Compensatory growth, known as catch-up growth and compensatory gain, is an accelerated growth of an organism following a period of slowed development, particularly as a result of nutrient deprivation. [1] [2] The growth may be with respect to weight or length (or height in humans). [1] [3] [4] [5] [6] [7] [8] For example, the body weights of animals who experience nutritional restriction will often over time become similar to those of animals who did not experience such stress. [1] It is possible for high compensatory growth rates to result in overcompensation, where the organism exceeds normal weight and often has excessive fat deposition. [9]
An organism can recover to normal weight without additional time. [1] Sometimes when the nutrient restriction is severe, the growth period is extended to reach the normal weight. [1] If the nutrient restriction is severe enough, the organism may have permanent stunted growth where it does not ever reach normal weight. [1] Usually in animals, complete recovery from carbohydrate and protein restriction occurs. [9]
Compensatory growth has been observed in a number of organisms including humans, [3] [4] [5] [6] [7] [8] other species of mammals, [10] birds, [10] reptiles, [11] fish, [12] [13] [14] plants (especially grasses and young tree seedlings and saplings), [15] fungi, [16] microbes, [17] pigs, [18] and damselflies. [19]
In 1911, Hans Aron performed the earliest study of growth after periods of undernourishment. [20] He underfed a dog and found that it still had the capacity to rapidly gain weight, though it did not reach the final weight of a dog that was fed normally. [20] [21] In 1915, Osborne and Mendel were the first to demonstrate that rats fed after growth restriction had an accelerated growth rate. [10] [20] [22] In 1945, Brody developed the idea of "homoestasis of growth" in the book Bioenergetics and Growth. [10] [20] [23] In 1955, Verle Bohman was the first to use the term "compensatory growth" in an article pertaining to beef cattle. [10] [24]
In animals, homeostatic and homeorhetic processes are involved in the abnormally high growth rates. Homeostatic processes usually affect compensatory growth in the short term, whereas homeorhetic processes usually have a long-term effect.
First, during nutrient starvation, a reduction of basal metabolism takes place. The gut tissues are the first tissues to be reduced in weight and activity. Then, during the realimentation (re-feeding) phase, an increase in feeding enables more dietary protein and energy to be contributed for tissue growth instead of basal metabolism. The gut tissues are the first to increase in weight, followed by muscle tissue and finally adipose tissue.
The exact biological mechanisms for compensatory growth remain poorly understood. However, it is known that during the restriction period, levels of growth hormone (GH) are increased by the pituitary gland, while the number of GH receptors decrease. [25] There is a decrease in insulin-like growth factor (IGF-1) as well. [25] When this restriction is severe, amino acids are released from muscle cells and catabolic hormones circulate to initiate gluconeogenesis processes. [25] Then, when compensation begins, the GH levels continue to remain high while insulin levels spike, allowing the GH to be used for growth processes. [25] At first, lean muscle is built, but after a few weeks of refeeding, fat begins to accumulate on the organism. [25] IGF-1 and thyroid hormones, on the other hand, approach normal levels much sooner. [25] This may be why animals often have increased fat deposition after a period of refeeding.
Compensatory growth in an organism can have impacts on the organism's behavior and muscle development. [14] These changes can occur during or after the period of compensation, and can lead to changes in behavior, movement, and body composition. [14] During compensation, animals may experience changes in food intake, body composition (increased fat and lessened muscle), metabolism, and the endocrine system. [26] Animals undergoing compensatory growth have been seen to have impaired muscle development after regrowth, which leads to impairments in locomotion and escape movements. [14] Behavioral impacts such as increased risk-taking and aggression have also been seen, both during and after regrowth. [14] Animals often have impaired movement due to lessened muscle development, yet they have been observed taking time during feeding, despite the risks of extended time spent eating. [14] Brown trout ( Salmon trutta) who have been treated with growth hormone after a period of deprivation have been observed to increase their growth rate but decrease their anti-predator responses, such as swimming in waters more accessible by predators. [14] Increased aggression and decreased sexual displays have also been seen in animals undergoing compensatory growth. [14]
Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation or prior to attaining peak bone mass. [27] Both height gain and pubertal development are dependent on the release of growth hormone and gonadotrophins (LH and FSH) from the pituitary gland. Suppression of gonadotropins in patients with anorexia nervosa has been frequently documented. [27] In some cases, especially where onset is pre-pubertal, physical consequences such as stunted growth and pubertal delay are usually fully reversible. [3] Height potential is normally preserved if the duration and severity of anorexia nervosa are not significant and/or if the illness is accompanied with delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may negate the deleterious effects of undernutrition on stature by allowing for a longer duration of growth compared to controls. [4] In such cases, appropriate early treatment can preserve height potential and may even help to increase it in some post-anorexic subjects due to the aforementioned reasons in addition to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels. [5] [6] [7] [8]
In 1960, Wilson and Osborne outlined six factors that could affect compensatory growth in a review article. [2] [10] The importance of each, some, or all of these factors is not well understood. [9] These factors are as follows: [2] [9] [10]
Animal factors that can affect compensatory growth may include the maturity level and fat proportion of the animal at the time of nutrient deprivation, the genotype, the gender, and the metabolic changes. [2] The stage of development of the animal when the nutrient restriction occurs greatly affects its body composition. [1]
The insulin-like growth factors (IGFs) are proteins with high sequence similarity to insulin. IGFs are part of a complex system that cells use to communicate with their physiologic environment. This complex system consists of two cell-surface receptors, two ligands, a family of seven high-affinity IGF-binding proteins, as well as associated IGFBP degrading enzymes, referred to collectively as proteases.
