16 Evolutionary biology of human adiposity

Mary Grace ‘D’ Tungdim

epgp books

 

 

 

Contents:

 

1.  Introduction

2.  Concept of Thrift

2.1.  Thrift & Control

2.2.  Human Genetic Variability

3.  Evaluation of Human Body Fatness

4.  Concept of Human Adiposity

4.1. Different types of Adipose tissue

4.1.1. Visceral fat

4.1.2. Subcutaneous fat

4.1.3. Human White adipose tissue (WAT)

4.1.4. Human Brown adipose tissue (BAT)

5. Use of Adipose tissues

5.1. Functions of Adipose tissue

5.1.1. Buffering starvation

5.1.2. Buffering short- and long-term fluctuations

5.1.3. Adaptation to the cold

5.1.4. Growth

5.1.5. Buffering the brain

5.1.6. Reproduction

5.1.7. Immune function

5.1.8. Psychosocial stress

5.1.9. Sexual selection

Summary

 

Learning Objectives:

    1.  To study the concept of thrift

2.  To study the human genetic variability

3.  To study the assessment of human body fatness

4.  To study the concept of human adiposity, its uses and functions

5.  To study the evolution of human adiposity

 

1. Introduction

 

Before we deal into the aspect of human adiposity it is important to understand the concept of human evolution. Evolution is derived from the Latin word- evolvere which means ‘to unfold’. In other words, evolution is also termed as ‘descent with modifications’. Evolutionary processes bring out changes in certain characteristics that eventually lead to development of dissimilarities between ancestral and the descendant population. Human evolution, from the genetic point of view, can be viewed as changes in gene frequency of human gene pool from one generation to the next with time. As a result of the process of evolution, humans had to pass several developmental stages so as to occupy the present taxonomic position that distinguishes man from other organisms.

 

Human beings have gone through different stages of foraging for their survival. So, almost all human civilization have surpassed as hunters, gatherers, pastoralists even before the discovery of agriculture. However, a fundamental theme throughout the human historical record has been preoccupation with the threat of food insecurity, hunger, undernutrition and disease induced anorexia. References to frequent famine, plaque and other instances of malnutrition are evident in the earliest world literature and many aspects of the first urban communities represented efforts to consolidate agricultural productivity and food supplies through systems of crop irrigation, food storage and redistribution, and social organisation (Newman et al., 1990).

 

Historical records from Mesopotamia from 3000 to 1400 BC, for example describe the rations given to workers in return for their labour on projects such as irrigation systems, which can be used to estimate dietary energy intake. These data suggest that Mesopotamia knew what it took to feed an adult and for the most part attempted to provide it. There are also instances of free food distribution during the times of scarcity in the late Roman Republic not for humanitarian reasons but in order to suppress popular unrest (Newman et al., 1990). The ‘stele of famine’, recovered from Ptolemaic Egypt and the Pharoah’s grieve over the lack of food grain is an early record of the social impact of agricultural failure (Keys et al., 1950). So, there is innumerable reference to and concern about famine in the past even prior to the origins of agriculture when humans subsisted on hunting and gathering. Therefore, recurring cycles of feast and famine was endured by humans since their existence on the planet.

 

The words chosen may be unfortunate, for anthropologists generally consider a feast to be a particular kind of ritualised occasion (Weissner and Schiefenhivel, 1996), whereas famine is a concept linked strongly with the failure of agricultural productivity (Dando, 1980).

 

2. Concept of Thrift

 

Previous evolutionary approaches to human obesity, hence relevant to adiposity in general, have been dominated by two hypotheses, each focusing on the concept of thrift. In the 1960s, the ‘thrifty genotype’ hypothesis or Gianfranco’s hypothesis suggested that populations varied genetically in their predisposition to store energy, on account of differential ancestral exposure to ‘cycles of feast and famine’ (Neel, 1962). Those experiencing more frequent famines were assumed to have undergone selection for thriftier genes. This hypothesis was somewhat abstract, with no discussion of when such cycles of feast and famine might have occurred. Nevertheless, it became extremely influential and is still widely cited today. An alternative hypothesis, focusing on life-course plasticity, proposed that low birth weight babies responded to their low level of nutritional intake in early life through alterations in growth and metabolism, which impact on subsequent obesity risk (Hales and Barker, 1992).

 

According to this ‘thrifty phenotype’ hypothesis, an increased risk of diabetes following low birth weight could be attributed to poor pancreatic development interacting with excess body weight in later life. Again, this hypothesis has been extremely influential. Although low birth weight babies are widely assumed to have an increased risk of adult obesity, a recent meta-analysis failed to support this assumption (Yu et al., 2011). In both of these hypotheses, fat and thrift were considered two sides of the same coin. Thrift remains a very useful concept in evolutionary approaches to human adiposity and metabolism; however, it is essential to emphasize from the outset that there is much more to thrift than fat, and much more to fat than thrift (Wells, 2011).

 

Thrift implies a degree of prosperity deriving from earlier frugality and careful management of resources (Wells, 2009a). It refers generically to the efficiency with which energy is used, and can derive either from reducing energy expenditure, or storing energy. Fat is only one strategy for storing energy, and organisms show a wide variety of other forms of thrift, including hibernation, torpor and a reduced activity level, along with manipulations of growth rate, body size and relative investment in expensive organs such as brains or secondary sexual characteristics (Wells, 2009a). Storing energy as fat allows some organisms to tolerate ecological uncertainty, however, many organisms respond to such uncertainty in a rather different way – for example, through variation in reproductive success.

 

Boom-bust population dynamics characterize species such as rabbits, which respond to increased energy supply by increasing reproductive rate rather than depositing fat (Wells, 2009a). For species with energy stores, the allocation of energy between competing functions is potentially subject to greater control, allowing more complex life-history strategies (Pond, 2003). Indeed, a recent study found that adipose tissue is negatively associated with brain size across mammals (Navarrete et al., 2011), highlighting that storing energy and processing information are alternative ways of dealing with ecological uncertainty. Humans, however, have both large brains and high adiposity level(Wells, 2009a), making both strategies possible.

 

2.1. Thrift & Control

 

Over what time-span fat stores were accumulated in our evolutionary past, how large they were and how they are related to patterns of gaining and expending energy remain difficult to reconstruct. In contemporary foraging societies, for example, the inherent relationship between physical effort and dietary food intake acts as a constraint on the accumulation of excess body weight. Famines have been common throughout the historical period and undernutrition has been the primary concern for most of the time in most populations till the early part of the nineteenth century.

 

The notion of body fatness as embodying the strategy of ‘thrift’ which is a store of energy for providing calories to accommodate starvation. Many other functions also benefit from these energy stores, but more importantly, adipose tissue also acts as a ‘control centre’, allocating energy between different biological processes. Adipose tissue is known to secrete numerous chemicals which act on the brain and other tissues, and it is this combined role in thrift and control that makes adiposity such an fascinating attribute.

 

2.2. Human Genetic Variability

 

Contemporary human genetic variability can be attributed to several different sources. First, some variability has persisted from Homo erectus, passing through the population bottleneck that characterized the origin of our own species (Garrigan and Hammer, 2006). Second, there is evidence that the gene pool of Homo sapiens received contributions through interbreeding with other hominin species, such as Neanderthals (Green et al., 2010) and a recently discovered type from Siberia (Abi-Rached et al., 2011). Because Neanderthals were well adapted to cold environments and a diet rich in protein, these genes might be very relevant to contemporary adiposity variability (Cochran and Harpending, 2009).

 

Third, the main proportion of global human genetic variability is assumed to have occurred following the exodus from Africa around 60,000 years ago, when populations migrated to most continents and adapted to a wide range of thermal environments, ecosystems, dietary niches and disease loads (Garrigan and Hammer, 2006). Fourth, the rapid expansion in global population size following the emergence of agriculture is predicted to have substantially increased the absolute number of new mutations in the last 10,000 years (Cochran and Harpending, 2009).

 

When a new mutation occurs, it can increase in frequency in the gene pool if it is beneficial, through a ‘selective sweep’. Recent evidence suggests that many local selective sweeps of genes influencing metabolism and adiposity only began relatively recently, and are still continuing (Bender et al., 2011). The specific functions of these genes converge on several important components of biology, including metabolism and digestion, immune defense, reproduction, and cognition (Voight et al., 2006; Cochran and Harpending, 2009). Genetic evidence indicates that adiposity is a continuous trait, much like other life-history traits such as stature and the timing of puberty (Lango Allen et al., 2010).

 

Continuous traits tend to have a polygenic architecture, with each associated gene contributing a small magnitude of effect. The polygenic basis of adiposity maintains numerous small sensitivities to diverse ecological stresses that are relevant to life-history strategy, integrating them into a single phenotype (Wells, 2009a). In this way, it might represent a moderate form of bet-hedging – i.e. increasing variance in offspring to reduce variance in fitness (Wells, 2009a). Perhaps more importantly, the same polygenic architecture further offers a stable platform on which mechanisms of plasticity can function, because the trait becomes robust to individual mutations by constraining their magnitude of effect (Wagner, 2005). Crucially, this perspective also suggests substantial common ground between the genetic and plastic components of adiposity variability. The genetic component integrates multiple ancestral influences on life-history traits such as growth, pubertal development, metabolism, adipocyte biology, etc., whereas the plastic component allows greater life-course flexibility in the same traits.

 

3. Evaluation of Human Body Fatness

 

The development on interest in body fatness started in the late nineteenth century after the great industrial revolution in the Western countries. During that time, there was great difficulty in evaluating body fatness, as adipose tissues are distributed within the human body in a number of depots which merge into one another and are difficult to differentiate (Pond, 1998). The scientific investigation of Wang et al. (1999) led to the identification of fat as a key body component.

Figure 1: Fat as a key component of body composition

(Source: Wang et al., 1999)

 

However, this does not ignore the formal attention to adiposity in the 1940s when Stuart et al. (1940) used two dimensional standard radiography to estimate adipose tissue mass in vivo, and Behnke et al. (1942) first applied the Archimedes’ principle to estimate relative proportion of fat and lean tissues. In the 1950s, Keys and Brozek (1953) gave a firm scientific basis to this densitometric approach.

 

The 1960s saw the development of a group of futher body composition methods, including whole body potassium counting (Forbes and Hursh, 1961), in vivo neutron analysis (Anderson et al., 1964) and dual photon absorptiometry (Mazees et al., 1970). Alongside, theoretical multicomponent models were also developed by combining different measurement technologies so as to improve overall accuracy (Siri, 1961; Brozek et al., 1963). Collectively, this research produced reliable and valuable data on whole body composition from the 1960s onwards, but it was in the 1980s that sophisticated in vivo techniques for discerning internal fat distribution emerged in the form of computed tomography (CT) scanning (Heymsfield et al., 1979) and magnetic resonance imaging (MRI) by Foster et al. (1984).

 

By the 1970s, the recognition of the role of fat as energy stores encouraged anthropologists to conduct widespread field measurements of adiposity using methodologies such as skinfold thicknesses, water displacement technique by Satwanti et al (1977),underwater weighing by Norgan et al. (1982). Interest in adiposity was further fuelled by identification that many non industrialised countries like Western Samoa were profoundly affected by exposure to the increasingly globalised economy. It was during this time that the British scientist Caroline Pond found the biology of adipose tissue to be a severely neglected field. So, she began her work on human cadavers and found considerable variability between species in adipose tissue distribution and a broadly common basic pattern in all mammals.

 

There are indications of different functional roles of energy stores but the discovery of hormone leptin in 1994 took many medical scientist by surprise (Zhang et al., 1994). Although functions of leptin are complex, there is little doubt that its key role is to signal the level of adipose energy to the brain. Recently adipose tissue has been considered an inert store of lipid – the fuel dump available for exploitation by metabolically active and functional lean tissues. However, increasingly adipose tissue, especially the small depots is considered to emit a range of biochemical factors exerting powerful effects on lean mass, and to integrate diverse physiological functions within a composite regulatory system.

 

4. Concept of Human Adiposity

 

Fat and adipose tissue are often interchanged in common usage, however in terms of body composition, fat and adipose tissue are distinct and at different levels and their taxanomic separation is important when measuring their mass and metabolic characteristics (Figure 1). Fat is found primarily in adipose tissue (Anderwald et al., 2002). Adipose tissue consists of adipocytes, extracellular fluid, nerves and blood vessels. Adipose tissue components are present throughout the body and the metabolic properties of these components vary across anatomic locations (Bjorntorp, 2000; Enevoldsen et al., 2001). Adipose tissue components are closely linked with health related conditions. For example, visceral adipose tissue is associated with insulin sensitivity, metabolic syndrome (Wajchenberg, 2000) and type 2 diabetes (Bermudez and Tucker, 2001).

Figure 2: Adipose tissue

(Source Link: http://www.cadiresearch.org/topic/obesity/abdominal-obesity/abdominal-obesity-causes)

 

Figure 3: The relationship between molecular level components lipid and fat and the tissue-organ-level component adipose tissue.

 

(Source: Heymsfield et al., 2005)

 

4.1. Different types of Adipose tissue

 

4.1.1. Visceral fat

 

As visceral fat is stored within the abdominal cavity and is stored around a number of important internal organs such as the liver, pancreas and intestines. Therefore, it is also known as abdominal fat ( also called as organ fat or intra-abdominal fat)

 

Visceral fat is sometimes referred to as ‘active fat’ because research has shown that this type of fat plays a distinctive and potentially dangerous role affecting how our hormones function.

 

Storing higher amounts of visceral fat is associated with increased risks of a number of health problems including type 2 diabetes and a risk for cardiovascular diseases.

 

4.1.2. Subcutaneous fat

 

The fat which is stored under the skin is known as subcutaneous fat. The subcutaneous fat is not necessarily hazardous to a person’s health.

  • The subcutaneous adipose tissue compartment can be further divided into superficial and deep depots or compartments. The superficial fat depot is present throughout the body, and constitutes the vast majority of the adipose tissue in the lower limb and is relatively inert metabolically.

Figure 4: Visceral fat vs Subcutaneous fat

(Source Link: https://www.google.co.in)

  • With energy excess, the secondary adipose tissue compartments—the deep subcutaneous (mainly upper body) and the visceral adipose tissue compartments—become more prominent. These two compartments are characterized by higher transmembrane fatty acid flux rates and thus are more closely linked to dyslipidemia and dysglycemia.
  • In some individuals, a disproportionate expansion of visceral relative to subcutaneous adipose tissue occurs. This manifests as an increased waist circumference (WC) and waist-to-hip ratio (WHR) and is associated with elevated risk of metabolic abnormalities. The mechanisms that support or limit the expandability of specific adipose tissue depots are not known.
  • The storage capacity of adipose tissue is determined by the combination of adipocytes hypertrophy and hyperplasia, which give rise to expanded tissue mass. However, in humans the expansion of adipose tissue in response to excess caloric intake is not always uniform.
  • Physical inactivity is an important contributor to abdominal obesity in every BMI category and both are independently associated with an increased risk of future coronary artery disease (CAD).

    4.1.3. Human White adipose tissue (WAT)

 

White adipose tissue (WAT) plays a role in lipid storage, hormone production, immune function, and local tissue architecture and is classified into two major depots: visceral (vWAT) and subcutaneous (scWAT). vWAT refers to the adipose tissue that surrounds the internal organs, whereas scWAT is primarily found around the thighs and buttocks.

