In biology, energy homeostasis, or the homeostatic control of energy balance, is a biological process that involves the coordinated homeostatic regulation of food intake (energy inflow) and energy expenditure (energy outflow). The human brain, particularly the hypothalamus, plays a central role in regulating energy homeostasis and generating the sense of hunger by integrating a number of biochemical signals that transmit information about energy balance. Fifty percent of the energy from glucose metabolism is immediately converted to heat.
Energy homeostasis is an important aspect of bioenergetics.
In the US, biological energy is expressed using the energy unit Calorie with a capital C (i.e. a kilocalorie), which equals the energy needed to increase the temperature of 1 kilogram of water by 1 °C (about 4.18 kJ).
The first law of thermodynamics states that energy can be neither created nor destroyed. But energy can be converted from one form of energy to another. So, when a calorie of food energy is consumed, one of three particular effects occur within the body: a portion of that calorie may be stored as body fat, triglycerides, or glycogen, transferred to cells and converted to chemical energy in the form of adenosine triphosphate (ATP - a coenzyme) or related compounds, or dissipated as heat.
Energy intake is measured by the amount of calories consumed from food and fluids. Energy intake is modulated by hunger, which is primarily regulated by the hypothalamus, and choice, which is determined by the sets of brain structures that are responsible for stimulus control (i.e., operant conditioning and classical conditioning) and cognitive control of eating behavior. Hunger is regulated in part by the action of certain peptide hormones and neuropeptides (e.g., insulin, leptin, ghrelin, and neuropeptide Y, among others) in the hypothalamus.
Energy expenditure is mainly a sum of internal heat produced and external work. The internal heat produced is, in turn, mainly a sum of basal metabolic rate (BMR) and the thermic effect of food. External work may be estimated by measuring the physical activity level (PAL).
The Set-Point Theory, first introduced in 1953, postulated that each body has a preprogrammed fixed weight, with regulatory mechanisms to compensate. This theory was quickly adopted and used to explain failures in developing effective and sustained weight loss procedures. A 2019 systematic review of multiple weight change interventions on humans, including dieting, exercise and overeating, found systematic "energetic errors", the non-compensated loss or gain of calories, for all these procedures. This shows that the body cannot precisely compensate for errors in energy/calorie intake, contrary to what the Set-Point Theory hypothesizes, and potentially explaining both weight loss and weight gain such as obesity. This review was conducted on short term studies, therefore such a mechanism cannot be excluded in the long term, as evidence is currently lacking on this timeframe.
The main preventable causes are:
A negative balance is a result of energy intake being less than what is consumed in external work and other bodily means of energy expenditure.
The main cause is undereating due to a medical condition such as decreased appetite, anorexia nervosa, digestive disease, or due to some circumstance such as fasting or lack of access to food. Hyperthyroidism can also be a cause.
Normal energy requirement, and therefore normal energy intake, depends mainly on age, sex and physical activity level (PAL). The Food and Agriculture Organization (FAO) of the United Nations has compiled a detailed report on human energy requirements: Human energy requirements (Rome, 17–24 October 2001) An older but commonly used and fairly accurate method is the Harris-Benedict equation.
Yet, there are currently ongoing studies to show if calorie restriction to below normal values have beneficial effects, and even though they are showing positive indications in primates it is still not certain if calorie restriction has a positive effect on longevity for primates and humans. Calorie restriction may be viewed as attaining energy balance at a lower intake and expenditure, and is, in this sense, not generally an energy imbalance, except for an initial imbalance where decreased expenditure hasn't yet matched the decreased intake.
There has been controversy over energy-balance messages that downplay energy intake being promoted by food industry groups.
Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited.
However, in normal individuals, body weight and body fat content are typically quite stable over time2,3 owing to a biological process termed 'energy homeostasis' that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas4 that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum.