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Map of Obesity in Adult Females (% of adult population with BMI>30) per country (2008).

Evolutionary approaches to obesity are attempts made by evolutionary theorists, anthropologists, biologists, and other scientists to explain the existence of obesity among humans. Obesity is becoming increasingly common in industrialized nations, especially with the onset of globalization and modernization. It is estimated that more than one-third (34.7% or 78.6 million) of adults in the United States are obese, with non-Hispanic African Americans with the highest age-adjusted rates of obesity (47.8%), followed by Hispanics (42.5%), non-Hispanic Whites (32.6%) and non-Hispanic Asians (10.8%)[1]. Obesity is associated with several chronic diseases including hypertension, stroke, type 2 diabetes, cardiovascular disease, and some cancers. It is also the leading cause of preventable death in the United States[1]. Obesity is now considered a disease, as well as a global epidemic and has been targeted by various public health organizations and initiatives, including the World Health Organization (WHO), the Center for Disease Control and Prevention (CDC), and the National Institute of Health (NIH). Identifying and understanding the various factors that favor the capacity for and predispose humans to obesity are important for implementing preventative health strategies. [2][3]

Background

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From an evolutionary perspective, the capacity for humans to accumulate fat has been viewed as an adaptive feature, though other theorists argue that it is maladaptive in a modern environment characterized by minimized fluctuations in energy supply and decreased physical effort in obtaining food sources. [2] Researchers argue that there are two salient contributory factors to the prevalence of obesity in modern society; an environmental change and a genetic predisposition that occurred during evolutionary history. Overall, it is commonly agreed that the modern-day obesity epidemic is a biocultural phenomenon. Various theories have been proposed to explain the existence and prevalence of obesity among humans. The thrifty gene hypothesis and the drifty gene hypothesis are among the most common theories proposed by evolutionary theorists to explain the genetics of obesity. Additionally, the existence of adipose tissue has been thought to serve various risk management purposes, thus suggesting that it is an adaptive feature of human evolution, though this is not necessarily the case with obesity. [3]

Adaptive Viewpoint: The Thrifty Gene Hypothesis

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The Thrifty Gene Hypothesis was proposed in 1962 by the geneticist James V. Neel to explain the genetic predisposition of some individuals to diabetes. This hypothesis has also been used as one possible explanation for obesity. Between the 1950s and 1970s, it was common for biological and evolutionary researchers to explain any means of biological variation with evolutionary adaptation. This hypothesis is a product of this time period. It states that during human evolutionary history, the accumulation of adipose tissue was genetically predisposed as a result of natural selection. This hypothesis predicts that when humans experienced periodic famine, such “thrifty genes” would allow for survival, though they are disadvantageous in modern societies and thus lead to obesity. Within the animal kingdom, various species apart from humans can also become obese, including several groups of birds and mammals that deposit fat in areas that would constitute obesity when compared to humans. This hypothesis has been heavily cited and critiqued in evolutionary literature. [4]

One major criticism of the thrifty gene hypothesis is that if humans were genetically predisposed to store fat or adipose tissue in order to prepare for potential food insecurity, the contemporary variation in those who live in industrialized environments without gaining weight is left unexplained. In other words, critics of this hypothesis contest that if such “thrifty genes” were adaptive, they would be present in all individuals, and all individuals living in Westernized environments would thus be overweight.

The Neutral Viewpoint: The Drifty Gene Hypothesis

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John Speakman proposed the drifty gene hypothesis in 2008 as a rebuttal to the thrifty gene hypothesis. The drifty gene hypothesis suggests that the majority of mutations in genes predisposing humans to obesity are neutral, or "drifty genes" and have been drifting over evolutionary time since the Pleistocene rather than having been positively selected by natural selection. The thrifty gene hypothesis and drifty gene hypothesis are incompatible due to the fact that genes cannot be both positively selected for (adaptive) and neutral. [4]

The Maladaptive Viewpoint

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The maladaptive viewpoint suggests that obesity never served an advantageous purpose in human history. It further suggests that obesity may never have historically existed except among a select few individuals under rare circumstances. The maladaptive viewpoint suggests that genes predisposing humans to obesity have been selected as a by-product of selection for another trait that is advantageous. An example of such a trait that may select obesity predisposition as a by-product is brown adipose tissue (BAT)[4].