 

The specific type of adipose tissue that accumulates in the body is critically important with regard to health risks. An accumulation of vWAT is associated with insulin resistance, an increased risk of type 2 diabetes, dyslipidemia, progression of atherosclerosis, and mortality (Wang et al., 2005; Zhang et al., 2008), whereas an accumulation of scWAT is associated with improved insulin sensitivity and a reduced risk for developing type 2 diabetes (Misra et al., 1997; Snijder et al., 2003). Recent studies have demonstrated that a number of conditions result in the presence of brown fat–like adipocytes in scWAT. These adipocytes have been termed “adaptive brown fat cells,” “recruitable brown fat cells,” “beige cells,”

 

or “brite cells” (Enerbäck, 2009; Ishibashi and Seale, 2010), and the increased presence of the these cells within the scWAT is referred to as “browning” or “beiging.” WAT browning is associated with increased expression of uncoupling protein 1 (UCP1), which uncouples mitochondrial respiration toward thermogenesis instead of ATP synthesis, leading to increased lipid mobilization and energy expenditure in cachectic mice (Petruzzelli et al., 2014).

Figure 5: Location of White fat and Brown fat in the human body.

 

(Source Link: https://www.google.co.in)

 

4.1.4. Human Brown adipose tissue (BAT)

 

Brown adipose tissue (BAT) is a unique tissue that is able to convert chemical energy directly into heat when activated by the sympathetic nervous system. While initially believed to be of relevance only in human newborns and infants, research during recent years provided unequivocal evidence of active BAT in human adults. Moreover, it has become clear that BAT plays an important role in insulin sensitivity in rodents and humans. This has opened the possibility for exciting new therapies for obesity and diabetes. BAT is a thermogenic tissue that allows small mammals to keep body core temperature constant at cold ambient temperatures without shivering. It differs markedly from white adipose tissue (WAT). While white adipocytes mainly consist of a single large lipid droplet and possess only a few mitochondria, brown adipocytes contain multiple lipid droplets per cell and are packed with mitochondria. BAT is densely innervated by the sympathetic nervous system (SNS) and is highly vascularized.

 

In rodents and human infants, a major depot is found between the scapulae, and more depots exist along the great vessels and in the retroperitoneum (Cannon and Nedergaard, 2004; Enerbäck, 2011). In short, the unique thermogenic capacity of the tissue is due to its high content of mitochondria and the expression of uncoupling protein 1 (UCP1). The relevance of BAT for human newborns and infants had been acknowledged and undisputed for decades (Merklin, 1974; Houstĕk et al., 1993), and even the presence of BAT in human adults was demonstrated in autopsy studies more than 40 years ago (Heaton, 1972).

 

5. Use of Adipose tissues

 

The notion that adiposity functions as a complex risk management system is supported by evaluations on how the tissue evolved in vertebrates. Other ecological stresses favoring fat stores include migration, breeding and hibernation, each of which temporarily overloads energy demand relative to intake (Pond, 1998). Adipose tissue stores are particularly valuable in cold environments, which are more vulnerable to fluctuations in energy supply (Pond, 1998). So important is fat to some hibernating animals that if they are starved as winter approaches, they preferentially preserve adipose tissue, and oxidize lean tissue instead (Dark, 2005).

 

We can therefore consider adipose tissue as a strategy for energy storage that responds to multiple ecological stresses, interacting with the characteristics of the animal. As body size increases, the energy expenditure per kg body weight decreases (Oftedal, 2000). Metabolic processes therefore become more efficient as body size increases. In this way, larger body size per se, along with both absolutely and relatively greater energy stores, increases the period of time over which adipose tissue stores can fund energy requirements.

 

Storing energy as fat is by no means the only strategy for managing the risk of uncertainty in energy supply. A highly social organism such as humans can store energy not only in the body but also extra-corporally (in food hoards) or in social relationships. This ‘redundancy’ of multiple mechanisms suggests that energy risk management was crucial in the evolution of our species; however, although the different approaches have much in common, they also address different situations. Storing energy in social relationships or food hoards buffers against individual uncertainty and misfortune, such that other group members alleviate the risk.

 

This scenario gives control over the social distribution of energy stores. Storing energy in the body buffers against situations that affect all individuals in the social group, such as major ecological stress. This scenario increases control over the internal distribution of energy, as discussed below. However, storing energy in the body also carries its own risks – the historical record has repeatedly documented widespread cannibalism during severe famine, with some individuals plundering the somatic energy stores of others (Keys, 1999).

 

5.1. Functions of Adipose tissue

 

Adipose tissue and metabolism are fundamental to each of the primary life-history functions and described as briefly below:

 

5.1.1. Buffering starvation

 

It is widely recognized that adipose tissue can buffer against starvation. A typical adult male and female store sufficient energy to meet daily requirements for several weeks, typically longer in females than males due to their higher average body fat content (Norgan, 1997). However, adipose tissue is by no means the only tissue that is broken down during starvation, and that, although it is the most plastic tissue, skeletal muscle, gut, spleen, heart and liver tissue all decrease substantially during prolonged starvation (Rivers, 1988). Fat is therefore only one of a wider range of energy stores.

 

Famines have been recorded regularly throughout human history (Keys et al., 1950), but only in certain circumstances there is death from starvation (i.e. extreme exhaustion of energy stores) common. Rather, death commonly occurs from infectious disease (Mokyr and O Grada, 2002), suggesting that, in addition to providing fuel for metabolism, a key role of adipose tissue is to maintain a viable immune system and protect vital homeostatic functions.

