As we grow older, our height weight and strength increases. There are a number of factors that can influence to what extent this occurs; including genetic factors, health and nutrition and environmental factors. However, the key mediators and regulators of growth are specific chemical messengers. Growth hormone is one of these key messengers. It is released from the pituitary gland, a pea-sized structure at the base of the brain. A lack of this hormone will stunt a child’s growth, while its excess can mediate increased growth, even gigantism. Growth hormone does not lose its function once we have stopped growing – it continues to work in adults, playing a role in repair and maintenance of many of the tissues in the body.
Growth hormone travels through the bloodstream and stimulates the liver to produce a protein called insulin-like growth factor (IGF-1), shown at the top of this page. This protein helps the cells that make up the cartilage at either end of our bones multiply. This leads to an increase in length of the bones, conveying growth in children. IGF-1, and hence growth hormone, has many other roles in a growing body, including acting on immature muscle cells to increase muscle mass and regulating metabolism so that adipose tissue stores less fat and sugar levels in the blood are regulated.
However, as we get older, growth hormone is no longer required to perform many of these actions and hence is produced in smaller quantities (see below). By the time we are in our late teens, much of the cartilage at the end of bones has become bone itself, meaning that IGF-1 cannot stimulate bone lengthening.
Hyper-secretion of growth hormone is the cause of gigantism and acromegaly. The former is caused by over-production of growth hormone in childhood, while the latter is associated with continued hyper-secretion even after the key stage of cartilage to bone transformation. In a large number of cases of both diseases, increased production is caused by a benign tumour in the pituitary gland called a pituitary adenoma, derived from a specific type of cell found in the gland (somatotrophs).
Robert Wadlow, shown on the right standing next to his 6 foot father, is the tallest known human to ever have lived and was an extreme case even for the kind of heights produced by gigantism. At the time of his death, which unfortunately came when Wadlow was just 22 years old after a sore from a leg brace became infected, he measured 8 feet 11 inches. Amazingly, he was just 7 inches shorter when he graduated high school and though his growth had indeed slowed, it had shown no signs of stopping. This is interesting, given that he had none of the signs of acromegaly, the most common of which are forehead and lower jaw protrusion and a visible swelling and enlargement of the hands, feet, nose and ears. Traditionally, people with gigantism suffer from accelerated growth but do eventually stop growing at around the same time as normal people. This suggests that Wadlow perhaps didn’t go through the processes that normally signify that the body has reached its final height.
Of course, the pituitary gland can also be affected to result in growth hormone deficiency. Children with this disorder may grow slowly and puberty may be delayed by several years or indefinitely. Growth hormone deficiency has no single definite cause. It can be caused by mutations of specific genes, damage to the pituitary gland, Turner’s Syndrome (when the body is missing an entire sex chromosome) poor nutrition, or even stress (which leads to a condition known as psycogenic dwarfism).
‘Til next time…