Adiposity and Risk Management

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Jonathan C. Wells, Professor of Anthropology and Pediatric Nutrition at University College London, argues that adiposity is associated with human risk management. Wells proposes the notion that adiposity works as a complete risk management strategy that mitigates many ecological stresses that interact with animal characteristics. Wells poses several adaptive benefits pertaining to adipose tissue, those these adaptive benefits do not necessarily pertain to obesity. These include: buffering starvation, buffering stochasticity, adaptation to the cold, growth, buffering the brain, reproduction, immune function, and sexual selection. [2]

The categories included below demonstrate that adipose tissue is associated with a variety of biological functions. It has been found that these functions can be integrated into the life history theoretical model[3]. Adipose tissue can provide the metabolic energy needed for each of these functions. This process is enabled by two key factors: its involvement in multiple signaling pathways through which energy availability and energy needs interact, and its interaction with fundamental feedback systems. Additionally, hormones such as leptin, insulin, and cortisol play fundamental roles in integrating adipose tissue with the competing biological functions. Other signaling molecules are also significant. [5][6][7][8][3]

Buffering Starvation

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Adipose tissue is commonly understood as a mechanism to counteract starvation. Adult humans store enough energy to last several weeks[9] However, the storage of fat is not the only means of energy storage. Other bodily components such as plastic tissue, skeletal muscle, heart and liver tissue, as well as the gut and spleen start decomposing when starvation in prolonged (Wells 2012:600, Rivers 1988). Additionally, even though famines were common throughout human history, death from starvation was only common under certain circumstances. Death during famine was mainly attributed to the shutting down of the immune system, thus leading to increased susceptibility to infectious diseases[3][10]. This further suggests that adipose tissue has additional functions in addition to solely serving as a means of providing metabolic fuel, and may also work to maintain the immune system and protect homeostatic functioning. [3][11]

Buffering Stochasticity

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Another possible function of adipose tissue is its role in buffering short- and long-term fluctuations in energy balance caused by seasonality in energy supply. It is suggested that this role is more significant than tolerating absolute famine.[3]

Adaptation to the Cold

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Some studies suggests that adipose tissue fat storage is beneficial in cold conditions. However, a recent study concerning non-Western populations concludes that additional ecological stresses apart from climatic variability play a central role in adiposity. Such stresses include: dietary ecology, food insecurity, and disease load. [3]

Growth

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Storing energy is essential in funding growth, whether it be through the energetics of reproduction or through the individual life-course[12][13]. Conception after reproduction is dependent on maternal nutritional status [6][8]and baseline adiposity and weight gained during pregnancy contribute to fetus growth.[14] Additionally, energy storage during early postnatal life is essential for growth, indicating that signals of energy availability relate more to the mother’s nutritional status than to the external environment[3][15].

Buffering the Brain

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Recent research suggests that the number of neurons in the human brain determine the amount of energy required for brain function [3][16]. At birth, the brain accounts for approximately 80 percent of total energy expenditure. This amount decreases to approximately 20 percent of total energy expenditure during adulthood[3]. Additionally, during early life, infection risk is quite high. It has been hypothesized that body fat may guarantee brain energy supply during early life and can provide ketones as an alternative substrate to combat starvation.[17][3].

