understanding of Genetic Factors: Our understanding of the genetic factors contributing to obesity is still evolving. Many of the genetic variants associated with obesity have been identified through genome-wide association studies (GWAS), but the individual effect sizes of these variants are often small, and the mechanisms by which they influence obesity risk are not always well understood. Critics argue that our current knowledge of genetic factors may not be comprehensive enough to fully explain the complexity of obesity.
Lack of Genetic Determinism: It’s important to emphasize that genetics does not determine an individual’s destiny when it comes to obesity. Genetic factors interact with environmental and lifestyle factors, and the resulting obesity risk is influenced by the interplay between these factors. While genetic factors may increase susceptibility to weight gain, lifestyle modifications can have a significant impact on weight management, even for individuals with a genetic predisposition.
Environmental factors
Environmental factors, such as the availability of high-calorie foods, increased portion sizes, sedentary lifestyles, and the prevalence of obesogenic environments, contribute to the development of obesity. Factors like easy access to unhealthy foods, sedentary jobs, limited physical activity opportunities, and built environments that discourage active lifestyles can contribute to weight gain.
Arguments in favour:
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Changes in Food Environment: The modern food environment is characterized by the widespread availability of energy-dense, nutrient-poor foods. Increased consumption of processed and fast foods, larger portion sizes, and the prevalence of sugary beverages contribute to excessive calorie intake. The easy access to these calorie-dense foods, coupled with aggressive food marketing and food pricing, creates an obesogenic environment that promotes weight gain.
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Sedentary Lifestyles: Technological advancements and changes in work and transportation patterns have resulted in reduced physical activity levels. Sedentary behaviors, such as prolonged sitting, increased screen time, and decreased engagement in physical activities, have become more prevalent. These lifestyle changes lead to reduced energy expenditure, contributing to the energy imbalance that can lead to weight gain.
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Built Environment: The built environment, including neighborhood design and urban planning, can influence physical activity levels. Environments with limited access to recreational spaces, parks, sidewalks, and safe areas for physical activity can discourage individuals from engaging in regular exercise. Lack of access to healthy food options, such as grocery stores with fresh produce, in certain neighborhoods also hinders individuals from making nutritious food choices.
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Social and Economic Factors: Social and economic factors can significantly impact obesity rates. Socioeconomic disparities, including lower income levels and limited educational opportunities, are associated with higher obesity rates. Limited access to affordable, nutritious foods, as well as an abundance of inexpensive, energy-dense foods, can contribute to unhealthy dietary patterns and weight gain.
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Cultural and Social Norms: Cultural and social norms surrounding food and physical activity influence behaviors and choices related to nutrition and exercise. These norms can vary across different cultures and communities, shaping individuals’ attitudes, preferences, and behaviors related to food consumption and physical activity. Social norms that promote unhealthy eating habits and sedentary lifestyles can contribute to the development of obesity.
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Family and Social Networks: Family and social networks have a significant influence on eating behaviors and lifestyle choices. Families and social groups can share similar dietary habits, physical activity levels, and attitudes toward body weight. Thus, social interactions and relationships can shape individual behaviors and contribute to obesity risk.
Contra arguments:
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Individual Responsibility: Critics argue that individuals have personal agency and should be held accountable for their own lifestyle choices. They contend that placing excessive emphasis on environmental factors may undermine personal responsibility and the importance of making healthy choices, including selecting nutritious foods and engaging in physical activity.
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Genetic Predisposition: Some argue that genetic factors play a more significant role in obesity than environmental factors. While environmental factors can influence weight gain, individuals with a genetic predisposition to obesity may be more susceptible to weight gain even in environments that are not considered obesogenic. This suggests that genetic factors may exert a stronger influence on weight regulation than the environment alone.
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Lack of Causal Evidence: Critics point out that although there is an association between environmental factors and obesity, establishing a direct causal link can be challenging. Many studies rely on observational data, making it difficult to definitively determine whether the environment directly causes obesity or if other confounding factors are at play. This lack of causal evidence raises questions about the extent to which environmental factors are solely responsible for obesity.
