Growth



Growth 3877
Photo by: Monia

Growth implies development, from the time of emergence or birth to the time of maturity and for many species, beyond maturity to eventual senescence or death. Growth also implies increase in size resulting from cell multiplication and cell expansion, as well as maturation of tissues. However, growth, while accentuating increased cell number and size, also necessitates programmed cell death, leading to the production of the final body form. Thus, growth is an incredibly complex phenomenon, which involves changes in body form, metabolism , and body processes.

Patterns of Growth

In most animals, the growth pattern follows an S-shaped curve. Slow early growth occurs from first emergence, or birth, which is followed by a long phase of rapid increase in body mass and maturation of organs, especially structural or somatic tissue that support the individual, up to about the time of puberty or reproductive maturity. Finally, growth slows, and in some species stops altogether after reproductive maturation. In many animals and most plants, however, growth continues throughout life, so that the oldest individuals in the population are generally the largest.

In birds and mammals, the young emerge looking vaguely like adults, but with different body proportions.
In birds and mammals, the young emerge looking vaguely like adults, but with different body proportions.

In many animals, young emerge looking like miniature adults, and gradually enlarge throughout their lifetime, going through alternating stages of rapid growth and plateaus. In contrast, in some vertebrate as well as many invertebrate species, the young emerge looking completely different from the adults and spend their early lives acquiring body mass as a larva, then go through a metamorphosis (complete rearrangement of body pattern) to emerge in the adult form. This is typical of some insects, such as butterflies and moths, and some amphibians, such as frogs.

In birds and mammals, young generally emerge looking vaguely like adults, but the body proportions are very different, characterized by an enlarged head and reduced supportive limb elements. During the rapid growth phase of these individuals, the head grows much less than the body, limbs elongate, and skin maturation results in the typical adult feather or fur patterns. Since young birds and mammals are usually dependent on their parents for a time after birth, the incomplete development at birth is not a disadvantage.

The pattern of human growth provides a good example of the change in body proportions throughout development from birth to adult (the ultimate size of the individual). At two months past conception, the head of the embryo makes up approximately 50 percent of its total length, and the limbs less than 25 percent. At birth, the head size makes up about 25 percent of the total length and the limbs approximately 37 percent. Throughout childhood, the head size to limb length ratio continues to decrease toward the adult pattern of head size about 12 percent of body length and limb size over 50 percent of body length.

Bone Growth

The increase in body size is supported by increased skeletal structure in vertebrates, as a soft and pliable cartilage matrix becomes invested with hard and resistive bone. In the early newborn, the cartilage model of the eventual skeletal structure serves as the template for bone deposition. Bone-forming cells called osteoblasts lay down a "collar" of calcium and phosphate crystals in a lattice matrix around the shaft of the cartilage. This provides the strength for the bone to bear weight. At the same time, the terminal ends of the cartilaginous model also develop centers of osteoblastic activity, called epiphyses (singular, epiphysis). As the bone elongates, the collar elongates and the epiphyses in the ends of the bones continue to deposit calcium and phosphate. Eventually, the cartilage between these two bony centers of ossification, called the epiphyseal plate, is completely replaced with the bony matrix, and growth (limb elongation) ceases.

The epiphyseal plate is maintained under the influence of a hormone from the pituitary gland (the master endocrine gland at the base of the brain) called growth hormone (GH). However, at puberty, the hormones

Computer color-enhanced X ray depicting the hand development of a two, six, and nineteen year old male.
Computer color-enhanced X ray depicting the hand development of a two, six, and nineteen year old male.
associated with reproductive maturity (estrogen and testosterone) cause an initial surge in GH release and in elongation of limbs, and then cause closure of the epiphyseal plate, causing growth to cease. This "growth spurt" tends to happen earlier in human females than in human males.

Hormonal Control

Growth hormone is essential to normal growth and development. It is regulated by two hormones released from the brain (in the hypothalamus) which cause daily peaks of GH in the blood. The peaks are most closely associated with the sleep cycle, large peaks appearing right after going to sleep and right before waking. Since growth hormone is associated not only with growth and differentiation but also tissue maintenance and repair, it makes sense that the peak of GH activity would occur during the nonactive period. In fact, the hypothalamic hormone that induces the release of GH (GH-releasing hormone) is a sleep inducer. Some researchers have suggested that the disappearance of deep sleep as we age and associated reduction of GH release may contribute to the physical decline that humans experience in old age.

GH represents about one-half the total hormone content of the anterior pituitary gland. GH stimulates the absorption of amino acids and protein synthesis necessary for development of skeletal muscle; stimulates breakdown of fat for energy utilization by cells of the body; stimulates the formation and maintenance of the epiphyseal plate in bone, and encourages lengthening of the long bones by stimulation of osteoblast cellular deposition of bone; and it stimulates the liver to make growth stimulating proteins, called insulin-like growth factors (IGF), which then affect the cellular metabolism of all cells in the body.

Growth Disorders

Abnormal secretion of GH can lead to growth disorders. Oversecretion of GH can lead to gigantism, marked by extreme limb elongation especially in the terminal elements (hands and feet) and enlargement of the face, especially the chin, nose, and ears, a condition called acromegaly . This condition can occur either because of a tumor of specific cells that manufacture GH or GH-like proteins or because of insufficient regulation by the hypothalamic releasing factors that control GH release. Not only are body proportions distorted with acromegaly, but hypersecretion of GH causes excessive sweating and secretion by the skin, enlargement of the heart, and sometimes high blood pressure. As a result of the many physiological effects of excessive GH secretion, life expectancy is shortened.

In contrast, lack of sufficient GH, especially during early years of development, can produce short stature or dwarfism. However, short stature with normal body proportions can be found throughout the human population and is probably associated with deficient production of IGF from the liver. For example, African pygmies are short, but normally proportioned people who have normal GH levels, but exhibit low levels of one form of IGF. Low GH release after birth can result in retarded growth, and these individuals are at risk for hypoglycemia (low blood sugar) as well. This condition severely impairs normal development, and these individuals are not only short but exhibit greatly retarded maturation of all tissues.

SEE ALSO Bone ; Development ; Fetal Development, Human ; Hypothalamus ; Insect ; Pituitary Gland ; Scaling

Susan B. Chaplin

Bibliography

Tanner, James M. Foetus into Man: Physical Growth from Conception to Maturity. Cambridge, MA: Harvard University Press, 1990.

Vlijasek, Stanley J., et al., eds. The Cambridge Encyclopedia of Human Growth and Development. New York: Cambridge University Press, 1998.



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