Additional global research concerning the global human diversity of eating patterns suggests that humans show a great deal of diversity in dietary regimes. Thus, finding food in nearly any type of environment is a cross-cultural characteristic of the homo sapien species. The high metabolic costs associated with the development of a large brain has led to the emergence of distinctive nutritional characteristics. Foraging strategies yielding high quality foods including large ranges and high levels of energy expenditure contributed to the development of the large hominid brain. Such strategies have become more efficient in obtaining energy with minimal time and effort involved. It is suggested that high levels of obesity in the United States are not only a product of lifestyle modernization but are also a result of both greater energy intakes and shifts in energy balance and diet composition.[1] [18]

Reproduction

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Wells also suggests that adipose tissue plays a significant role in reproduction. Among adult humans, there is substantial sexual dimorphism of visible adipose tissue. The fact that adult females tend to have more adipose tissue compared to males suggests that body fat is related to the primary role played by females in providing energy for reproduction[12][3][19]

Immune Function

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Recent research suggests that adipose tissue provides energy for the functioning of the human immune system, including aiding in immune defense and aiding in the repair of damaged tissues. Immune function requires vast amounts of metabolic energy, as well as other costs including the defense and repair of specific tissues, the production of lymphocytes and other immune agents and the metabolic cost of fever. In addition to providing energy for immune function, adipose tissue also provides anatomically specific precursors for immune agents[20] [21][3][22]Cite error: A <ref> tag is missing the closing </ref> (see the help page).[23]

Sexual Selection

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One of adiposity’s key traits is that it is subject to sexual selection in females. This pertains to the fact that women pay direct reproductive costs[3][9]. Cross-culturally, adiposity among females is considered attractive to a certain extent. The association of adiposity and attractiveness is ecogeographically and culturally variable, further suggesting that male preferences can shift depending on local ecological conditions. [3][24]

Ethnological Approach

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Nikolaas Tinbergen proposed an ethological model to obesity in 1963 which was designed to address the difficulty associated with adopting evolutionary approaches to factors not preserved in the fossil record. This model investigates proximate causation, ontogeny, the evolutionary history of a trait, and survival value[25]. The various subfactors integrated into this model include: genetic factors, dietary consumption, physical activity level, feeding behavior, endocrine factors, inflammation, psychological factors, and social and environmental factors, as proposed by Jonathan Wells.

Genetic Factors

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Genes play a large role in the variability in human fatness in that they determine both differences in susceptibility as well as determine the pathways leading to weight gain among individuals. Studies conducted on twins and adopted individuals indicate that approximately half of the variation in total fatness and the distribution of fat is genetic[26]. Additionally, it has been shown that variability in human fatness is evident within all ecological environments. Increased adipose tissue is a recent concern effecting individuals in Western populations, as depicted by an increase in median body mass, as well as an increase in the overall number of overweight and obese individuals[2].

Dietary Composition

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Researchers generally agree that obesity results from a combination of both genetic and environmental factors. The composition of one’s diet has also been investigated as a possible cause of positive energy balance. Dietary composition influences weight gain through two distinct pathways: stimulating one’s appetite or altering one’s metabolism. Both of these pathways can lead to over-consumption of energy compared to one’s daily requirements. Protein consumption is not typically associated with obesity, though in early postnatal life, it is associated with higher growth rates[2]. Recent findings also suggest that high protein intake early in life may lead to programmed obesity later on in life[2]. Diets rich in carbohydrates are typically assumed to be beneficial in reducing dietary fat content, though the types of carbohydrates that are consumed may influence one’s adiposity or weight gain. Foods containing carbohydrates are categorized by their glycemic index and their glycemic load. These terms pertain to blood glucose level variability after ingestion and insulin production[12][27]. Some research suggest that food with a high glycemic load fosters weight gain through the distortion of food volume and metabolic response[28].Liquid carbohydrates such as drinks containing sucrose have been linked to weight gain among children[2][29]. Alcohol has also been found to promote positive energy balance, thus leading to metabolic pathway imbalances due to the failure to compensate for extra energy intake elsewhere in one’s diet[2][30]. From a global standpoint, feeding behavior varies due to various interrelated social, cultural and psychological factors. Fast foods, often associated with the Western diet, are also a leading cause to obesity. On average, calorically-dense fast foods are 145% more dense than foods consumed in the traditional African diet[2][31]Cultural behaviors and factors such as increasing food portion sizes, fast-food consumption, and snacking behavior have all led to weight gain[2][32]. Westernization has led to food choice being dependent on taste, convenience, and cost effectiveness, which has further led to the overconsumption of affordable, calorically-dense foods.