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Individual Variability: Critics argue that not all individuals respond to the same environmental factors in the same way. While certain environmental factors may contribute to obesity in some individuals, others may be more resilient or exhibit different responses due to genetic, physiological, or behavioral differences. This individual variability suggests that the impact of environmental factors on obesity can vary widely.
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Cultural and Social Factors: Critics contend that cultural and social factors can influence obesity rates independently of environmental factors. Cultural norms, beliefs, and social influences surrounding body image, food preferences, and eating behaviors may play a significant role in weight management, separate from the impact of environmental factors.
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Insufficient Focus on Treatment: Critics argue that an excessive focus on environmental factors may divert attention and resources away from treatment options for individuals already living with obesity. While prevention efforts are essential, addressing the underlying causes and providing effective treatment options for those already affected by obesity is equally important.
It’s important to note that these counterarguments do not dismiss the role of environmental factors in obesity but rather highlight the need for a balanced approach that acknowledges the complex interplay of genetic, environmental, and individual factors.
The insulin theory
The insulin theory of obesity proposes that obesity is primarily caused by chronically elevated levels of insulin in the blood. According to this theory, when insulin levels are consistently high, it promotes the storage of excess energy in fat cells, leading to weight gain. Here are the key points of the insulin theory of obesity:
- Role of Insulin: Insulin is a hormone secreted by the pancreas in response to elevated blood glucose levels. Its primary function is to regulate blood sugar levels by facilitating the uptake of glucose into cells. Insulin also plays a role in lipid metabolism and the storage of energy in fat cells.
- Insulin and Lipogenesis: Insulin promotes the synthesis of fatty acids (lipogenesis) and inhibits the breakdown of stored fat (lipolysis). When insulin levels are elevated, it signals to the body that there is an abundance of energy available and encourages the conversion of excess glucose into fatty acids for storage as triglycerides in adipose tissue.
- Insulin Resistance: Insulin resistance is a condition where cells become less responsive to the effects of insulin, requiring higher levels of insulin to achieve the same glucose uptake. Insulin resistance is often associated with obesity and is believed to be a key driver of the insulin theory. As insulin resistance develops, the body compensates by producing more insulin, leading to higher insulin levels in the blood.
Arguments in favour:
- Hyperinsulinemia and Weight Gain: Proponents of the insulin theory argue that chronically elevated insulin levels, known as hyperinsulinemia, contribute to weight gain and the development of obesity. The persistent presence of high insulin levels promotes increased fat storage, inhibits fat breakdown, and stimulates hunger, leading to overeating and a positive energy balance.
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Carbohydrate Intake: The insulin theory suggests that high carbohydrate diets, particularly those rich in refined carbohydrates and sugars, can lead to elevated insulin levels and subsequent weight gain. Carbohydrates cause a rise in blood glucose, which triggers insulin release. High carbohydrate diets, especially those with a high glycemic load, are believed to exacerbate insulin resistance and contribute to hyperinsulinemia.
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Treatment with Low Carbohydrate Diets: The insulin theory suggests that reducing carbohydrate intake, particularly refined carbohydrates and sugars, can lower insulin levels, improve insulin sensitivity, and lead to weight loss. Low carbohydrate diets, such as the ketogenic diet or low-carb high-fat (LCHF) diets, are often advocated as a way to regulate insulin levels and promote weight loss in individuals with insulin resistance or obesity.
Counter arguments against the insulin theory:
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Caloric Intake and Energy Balance: Critics argue that weight gain and obesity primarily result from a positive energy balance—consuming more calories than expended—rather than solely focusing on insulin levels. According to this viewpoint, obesity can occur irrespective of insulin levels as long as there is an excess intake of calories. The total caloric intake and energy balance remain critical factors in weight regulation.
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Individual Variability: The response to insulin and its effect on weight regulation can vary significantly among individuals. Critics argue that not everyone with insulin resistance or high insulin levels becomes obese. Genetic, environmental, and metabolic factors can influence how the body responds to insulin, and some individuals may compensate for insulin resistance by increasing energy expenditure or exhibiting other metabolic adaptations.