Anorexia is a medical term for a loss of appetite. While the term outside of the scientific literature is often used interchangeably with anorexia nervosa, many possible causes exist for a loss of appetite, some of which may be harmless, while others indicate a serious clinical condition or pose a significant risk.
An eating disorder is a mental disorder defined by abnormal eating behaviors that adversely affect a person's physical or mental health. These behaviors include eating either too much or too little. Types of eating disorders include binge eating disorder, where the patient keeps eating large amounts in a short period of time typically while not being hungry; anorexia nervosa, where the person has an intense fear of gaining weight and restricts food or overexercises to manage this fear; bulimia nervosa, where individuals eat a large quantity (binging) then try to rid themselves of the food (purging); pica, where the patient eats non-food items; rumination syndrome, where the patient regurgitates undigested or minimally digested food; avoidant/restrictive food intake disorder (ARFID), where people have a reduced or selective food intake due to some psychological reasons; and a group of other specified feeding or eating disorders. Anxiety disorders, depression and substance abuse are common among people with eating disorders. These disorders do not include obesity. People often experience comorbidity between an eating disorder and OCD. It is estimated 20–60% of patients with an ED have a history of OCD.
Development of the human body is the process of growth to maturity. The process begins with fertilization, where an egg released from the ovary of a female is penetrated by a sperm cell from a male. The resulting zygote develops through mitosis and cell differentiation, and the resulting embryo then implants in the uterus, where the embryo continues development through a fetal stage until birth. Further growth and development continues after birth, and includes both physical and psychological development that is influenced by genetic, hormonal, environmental and other factors. This continues throughout life: through childhood and adolescence into adulthood.
Intrauterine growth restriction (IUGR), or fetal growth restriction, is the poor growth of a fetus while in the womb during pregnancy. IUGR is defined by clinical features of malnutrition and evidence of reduced growth regardless of an infant's birth weight percentile. The causes of IUGR are broad and may involve maternal, fetal, or placental complications.
Eating is the ingestion of food. In biology, this is typically done to provide a heterotrophic organism with energy and nutrients and to allow for growth. Animals and other heterotrophs must eat in order to survive — carnivores eat other animals, herbivores eat plants, omnivores consume a mixture of both plant and animal matter, and detritivores eat detritus. Fungi digest organic matter outside their bodies as opposed to animals that digest their food inside their bodies.
Leptin, also known as obese protein, is a protein hormone predominantly made by adipocytes. Its primary role is likely to regulate long-term energy balance.
Appetite is the desire to eat food items, usually due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety. Appetite exists in all higher life-forms, and serves to regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the digestive tract, adipose tissue and the brain. Appetite has a relationship with every individual's behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia is increased eating. Dysregulation of appetite contributes to ARFID, anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.
A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behaviour of the offspring. These adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.
Adipose tissue is a loose connective tissue composed mostly of adipocytes. It also contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body.
Delayed puberty is when a person lacks or has incomplete development of specific sexual characteristics past the usual age of onset of puberty. The person may have no physical or hormonal signs that puberty has begun. In the United States, girls are considered to have delayed puberty if they lack breast development by age 13 or have not started menstruating by age 15. Boys are considered to have delayed puberty if they lack enlargement of the testicles by age 14. Delayed puberty affects about 2% of adolescents.
Cat food is food specifically formulated and designed for consumption by cats. As obligate carnivores, cats have specific requirements for their dietary nutrients, namely nutrients found only in meat or synthesised, such as taurine and Vitamin A. Certain nutrients, including many vitamins and amino acids, are degraded by the temperatures, pressures and chemical treatments used during manufacture, and hence must be added after manufacture to avoid nutritional deficiency. Cat food is typically sold as dry kibble, or as wet food in cans and pouches.
An underweight person is a person whose body weight is considered too low to be healthy. A person who is underweight is malnourished.
Protein–energy undernutrition (PEU), once called protein-energy malnutrition (PEM), is a form of malnutrition that is defined as a range of conditions arising from coincident lack of dietary protein and/or energy (calories) in varying proportions. The condition has mild, moderate, and severe degrees.
Human body shape is a complex phenomenon with sophisticated detail and function. The general shape or figure of a person is defined mainly by the molding of skeletal structures, as well as the distribution of muscles and fat. Skeletal structure grows and changes only up to the point at which a human reaches adulthood and remains essentially the same for the rest of their life. Growth is usually completed between the ages of 13 and 18, at which time the epiphyseal plates of long bones close, allowing no further growth.
Functional hypothalamic amenorrhea (FHA) is a form of amenorrhea and chronic anovulation and is one of the most common types of secondary amenorrhea. It is classified as hypogonadotropic hypogonadism. It was previously known as "juvenile hypothalamosis syndrome," prior to the discovery that sexually mature females are equally affected. FHA has multiple risk factors, with links to stress-related, weight-related, and exercise-related factors. FHA is caused by stress-induced suppression of the hypothalamic-pituitary-ovarian (HPO) axis, which results in inhibition of gonadotropin-releasing hormone (GnRH) secretion, and gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Severe and potentially prolonged hypoestrogenism is perhaps the most dangerous hormonal pathology associated with the disease, because consequences of this disturbance can influence bone health, cardiovascular health, mental health, and metabolic functioning in both the short and long-term. Because many of the symptoms overlap with those of organic hypothalamic, pituitary, or gonadal disease and therefore must be ruled out, FHA is a diagnosis of exclusion; "functional" is used to indicate a behavioral cause, in which no anatomical or organic disease is identified, and is reversible with correction of the underlying cause. Diagnostic workup includes a detailed history and physical, laboratory studies, such as a pregnancy test, and serum levels of FSH and LH, prolactin, and thyroid-stimulating hormone (TSH), and imaging. Additional tests may be indicated in order to distinguish FHA from organic hypothalamic or pituitary disorders. Patients present with a broad range of symptoms related to severe hypoestrogenism as well as hypercortisolemia, low serum insulin levels, low serum insulin-like growth factor 1 (IGF-1), and low total triiodothyronine (T3). Treatment is primarily managing the primary cause of the FHA with behavioral modifications. While hormonal-based therapies are potential treatment to restore menses, weight gain and behavioral modifications can have an even more potent impact on reversing neuroendocrine abnormalities, preventing further bone loss, and re-establishing menses, making this the recommended line of treatment. If this fails to work, secondary treatment is aimed at treating the effects of hypoestrogenism, hypercortisolism, and hypothyroidism.
The diet-induced obesity model is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets. It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models. These animals can then be used to study in vivo obesity, obesity's comorbidities, and other related diseases. Users of such models must take into account the duration and type of diet as well as the environmental conditions and age of the animals, as each may promote different bodyweights, fat percentages, or behaviors.
Compensatory growth is a type of regenerative growth that can take place in a number of human organs after the organs are either damaged, removed, or cease to function. Additionally, increased functional demand can also stimulate this growth in tissues and organs. The growth can be a result of increased cell size or an increase in cell division or both. For instance, if one kidney is surgically removed, the cells of the other kidney divide at an increased rate. Eventually, the remaining kidney can grow until its mass approaches the combined mass of two kidneys. Along with the kidneys, compensatory growth has also been characterized in a number of other tissues and organs including:
Puberty is the process of physical changes through which a child's body matures into an adult body capable of sexual reproduction. It is initiated by hormonal signals from the brain to the gonads: the ovaries in a female, the testicles in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, bones, muscle, blood, skin, hair, breasts, and sex organs. Physical growth—height and weight—accelerates in the first half of puberty and is completed when an adult body has been developed. Before puberty, the external sex organs, known as primary sexual characteristics, are sex characteristics that distinguish males and females. Puberty leads to sexual dimorphism through the development of the secondary sex characteristics, which further distinguish the sexes.
Anorexia nervosa (AN), often referred to simply as anorexia, is an eating disorder characterized by food restriction, body image disturbance, fear of gaining weight, and an overpowering desire to be thin.