 

5.1.2. Buffering short- and long-term fluctuations

 

Rather than tolerating absolute famine, energy stores can be considered more important for buffering short- and long-term fluctuations in energy balance that are caused by seasonality in energy supply or other similar stresses. Studies of farming populations in seasonal environments show typical average fluctuations in body weight of 2-3 kg (Ferro-Luzzi and Branca, 1993), with 4-5 kg occurring under more extreme conditions (Singh et al., 1989). Detailed studies of Gambian women showed that the majority of such weight change was attributable to losses and gains in fat (Lawrence et al., 1987). Although suppression of basal metabolic rate during pregnancy provides another dimension of thrift in this population (Poppitt et al., 1994). Other studies have shown the extraordinary rapidity with which weight can be gained through voluntary over-feeding for brief periods, as demonstrated by the Guru Walla ceremony in rural Cameroon, where daily weight gains approaching 0.25 kg were observed in some individuals (Pasquet et al., 1992).

 

5.1.3. Adaptation to the cold

 

Body fatness tends to be greater in populations inhabiting colder environments (Wells, 2012). Although some have suggested that fat is favored as insulation in such conditions, this is not well supported by evidence, and high fatness impedes heat loss during exercise (Pond, 1998). Instead, increased energy stores in cold environments can ensure a supply of energy for thermogenesis as well as providing greater buffering against negative energy balance, which is potentially more harmful in cold environments.

 

Several stresses co-vary with climate, including dietary ecology, food insecurity and disease load. A recent analysis of non-Western populations showed that climatic variability was more strongly associated with peripheral than central adiposity, suggesting that central adiposity is more strongly influenced by other ecological stresses (Wells, 2012).

 

5.1.4. Growth

 

Energy stores are important in funding growth, both via the energetics of reproduction and through the individual life-course (Wells, 2009b). Maternal nutritional status regulates the probability of conception (Wade et al., 1996; Schneider 2004), whereas baseline adiposity and pregnancy weight gain contribute to growth of the fetus (Anderson et al., 1984). In early postnatal life, storing energy predicts the amount of lean mass accreted subsequently. This suggests that growth strategy is sensitive to signals of energy availability, although in early life these signals relate more strongly to maternal nutritional status than to the external environment per se (Wells, 2010).

 

5.1.5. Buffering the brain

 

Recent studies suggest that brain energy requirements are a function of neuron number (Herculano-Houzel, 2011). Hence, the high neuron number in the human brain which is associated with upregulation of many brain genes compared with non-human apes (Caceres et al., 2003) generates a particularly high energy requirement, equivalent to 20% of basal metabolism even in adult life. The high level of adiposity in early life has been attributed to the benefits of buffering the heightened energy needs of the brain at this age (Kuzawa, 1998). At birth, the brain accounts for ~80% of total energy expenditure, a value which decreases to ~20% by adulthood (Holliday, 1978). The brain is not insulin sensitive and has obligatory energy requirements. Body fat might guarantee brain energy supply during early life when infection risk is high, and can provide ketones as an alternative substrate during starvation (Kuzawa, 1998).

 

5.1.6. Reproduction

 

The substantial sexual dimorphism that is observable for adult adiposity can be attributed to the primary role that females play in the direct provision of energy for reproduction (Lassek and Gaulin, 2006; Wells, 2009c). The magnitude of dimorphism varies substantially, in accordance with ecological factors such as energy availability and climate, but the mean female triceps skinfold thickness is greater than that of males in the vast majority of these 96 populations. Importantly, specific fat depots such as gluteo-femoral adiposity might be particularly important in providing essential fatty acids for offspring brain growth (Rebuffe-Scrive et al., 1985; Lassek and Gaulin, 2007), indicating that fat often supplies more than mere energy for biological functions. Notably, such gluteo-femoral fat also seems to be less detrimental to cardiovascular risk than central abdominal fat (Snijder et al., 2004a; Snijder et al., 2004b).

 

5.1.7. Immune function

 

There are evidences that adipose tissue has a fundamental contribution to the immune system. Immune function is metabolically expensive, involving a variety of costs, including the defense and repair of specific tissues, the metabolic cost of fever, and the production and maintenance of lymphocytes and other immune agents (Romanyukha et al., 2006). Ironically, these costs also include the growth and metabolism of the pathogens themselves. Again, adipose tissue not only provides energy for immune function, but also anatomically specific molecular precursors for immune agents (Pond, 2003; Mattacks et al., 2004) and a range of pro- and anti-inflammatory cytokines that play numerous roles in both immune defense and the repair of damaged tissues (Atanassova et al., 2007; Permana and Reardon, 2007).

 

5.1.8. Psychosocial stress

 

Like many other mammals, humans live in social groups characterized by varying degrees of social hierarchy. In this context, the feeding behavior and metabolism of subordinate individuals is sensitive to behavioral signals from dominant individuals. In humans, as in other primates, subordinate individuals show a different neuroendocrine profile to dominant individuals, having increased cortisol and neuropeptide Y (NPY) levels, leptin resistance, and a greater appetite and central adiposity (Adam and Epel, 2007; Siervo et al., 2009). Patterns of fat metabolism and deposition therefore represent an adaptive response to the psychosocial environment.

 

5.1.9. Sexual selection

 

Given the multiple functions of adiposity, it is of no surprise that it represents a key trait that is subject to sexual selection in females, who bear the direct costs of reproduction (Norgan, 1997). Across human populations, female adiposity is generally considered attractive up to a point. However, this association of adiposity and attractiveness is also subject to eco geographical and cultural variability, indicating that males can facultatively shift their preferences according to local ecological conditions (Tovee et al., 2006). We have seen that adipose tissue is associated with numerous different biological functions. Importantly, they can all be integrated within the theoretical model of life-history.