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Protein and Fat Intake: The insulin theory primarily focuses on carbohydrate intake as the main driver of insulin secretion and subsequent weight gain. However, critics argue that protein and fat intake also stimulate insulin release, although to a lesser extent. They contend that excessive intake of any macronutrient can lead to weight gain, regardless of insulin levels.
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Satiety and Hunger Regulation: Critics argue that the insulin theory overlooks the complex mechanisms involved in appetite regulation. While insulin plays a role in hunger and satiety signaling, it is not the sole determinant. Other hormones, such as leptin and ghrelin, as well as psychological and environmental factors, also influence appetite and food intake.
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Long-Term Sustainability: Critics raise concerns about the long-term sustainability and practicality of very low carbohydrate diets advocated by the insulin theory. Restricting carbohydrates to a significant extent may lead to dietary imbalances, nutritional deficiencies, and challenges in meeting essential nutrient needs. Additionally, adherence to such diets over the long term can be challenging for some individuals.
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Weight Loss Mechanisms: Critics argue that while reducing carbohydrate intake may lead to initial weight loss, the mechanisms behind it may not solely be attributed to insulin reduction. Low carbohydrate diets often result in reduced calorie intake due to increased satiety and the elimination of high-calorie, carbohydrate-rich foods. The resulting calorie deficit, rather than changes in insulin levels alone, may drive initial weight loss.
Ultra processed food (UPF) as cause of obesity
Ultra-processed foods are food products that undergo extensive industrial processing, often involving multiple stages and the addition of various ingredients. These foods are typically highly convenient, have long shelf lives, and are ready-to-eat or require minimal preparation. They often contain additives, preservatives, and flavor enhancers.
Arguments in favour of the UPFs explanation
- Energy-Dense and Nutrient-Poor: Ultra-processed foods tend to be high in calories but low in essential nutrients. They often provide empty calories, meaning they contribute to calorie intake without providing significant nutritional value. Examples include sugary beverages, pre-packaged snacks, fast food items, frozen meals, processed meats, and certain breakfast cereals.
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Ready-to-Eat and Convenience: Ultra-processed foods are designed for convenience and require minimal preparation. They are often packaged as single servings or individually wrapped portions, making them easy to grab and consume on the go.
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Palatability and Food Appeal: Ultra-processed foods are engineered to have highly appealing tastes, textures, and aromas. They often contain combinations of salt, sugar, and unhealthy fats to create a desirable flavor profile that can be addictive. This palatability can contribute to overeating and a decreased ability to regulate food intake.
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Widespread Availability and Marketing: Ultra-processed foods are extensively marketed and widely available in supermarkets, convenience stores, and fast-food outlets. They are often promoted through aggressive advertising campaigns targeting various age groups, including children. The pervasive marketing and easy accessibility of these foods contribute to their consumption and influence dietary choices.
Counter-arguments against the UPF explanation
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Individual Differences: Critics argue that not everyone who consumes UPFs becomes obese or experiences negative health outcomes. There are individual variations in metabolic response, genetic factors, and lifestyle choices that can influence how individuals respond to UPFs. Some individuals may consume UPFs in moderation as part of an overall healthy diet without experiencing adverse effects.
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Nutritional Quality: Critics contend that not all UPFs are inherently unhealthy or devoid of nutrients. While many UPFs are calorie-dense and nutrient-poor, there are exceptions. For example, some fortified breakfast cereals or packaged foods may contain added vitamins and minerals to improve their nutritional profile. It’s important to differentiate between highly processed foods with low nutritional value and those that may still offer some health benefits.
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Dietary Patterns and Lifestyle: Critics argue that focusing solely on UPFs neglects the broader dietary patterns and lifestyle factors that contribute to obesity and poor health. It is not solely the presence of UPFs but also the overall dietary quality, portion sizes, frequency of consumption, and other lifestyle factors (such as physical activity) that influence health outcomes. Placing sole emphasis on UPFs may overshadow the importance of adopting a balanced, varied, and nutrient-dense diet.
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Socioeconomic Factors: Critics contend that the UPF explanation overlooks the influence of socioeconomic factors on food choices and dietary habits. Individuals with lower incomes may rely more on UPFs due to cost, accessibility, and time constraints. Addressing the impact of UPFs on health should also consider addressing socioeconomic disparities, improving food access, and promoting nutrition education.