Physical Activity Level

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Indirect evidence increasingly supports the hypothesis that physical activity is an additional contributory factor to one’s overall weight, though research directly demonstrating that reduced activity directly causes obesity is lacking[33][2]. Physical activity includes various dimensions such as frequency, duration, energy cost, intensity, locomotory effects, and efficiency. Increase in physical activity is commonly suggested and recommended for weight loss, though evidence of their efficacy remains inconclusive. Existing research suggests that increasing physical activity may contribute more to preventing and reducing age-related weight gain than to promoting weight loss for all individuals[33][2].

Psychological Factors

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Recent studies on obese and non-obese individuals have found significant relationships between psychological traits and causational factors of obesity[2]. While earlier studies examining the possible relationship between obesity and mental illnesses such as depression and anxiety were inconclusive[2][34], recent studies on obese and non-obese individuals have found significant relationships between psychological traits and causational factors of obesity[2]. It has also been suggested that emotional issues experienced by individuals with obesity may be associated with negative treatment by others[2]. Some research suggests that cross-sectional associations exist between the internalization of racism among women and abdominal obesity[2][35]. Research also suggests that there is a positive correlation between psychosocial stress and abdominal obesity[36][2].

Toxic Environment Hypothesis

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The toxic environment hypothesis, also known as the toxic food environment hypothesis, suggests that the mismatch between human evolved dietary and energetic adaptation and the current environment has led to an increased prevalence in obesity among individuals living in modern, industrial environments. This hypothesis infers that the modern food environment that humans have created in recent years, characterized by calorically dense, sugary and fatty foods contrasts sharply with the human ancestral food environment. Additionally, this hypothesis proposes the notion that humans cannot modulate food consumption due to the fact that humans did not evolve in an environment with a surplus of calorie-dense foods. This hypothesis has been utilized by public policy makers in terms of defining the "healthy diet"[37][38]." One assumption of this argument is the fact that food was indeed scarce in the evolved evolutionary environment (EEA). While it is difficult to fully demonstrate such scarcity through evidence provided by the fossil record, data collected from modern hunter-gatherer groups provide insight to the average daily caloric intake of ancestral hunter-gatherers. Such data reveals that the average hunter-gatherer adult consumes about 2580 calories per day, while the average adult in the United States consumes approximately 2248 calories per day. Physical activity level (PAL) is another significant factor to consider when comparing hunter-gatherer groups with individuals living in modern, industrialized environments. PAL is calculated by dividing total daily energy expenditure by basal metabolic rate. Research suggests that the PAL of hunter-gatherers is higher than that of industrialized nations, with an average of 1.82 compared to a PAL of 1.73 in industrialized societies. This data infers that higher physical activity levels among hunter-gatherers can possibly cancel out their higher calorie consumption, though it is not commonly agreed that humans are evolution arily adapted to food scarcity based on evidence from ancestral and modern hunter-gatherer groups[38].

Public Health Efforts for Obesity Prevention

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Obesity has become a salient public health concern both globally and within Western societies, especially in the United States. Originally a “first world problem,” obesity and overweight are now becoming increasingly common in low- and middle-income countries, particularly in urban areas. The World Health Organization (WHO) defines overweight and obesity as “abnormal or excessive fat accumulation that presents a risk to health.” A common mechanism for measuring obesity is the body mass index (BMI), which is calculated by taking a person’s weight in kilograms and dividing it by his or her height in meters. To be considered obese, a person’s BMI must be above 30, while a person with a BMI of 25 is considered overweight[39].Obesity and overweight are becoming the targets of many global and national public health efforts, though they are still considered some of the most neglected public health problems, despite their visibility[40]. The Center for Disease Control (CDC)’s Division of Nutrition, Physical Activity, and Obesity is implementing both environmental and policy-related strategies to draw attention to the importance of engaging in physical activity and eating a healthy, well-balanced diet. Additionally, First Lady Michelle Obama has gained national fame with her Let’s Move campaign. This campaign has focused on preventing obesity and overweight among children within the United States, and involves the dissemination of key nutrition and fitness-related information[41].

