[Show abstract][Hide abstract] ABSTRACT: The food reward centres in the brain play a central role in the regulation of food intake and thereby obesity. In the modern lifestyle, a number of artificial rewards such as money have been introduced and brain areas evolved for handling food rewards appear to be exapted to handle money and other rewards. This implies that the changing behaviour related to these rewards could influence obesity. Considering money as a reward, we conducted a survey of 211 full-time cashiers to test whether ownership over cash, amount of cash handled and duration of cash-handling work correlated with obesity parameters. Body mass index was significantly affected by sex, ownership, amount of money handled and duration of cash-handling service. Waist-to-hip ratio was significantly affected by sex, amount of money handled and marginally by ownership. The results are compatible with the exaptation hypothesis. It is possible that increasing importance of non-food rewards may play a significant role in the obesity epidemic.
[Show abstract][Hide abstract] ABSTRACT: Obesity and related disorders are thought to have their roots in metabolic "thriftiness" that evolved to combat periodic starvation. The association of low birth weight with obesity in later life caused a shift in the concept from thrifty gene to thrifty phenotype or anticipatory fetal programming. The assumption of thriftiness is implicit in obesity research. We examine here, with the help of a mathematical model, the conditions for evolution of thrifty genes or fetal programming for thriftiness. The model suggests that a thrifty gene cannot exist in a stable polymorphic state in a population. The conditions for evolution of thrifty fetal programming are restricted if the correlation between intrauterine and lifetime conditions is poor. Such a correlation is not observed in natural courses of famine. If there is fetal programming for thriftiness, it could have evolved in anticipation of social factors affecting nutrition that can result in a positive correlation.
Full-text · Article · May 2011 · Journal of obesity
[Show abstract][Hide abstract] ABSTRACT: The metabolic syndrome disorders (MSD) including type 2 diabetes, hypertension, hypercholesterolemia, atherosclerosis and cardiovascular disease are known to be triggered by lifestyle change. We state and support a hypothesis here that changes in behavior rather than changes in diet and metabolism are central to MSD. We provide and discuss evidence in support of the following sequence of arguments. (i) Diet, thriftiness and obesity centered paradigm is inadequate to explain most of the physiological and immunological changes associated with metabolic syndrome disorders (MSD). (ii) Comparative studies show that relative obesity rather than absolute obesity is strongly associated with various parameters of MSD and further perception of calories without actual change in intake of calories can induce physiological changes. (iii) Alternative behavioral strategies co-exist in animal populations which are associated with characteristic metabolic states and some of these states show close resemblance with MSD in humans. (iv) Obesity and MSD are strongly and cross culturally associated with certain behavioral traits. (v) Deficiencies of certain behaviors that evolved with hunter gatherer life as adaptive behaviors but that are deficient in modern life lead to corresponding dysfunctions of neuro-endocrine mechanisms. Through a meta-analysis study we show that deficiency of physical aggression is strongly associated with MSD as seen by neuro-endocrine mechanisms as well as epidemiological data. This raises a possibility that the effects of behavioral deficiencies may be reversed by behavioral supplementation. (vi) On a pilot scale, behavioral interventions substantially ameliorated many components of MSD without significantly changing body weights. All the evidence collectively indicates that MSD originates due to behavioral deficiencies rather than metabolic thriftiness and therefore behavioral supplementation may be effective in reversing the chronic conditions.
Full-text · Article · Aug 2010 · Nature Precedings
[Show abstract][Hide abstract] ABSTRACT: In most insect-pollinated flowers, pollinators cannot detect the presence of nectar without entering the flower. Therefore, flowers may cheat by not producing nectar and may still get pollinated. Earlier studies supported this 'cheater flower' hypothesis and suggested that the cost saving by cheater flowers could be the most predominant selective force in the evolution of nectarless flowers. Previous models as well as empirical studies have addressed the problem of optimizing the proportion of nectarless and nectarful flowers. However, there has been no attempt to optimize the investment in nectar production along with that in floral display. One of the key questions that arises is whether the floral display will evolve to be an honest indicator of nectar reward. We use a mathematical model to cooptimize the investments in nectar and floral display in order to achieve maximum reproductive success. The model assumes that pollinators rely on a relative rather than an absolute judgement of reward. A conspicuous floral display attracts naive pollinators on the one hand and enhances pollinator learning on the other. We show that under these assumptions, plant-pollinator co-evolution leads to honest signalling, i.e. a positive correlation between display and reward.