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Limited Causal Evidence: While observational studies have found associations between UPF consumption and adverse health outcomes, establishing a direct causal relationship can be challenging. Many studies rely on self-reported dietary data, which can be subject to recall bias. Controlled intervention studies specifically designed to examine the effects of UPFs on health outcomes are limited, making it difficult to definitively establish causality.
Poverty as a cause of obesity
Poverty can contribute to obesity through various interconnected mechanisms and factors. While obesity is a complex condition influenced by multiple factors, the relationship between poverty and obesity is well-established, particularly in low- and middle-income countries. Here are some ways poverty can lead to obesity:
Limited Access to Healthy Foods: Individuals living in poverty often have limited access to affordable and nutritious foods. In many low-income neighborhoods, there may be a scarcity of grocery stores with fresh produce and healthy food options, making it challenging to maintain a balanced diet. As a result, people may rely more on cheaper, calorie-dense, and nutrient-poor foods, such as ultra-processed foods, which can contribute to weight gain.
Food Insecurity: Poverty is closely associated with food insecurity, which refers to the inability to access enough nutritious food for an active and healthy life. In food-insecure households, there may be irregular meals, dependence on low-cost high-calorie foods, and a higher risk of overeating during times of food abundance. This pattern of inconsistent food intake can disrupt hunger and satiety signals, contributing to weight gain.
High Caloric Cost of Nutrient-Dense Foods: Nutrient-dense foods such as fresh fruits, vegetables, and lean proteins can be more expensive than calorie-dense processed foods. For those on a tight budget, it may be more economically feasible to opt for less nutritious, energy-dense options that provide more calories per dollar spent. This can contribute to the consumption of excess calories and, consequently, weight gain.
Lack of Safe Places for Physical Activity: Low-income neighborhoods may have limited access to safe parks, playgrounds, or recreational facilities. The absence of safe and accessible spaces for physical activity can discourage regular exercise and promote sedentary behaviors, which are associated with weight gain and obesity.
Stress and Mental Health: Poverty is often accompanied by chronic stress, financial strain, and limited access to healthcare. Stress and mental health issues, such as depression and anxiety, can influence eating behaviors and lead to emotional eating and weight gain. Moreover, individuals facing stress and adversity may adopt coping strategies that involve consuming high-calorie comfort foods.
Limited Nutrition Education: Nutrition education and awareness of healthy eating practices may be lacking in impoverished communities. Without sufficient knowledge about nutrition and portion control, individuals may make less informed dietary choices that contribute to obesity.
Generational Impact: Poverty can lead to intergenerational cycles of obesity and poor health. Children growing up in low-income households may develop eating habits and lifestyle behaviors that persist into adulthood, perpetuating the cycle of obesity and related health issues.
Addressing obesity in the context of poverty requires comprehensive strategies that address the broader socioeconomic determinants of health. These strategies may include improving food access, enhancing nutrition education, promoting community-based programs for physical activity, and implementing social policies that reduce poverty and improve overall living conditions.
Summary
What is the takeaway message?
It’s complicated!?
The explanations above are likely just some of the reasons contributing to obesity. I expect that the causes includes a combination of factors for many people.
What’s my view on it?
I don’t think genetics massively changed over the last few decades, so it’s unlikely to be a significant contributor, but it can play a role.
What definitely changed is replacing home-cooked whole foods with pre-packed meals full of flavours, which are less satiating, leading to overeating. We also have way more access to sweet foods as a dessert because sugar and its derivates are added to many foods. So I mainly blame ultra-processed foods and sugar.
But this doesn’t explain why my grandmothers and people from her generation gained weight when they didn’t have access to UPFs and didn’t eat sweets. In my culture, it is a phenomenon observed in many women above 40-50. So too much healthy foods increase the risks of obesity too, significantly as the metabolism slows down with ageing.
The takeaway message is that there is a combination of factors in many cases, and population-based approaches must address the problem from multiple angles.
On an individual level, change is possible with access to the right information and determination to improve health.
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