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  15. ^ Wells, Jonathan C. K. (2010). "Maternal Capital and the Metabolic Ghetto: An Evolutionary Perspective on the Transgenerational Basis of Health Inequalities". Am. J. Hum. Biol. 22: 1–17.
  16. ^ Herculano-Houzel, S. (2011). "Scaling of Brain Metabolism with a Fixed Energy Budget Per Neuron: Implications for Neuronal Activity, Plasticity, and Evolution". PLoS ONE. 6: e17514.
  17. ^ Kuzawa, C. W. (1998). "Adipose Tissue in Human Infancy and Childhood: An Evolutionary Perspective". Am. J. Phys. Anthropol. 27 (Suppl.): 117–209.
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  19. ^ Lassek & Gaulin (2006). "Changes in Body Fat Distribution in Relation to Parity in American Women: A Covert Form of Maternal Depletion". Am. J. Phys. Anthropol. 131: 295–302.
  20. ^ Mattacks; et al. (2004). "Site-Specific Differences in Fatty Acid Composition of Dendritic Cells and Associated Adipose Tissue in Popliteal Depot, Mesentery, and Omentum and their Modulation by Chronic Inflammation and Dietary Lipids". Lymphat. Res. Biol. 2: 107–129. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  21. ^ Pond, C.M. (2003). "Paracrine Interactions of Mammalian Adipose Tissue". J. Exp. Zool. 295A: 99–110.
  22. ^ Atanassova; et al. (2007). "What are Subcutaneous Adipocytes Really Good For?". Ext. Dermatol. 16: 56–59. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  23. ^ Romanyukha; et al. (2006). "Energy Cost of Infection Burden: An Approach to Understanding the Dynamics of Hot-Pathogen Interactions". J. Theor.Biol. 241: 1–13. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  24. ^ Tovee; et al. (2006). "Changing Perceptions of Attractiveness as Observers are Exposed to a Different Culture". Evol. Hum. Behav. 27: 443–456. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  25. ^ Tinbergen, N. (1963). "On Aims and Methods of Ethology". Zeischrift Teirpsycologie. 20: 410–433.
  26. ^ Bouchard, C. (2007). "The Biological Predisposition to Obesity: Beyond the Thrifty Genotype Scenario". Int. J. Obes. 31: 1337–1339.
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  28. ^ Bell & Sears (2003). "Low-Glycemic-Load Diets: Impact on Obesity and Chronic Diseases". Critical Review of Food Science and Nutrition. 43: 357–377.
  29. ^ Ludwig; et al. (2001). "Relation between Consumption of Sugar-Sweetened Drinks and Childhood Obesity: A Prospective, Observational Analysis". Lancet. 357: 505–508. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  30. ^ Astrup, A. (2001). "The Role of Dietary Fat in the Prevention and Treatment of Obesity. Efficacy and Safety of Low-Fat Diets". International Journal of Obesity. 25: 46–50.
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  34. ^ Friedman & Brownell (1995). "Psychological Correlates of Obesity: Moving to the Next Research Generation". Psychological Bulletin. 117: 3–20.
  35. ^ Tull; et al. (1999). "Relationship of Internalized Racism to Abdominal Obesity and Blood Pressure in Afro-Caribbean Women". Journal of the National Medial Assocation. 91: 447–452. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  36. ^ Raikkonen; et al. (1996). "Psychosocial Stress and the Insulin Resistance Syndrome". Metabolism. 45: 1553–1558. {{cite journal}}: Explicit use of et al. in: |last1= (help)
  37. ^ Poston and Foreyt (1999). "Obesity is an Environmental Issue". Atherosclerosis. 146 (2): 201–209.
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  39. ^ WHO. "Obesity".
  40. ^ WHO. "Controlling the Global Obesity Epidemic". World Health Organization.
  41. ^ "Let's Move Campaign".
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