 

Adipose tissue can provide energy for each of these functions, and its ability to do so is enabled by two key factors: its involvement in multiple signaling pathways through which energy needs and energy availability interact, and its interaction with fundamental feedback systems that proactively allocate energy between these functions. Hormones such as leptin (secreted by adipose tissue itself), insulin (responsive both to adiposity and ongoing metabolic dynamics) and cortisol (sensitive to a variety of ecological stressors) play key roles in integrating adipose tissue with these competing functions (Schneider, 2004; Harshman and Zera, 2007), but many other signaling molecules are also important.

 

Summary

 

Storing energy as fat is a characteristic of many organisms. It is best considered a strategy – a strategy that humans use in general, but one in which they also demonstrate substantial variability. Chronic food shortage and malnutrition have been the scourge of humankind from the dawn of history. Mankind has dealt with food scarcity and potential starvation for most of the time we have been on earth. For much of civilization, being overweight or obese was lauded as a symbol of wealth and prosperity — something to celebrate. Only as countries developed in the 18th century and food became more readily available the growth in population escalated.

 

At first, the greater availability of food created a stronger, healthier population. But, in the 19th century, it is developed into a full-blown health problem. For example, in the United States during the 1930s, life insurance companies started screening potential clients for body weight, and in the 1950s, doctors openly linked increasing rates of obesity with subsequent increases in the diagnosis of heart diseases. It was not until the year 2000, that the number of people who were overweight or obese was greater than the number of those who were underweight.

 

The scarcity of food throughout most of history had led to connotations that being fat was good, and that corpulence and increased “flesh” were desirable as reflected in the arts, literature and medical opinion of the times. Only in the latter half of the nineteenth century did being fat begin to be stigmatized for aesthetic reasons and in the twentieth century, its association with increased mortality was recognized. WAT and BAT have essentially antagonistic functions: WAT stores excess energy as triglycerides and BAT is specialized in the dissipation of energy through the production of heat. Considerable amounts of BAT are present in a substantial proportion of adult humans and relatively high quantities of BAT are associated with lower body weight. With increasing age, BAT decreases and body weight increases.

you can view video on Evolutionary biology of human adiposity

 

Glossary:

 

Evolutionary biology is the subfield of biology that studies the evolutionary processes that produced the diversity of life on Earth, starting from a single origin of life. These processes include natural selection, common descent, and speciation.

 

White fat: White fat is the type of fat that most of us try to avoid accumulating. White fat cells store energy in the form of a single large, oily droplet. White fat does help us to regulate our temperature by insulating organs, but it does little to burn calories like brown fat does. White fat is found below the skin (subcutaneous) and around the organs (visceral fat, which can be especially dangerous) and accumulates from a surplus of calories. White fat has an effect on hormone production and hunger levels, and in healthy, non-overweight humans, it can comprise up to 20 percent of body weight in men and 25 percent in women.

 

Brown fat: Brown fat cells contain mitochondria and are made of a larger number of oily droplets, which are also smaller than those that make up white fat. Brown fat seems to act similarly to muscle tissue in many ways, and actually uses white fat for fuel at times. Within brown fat’s mitochondria (which are often nicknamed the “power house” of cells), heat is able to be generated that helps regulate the body’s internal temperature in response to the changing environment outside. The creation of body heat takes a lot of energy and this calls upon using the body’s excess fat stores for fuel. Brown fat is responsible for “thermoregulatory thermogenesis,” in other words regulation of temperature without shivering (or nonshivering thermogenesis). It also helps release the hormone norepinephrine when we are very cold in order to let us know we are uncomfortable and potentially in danger, so we need more heat.

 

Uncoupling protein 1 (UCP1): UCP1 is a proton channel within the inner mitochondrial membrane that, upon activation, short circuits the respiratory chain, thereby dissipating chemical energy as heat.

 