Full-text · Article · Dec 2009 · Journal of Biosciences
[Show abstract][Hide abstract] ABSTRACT: An upcoming hypothesis about the evolutionary origins of metabolic syndrome is that of a 'soldier' to 'diplomat' transition in behaviour and the accompanying metabolic adaptations. Theoretical as well as empirical studies have shown that similar to the soldier and diplomat dichotomy, physically aggressive and non-aggressive strategists coexist in animal societies with negative frequency dependent selection. Although dominant individuals have a higher reproductive success obtained through means such as greater access to females, subordinate individuals have alternative means such as sneak-mating for gaining a substantial reproductive success. The alternative behavioural strategies are associated with different neurophysiologic and metabolic states. Subordinate individuals typically have low testosterone, high plasma cholesterol and glucocorticoids and elevated serotonin signalling whereas dominant ones are characterized by high testosterone, low brain serotonin and lower plasma cholesterol. Food and sex are the main natural causes of aggression. However, since aggression increases the risk of injury, aggression control is equally crucial. Therefore chronic satiety in the form of fat should induce aggression control. It is not surprising that the satiety hormone serotonin has a major role in aggression control. Further chronically elevated serotonin signalling in the hypothalamus induces peripheral insulin resistance. Meta-analysis shows that most of the anti-aggression signal molecules are pro-obesity and pro-insulin-resistance. Physical aggression is known to increase secretion of epidermal growth factor (EGF) in anticipation of injuries and EGF is important in pancreatic beta cell regeneration too. In anticipation of injuries aggression related hormones also facilitate angiogenesis and angiogenesis dysfunction is the root cause of a number of co-morbidities of insulin resistance syndrome. Reduced injury proneness typical of 'diplomat' life style would also reorient the immune system resulting into delayed wound healing on the one hand and increased systemic inflammation on the other. Diabetes is negatively associated with physically aggressive behaviour. We hypothesize that suppression of physical aggression is the major behavioural cue for the development of metabolic syndrome. Preliminary trials of behavioural intervention indicate that games and exercises involving physical aggression reduce systemic inflammation and improve glycemic control.
Full-text · Article · Oct 2009 · Medical Hypotheses
[Show abstract][Hide abstract] ABSTRACT: We examine here, using a simple mathematical model, the conditions under which thrifty genes or fetal programming could evolve. Obesity and related disorders are thought to have their roots in metabolic thirftiness that evolved to combat periodic starvation. The failure to detect any thrifty genes and the association of low birth weight with type 2 diabetes, caused a shift in the concept from thrifty gene to thrifty phenotype and fetal programming. This hypothesis assumes that intra-uterine undernutrition programs the body to be thrifty, predicting and preparing for starvation in later life. However, there are reproductive costs associated with thriftiness. Results of the model suggest that under no condition thrifty and non-thrifty genes would co-exist stably in a population. The conditions for evolution of fetal programming are also very restricted. For species with longer life spans, programming for thriftiness is unlikely to evolve if starvation is decided by seasonality or stochastic annual climatic variations since the correlation between intra-uterine and life-time conditions is poor. On the other hand, if starvation is governed by longer periodicity factors such as population oscillations or social hierarchies, there can be better correlation between intra-uterine and life time conditions. Therefore social and population processes are more likely to have selected for fetal programming rather than seasonal and climatic “feast and famine” conditions. Since social and population processes can have cues other than diet, these cues may also influence the incidence of obesity related disorders as some recent evidence suggest.
No preview · Article · Dec 2008 · Nature Precedings
[Show abstract][Hide abstract] ABSTRACT: The adipose tissue is an active endocrine organ which secretes proinflammatory cytokines and chemokines resulting into raised serum levels. Hypercytokinemia has been interpreted as raised level of innate immunity and its evolution is interpreted as a response to increased chances of infection under starvation conditions in which the thrifty phenotype evolved. If starvation and infection challenges co-occurred during hunter gatherer life, thrifty genotype and infection resistant genotype may have co-evolved. An inherent weakness of this explanation is that in obesity or insulin resistance there is no evidence of increased resistance to infections. The raised levels of inflammatory cytokines have not been demonstrated to combat infections or enhance wound healing. We suggest that the raised chemokine levels actually decrease peripheral innate immunity. The normal movement of monocyte-macrophages and neutrophils from blood vessels to injured tissue is under a chemokine gradient. A gradient results from the difference between the basal levels of chemokines and those secreted by the injured tissue. Increase in the basal level is expected to weaken the gradient thereby decreasing extravasation and infiltration. Using diffusion kinetics we show that a small rise in basal levels can cause substantial reduction in cell infiltration. This interpretation is consistent with the behavioural switch hypothesis proposed by Watve and Yajnik which suggests that obesity and insulin resistance mark a transition from “soldier” to “diplomat” lifestyle. Hypercytokinemia may have evolved as a mechanism of disinvestment in peripheral innate immunity since the diplomat lifestyle is less injury prone. We evaluate the two alternative hypotheses by available evidence.
Full-text · Article · Dec 2008 · Nature Precedings
[Show abstract][Hide abstract] ABSTRACT: Fat accumulation has been classically considered as a means of energy storage. Obese people are theorized as metabolically 'thrifty', saving energy during times of food abundance. However, recent research has highlighted many neuro-behavioral and social aspects of obesity, with a suggestion that obesity, abdominal obesity in particular, may have evolved as a social signal. We tested here whether body proportions, and abdominal obesity in particular, are perceived as signals revealing personality traits. Faceless drawings of three male body forms namely lean, muscular and feminine, each with and without abdominal obesity were shown in a randomized order to a group of 222 respondents. A list of 30 different adjectives or short descriptions of personality traits was given to each respondent and they were asked to allocate the most appropriate figure to each of them independently. The traits included those directly related to physique, those related to nature, attitude and moral character and also those related to social status. For 29 out of the 30 adjectives people consistently attributed specific body forms. Based on common choices, the 30 traits could be clustered into distinct 'personalities' which were strongly associated with particular body forms. A centrally obese figure was perceived as "lethargic, greedy, political, money-minded, selfish and rich". The results show that body proportions are perceived to reflect personality traits and this raises the possibility that in addition to energy storage, social selection may have played some role in shaping the biology of obesity.
[Show abstract][Hide abstract] ABSTRACT: Aging is one of the most intriguing processes of biology and despite decades of research, many aspects of aging are poorly understood. Aging is known to occur in bacteria and yeast that divide with morphological asymmetry. Morphologically symmetrically dividing bacteria such as _Escherichia coli_ were assumed not to age until they were shown to divide with functional asymmetry leading to aging and death of some of the cells even in exponentially growing cultures. In asymmetrically dividing _E. coli_ the newly synthesized components are presumed to occupy one pole so that after division one of the daughter cells receives newly synthesized components whereas the other retains the older components. Mathematical models predicted that at the population level, asymmetric growth should result in higher growth rate and symmetric growth in higher growth yield. Therefore, arguably symmetric cell division should be selected in low nutrient environments and asymmetric division in nutrient rich environments. A further prediction was that lower substrate concentrations should strengthen repair mechanisms and suppress aging whereas higher substrate concentrations suppress repair and enhance aging. We show here that _E. coli_ divides more symmetrically under caloric restriction, that both genetic selection and phenotypic plasticity are important determinants of cell division symmetry and also that the proportion of cells that stop dividing and therefore are presumably dead is significantly lower in symmetrically dividing cultures. However, contrary to the prediction, symmetry was not always accompanied by reduced growth rate. These results demonstrate that asymmetry of division in _E. coli_ is not hardwired but responsive to the nutritional environment. This provides a new perspective on why caloric restriction increases lifespan in organisms ranging from microbes to mammals. Symmetry of division may be a mechanism spanning across the width of life forms but regulating aging in different ways in different forms.