References

  • Abi-Rached L, Jobin MJ, Kulkarni S, McWhinnie A, Dalva K, Gragert L, Babrzadeh F, Gharizadeh B, Luo M, Plummer FA et al. (2011). The shaping of modern human immune systems by multiregional admixture with archaic humans. Science. 334: 89-94.
  • Anderson J, Osborn SB, Tomlinson RW, Newton D, Rundo J, Salmin L, Smith JW (1964). Neutron activation analysis in man in vivo: a new technique in medical investigation. Lancet 2 (7371): 1201-1205.
  • Behnke AR, Feen BG, Welham WC (1942). The specific gravity of the healthy men. Journal of the American Medical Association. 118: 495-498.
  • Bermudez OI, Tucker KL (2001). Total and central obesity among elderly Hispanics and the association with Type 2 diabetes. Obes Res. Aug; 9(8):443-51.
  • Brozek J, Grande F, Anderson JT, Keys A (1963). Densitometric analysis of body composition: revision of some quantitative assumptions. Annals of the New York Academy of Sciences. 110:113-140.
  • Caceres M, Lachuer J, Zapala MA, Redmond JC, Kudo L, Geschwind DH, Lockhart DJ, Preuss TM, Barlow C (2003). Elevated gene expression levels distinguish human from non-human primate brains. Proceedings of the National Academy of Sciences, USA. 100: 13030–13035.
  • Cannon  B,  Nedergaard  J  (2004).  Brown  adipose  tissue:  function  and  physiological  significance. Physiological Reviews. 84 (1): 277-359.
  • Dark J (2005). Annual lipid cycles in hibernators: integration of physiology and behaviour. Annual Review of Nutrition. 25: 469-497.
  • Ferro-Luzzi A, Branca F (1993). Seasonal energy stress in marginally nourished rural women: interpretation and integrated conclusions of a multicentre study in three developing countries. European Journal of Clinical Nutrition. 44 Suppl 1: 41-46.
  • Forbes GD, Hursh JB (1961). Estimation of total body fat from potassium 40 content. Science 133: 1918.
  • Foster MA, Hutchnson JM, Mallard JR, Fuller M (1984). Nuclear magnetic resonance pulse sequence and discrimination of high and low fat tissues. Magnetic Resonance Imaging 2 (3): 187-192.
  • Garrigan D, Hammer M F (2006). Reconstructing human origins in the genomic era. Nature Reviews Genetics. 7: 669–680.
  • Green RE, Krause J, Briggs AW, Maricic T, Stenzel U, Kircher M, Patterson N, Li H, Zhai W, Fritz MH, et al. (2010). A draft sequence of the Neandertal genome. Science. 328: 710–722.
  • Hales CN, Barker DJ (1992). Type 2 (non-insulin dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 35 (7): 1097-1101.
  • Heymsfield SB, Olafson RP, Kutner MH, Nixon DW (1979). A radiographic method of quantifiying protein-calarie undernutrition. American Journal of Clinical Nutrition. 32 (3): 693-702.
  • Heymsfield SB, Lohman TG, Wang Z, Going SB (eds) (2005). In : Human Body Composition. Human Kinetics, UK.
  • Holliday MA (1978). Metabolic rate and organ size during growth from infancy to maturity and during late gastation and early infancy. Pediatrics. 47 (1); Suppl 2: 169-179.
  • Keys D. (1999). Catastrophe: An Investigation into the Origins of the Modern World. London: Century (Random House).
  • Keys A, Brozek J (1953). Body fat in adult man. Physiological Reviews 33 (3): 245-325.
  • Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HI (1950). The biology of human starvation, University of Minnesota Press, Minneapolis.
  • Kuzawa CW (1998). Adipose tissue in human infancy and childhood: an evolutionary perspective. American Journal of Physical Anthropology. Suppl 27: 177-209.
  • Lango Allen, H., Estrada, K., Lettre, G., Berndt, S. I., Weedon, M. N., Rivadeneira, F., Willer, C. J., Jackson, A. U., Vedantam, S., Raychaudhuri, S. et al. (2010). Hundreds of variants clustered in genomic loci and biological pathways affect human height. Nature. 467: 832-838.
  • Lassek WD, Gaulin SJ (2006). Changes in body fat distribution in relation to parity in American women: a covert form of maternal depletion. American Journal of Physical Anthropology. 131: 295-302.
  • Lassek WD, Gaulin SJ (2007). Waist-hip ratio and cognitive ability: is gluteofemoral fat a privileged store of neurodevelopmental resources? Evolution and Human Behavior. 29: 26-34.
  • Mattacks CA, Sadler D, Pond CM (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. Lymphatic Research and Biology. 2: 107-129.
  • Misra et al., 1997; Misra A, Garg A, Abate N, Peshock RM, Stray-Gundersen J, Grundy SM (1997). Relationship of anterior and posterior subcutaneous abdominal fat to insulin sensitivity in nondiabetic men. Obesity Research. 5:93–99.
  • Mokyr J, O Grada C (2002). What do people die of during famines: the Great  Irish Famine in comparative perspective. European Review of Economic History. 6: 339-363. Navarrete, A., van Schaik, C. P. and Isler, K. (2011). Energetics and the evolution of human brain size. Nature. 480: 91-93.
  • Neel V (1962). Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”? American Journal of Human Genetics. 14: 353-362.
  • Norgan NG (1997). The beneficial effects of body fat and adipose tissue in humans. International Journal of Obesity and Related Metabolic Disorders. 21: 738-746.
  • Oftedal OT (2000). Use of maternal reserves as a lactation strategy in large mammals. Proceedings of the Nutrition Society. 59: 99-106.
  • Pasquet P, Brigant L, Froment A, Koppert GA, Bard D, de Garine I, Apfelbaum M (1992). Massive overfeeding and energy balance in men: the Guru Walla model. American Journal of Nutrition. 56: 483-490.
  • Permana PA, Reardon CL (2007). What are subcutaneous adipocytes really good for? Viewpoint 2. Experimental Dermatology.16: 53-55.
  • Petruzzelli M, Schweiger M, Schreiber R, Campos-Olivas R, Tsoli M, Allen J, et al. (2014). A Switch from White to Brown Fat Increases Energy Expenditure in Cancer-Associated Cachexia. Cell Metabolism. 20; 433–447.
  • Pond CM (1998). The Fats of Life. Cambridge: Cambridge University Press.
  • Pond, C. M. (2003). Paracrine interactions of mammalian adipose tissue. Journal of Experimental Zoology. 295A: 99-110.
  • Poppitt SD, Prentice AM, Goldberg GR, Whitehead RG, (1994). Energysparing strategies to protect human fetal growth. American Journal of Obstetrics & Gynecology. 171: 118-125.
  • Rebuffe-Scrive M, Enk L, Crona N, Lonnroth P, Abrahamsson L, Smith U, Bjorntorp P (1985). Fat cell metabolism in different regions in women. Effect of menstrual cycle, pregnancy, and lactation. Journal of Clinical Investigation. 75: 1973-1976.
  • Romanyukha AA, Rudnev SG, Sidorov IA (2006). Energy cost of infection burden: an approach to understanding the dynamics of host-pathogen interactions. Journal of Theoretical Biology. 241: 1-13. Schneider JE (2004). Energy balance and reproduction. Physiology and Behaviour. 81, 289-317. Siervo M, Wells JC, Cizza G (2009). The contribution of psychosocial stress to the obesity epidemic: an evolutionary approach. Hormone and Metabolic Research. 41: 261-270.
  • Singh J, Prentice AM, Diaz E, Coward WA, Ashford J, Sawyer M, Whitehead RG (1989). Energy expenditure of Gambian women during peak agricultural activity measured by the doubly-labelled water method. British Journal of Nutrition. 62: 315-329.
  • Siri WE (1961). Body composition from fluid spaces and density. In: Brozej J and Henschel A (eds) Techniques for measuring body composition. National Academy of Sciences. Washington, DC, pp 223-244.
  • Snijder MB, Dekker JM, Visser M, et al. (2003). Associations of hip and thigh circumferences independent of waist circumference with the incidence of type 2 diabetes: the Hoorn Study. American Journal of Clinical Nutrition. 77:1192–1197.
  • Snijder MB, Dekker JM, Visser M, Bouter LM, Stehouwer CD, Yudkin JS, Heine RJ, Nijpels G, Seidell JC (2004a). Trunk fat and leg fat have independent and opposite associations with fasting and postload glucose levels: the Hoorn study. Diabetes Care 27, 372-377.
  • Snijder MB, Zimmet PZ, Visser M, Dekker JM, Seidell JC, Shaw JE (2004b). Independent and opposite associations of waist and hip circumferences with diabetes, hypertension and dyslipidemia: the Aus. Diab Study. International Journal of Obesity and Related Metabolic Disorders. 28, 402-409.
  • Stuart HC, Hill P, Shaw C (1940). The growth of bone, muscle and overlying tissue as revealed by studies of roentgenograms of the leg areas. Monograph of the Society for Research in Child Development. 5: 1-90.
  • Tovee MJ, Swami V, Furnham A, Mangalparsad R (2006). Changing perceptions of attractiveness as observers are exposed to a different culture. Evolution and Human Behavior. 27: 443-456.
  • Voight BF, Kudaravalli S, Wen X, Pritchard JK (2006). A map of recent positive selection in the human genome. PLoS Biology. 4: e72.
  • Wade GN, Schneider JE, Li HY (1996). Control of fertility by metabolic cues. American Journal of Physiology. 270: E1-E19.
  • Wagner A (2005). Robustness and Evolvability in Living Systems. Princeton: Princeton University Press.
  • Wang Z, Wang ZM, Heymsfield SB (1999). History of the study of human body composition: abrief review. American Journal of Human Biology. 11: 157-165.
  • Wang Y, Rimm EB, Stampfer MJ, Willett WC, Hu FB (2005). Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men. American Journal of Clinical Nutrition. 81:555–563.
  • Wells JC (2009a). Ethnic variability in adiposity and cardiovascular risk: the variable disease selection hypothesis. International Journal of Epidemiology. 38: 63-71.
  • Wells JC (2009b). Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms. International Journal of Obesity. 33: 1331-1338.
  • Wells JC (2009c). The Evolutionary Biology of Human Body Fatness: Thrift and Control. Cambridge: Cambridge University Press.
  • Wells JC  (2010). Maternal  capital and the metabolic ghetto: An evolutionary perspective on the transgenerational basis of health inequalities. American Journal Human Biology. 22: 1-17.
  • Wells JC (2011). An evolutionary perspective on the trans-generational basis of obesity. Annals of Human Biology. 38: 400-409.
  • Wells JC (2012). Sexual dimorphism in body composition across human populations: associations with climate and proxies for short- and long-term energy supply. . American Journal Human Biology. 2: 411-419.
  • Yu ZB, Han SP, Zhu GZ, Zhu C, Wang XJ, Cao XG, Guo XR (2011). Birth weight and subsequent risk of obesity: a systematic review and meta-analysis. Obes. Rev. 12, 525-542.
  • Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (1994). Positional cloning of the mouse obese gene and its human homologue. Nature. 372:425–432.
  • Zhang C, Rexrode KM, van Dam RM, Li TY, Hu FB (2008). Abdominal obesity and the risk of all-cause, cardiovascular, and cancer mortality: sixteen years of follow- up in US women. Circulation.117:1658–1667.

    Suggested Readings

  1. The Evolutionary Biology of Human Body Fatness: Thrift and Control by Jonathan C. K. Wells, Cambridge University Press, 2010 – Nature.
  2. The Metabolic Ghetto: An Evolutionary Perspective on Nutrition, Power relations and chronic disease. By Jonathan C. K. Wells. Cambridge University press. 2016.
  3. 3. Human Biology: An Evolutionary and Biocultural Perspective, 2nd Edition By: Sara Stinson , Barry Bogin and Dennis H. O’Rourke. Wiley Blackwell, March 2012.
  4. Adipose Tissue Biology edited by Michael E. Symonds. Springer nature, USA, 2017.
  5. Human Evolutionary Biology. edited by Michael P. Muehlenbein. Cambridge University Press, 2010.