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Do Humans Undergo Metamorphosis?

Here is another speculation concerning the remarkable human life cycle. Do humans undergo metamorphosis or are we direct developers?

Puberty as a variation on the theme of metamorphosis

In mammals, one of the most striking displays of hormonal control of differentiation occurs during human puberty. If metamorphosis is understood to comprise the processes of dramatic change whereby a juvenile reaches maturity, both sexually and biochemically, then human puberty may be considered a variation of the metamorphic theme. Recent research suggests that the processes of metamorphosis and puberty may, in fact, be quite similar. A good summary of puberty is given by Styne and Grumbach (1978):

Puberty is the transition between the juvenile state and adulthood; during this stage of development, secondary sex characteristics appear and mature, the adolescent growth spurt occurs, fertility is achieved, and profound psychologic effects are observed. These changes result directly or indirectly from maturation of the hypothalamic-pituitary gonadotropin unit, stimulation of the sex organs, and the secretion of sex steroids.

Certainly, striking changes in body form occur during this time. At the beginning of puberty, boys and girls have the same proportion of muscle mass, skeletal mass, and body fat. By the end of puberty, men have 1.5 times the skeletal and muscle mass of women, whereas women develop twice as much body fat as men (Forbes, 1975). Secondary sex characteristics* also develop at this time, marking the change from the juvenile form to the sexually mature adult. In women, the development of breasts is controlled by a surge of estrogen secreted by the ovaries; and in men, the maturation of the penis and testes is controlled by the testosterone released from the testes. In both sexes, pubic and axillary (underarm) hair development is regulated by testosterone, which is secreted by the testes in males and by the adrenal glands in females. Men also undergo testosterone-dependent enlargement of the larynx and its associated muscles and cartilage, leading to a deepening of the voice. In both sexes, puberty is the time when major sexual development takes place. In females, menarcheothe first menstrual periodorepresents the new integration of the hormonal cycles releasing the developing egg from the ovary. In males, fertility is achieved when meiosis begins in the male germ cells and the spermatic ducts hollow out to form a channel for the sperm cells to pass from the testes into the urethra.

The hormonal basis of puberty is thought to be very similar to that of metamorphosis. The metamorphoses of amphibians and insects were both seen to be regulated by hormonal changes that were initiated by the neurohormones of the brain (TSH-RF and PTTH, respectively). The changes of human puberty in both sexes are initiated by luteinizing hormone releasing factor (LH-RF) from the hypothalamus of the brain* (Figure 1). Like TSH-RF, this factor is released from the hypothalamic neurons to the medial eminence (infudibulum) of the pituitary gland. Similarly, the LH-RF is then transported by the blood vessels of the pituitary to the anterior lobes of that gland. Once in the anterior pituitary, the releasing factor causes the release of a tropic hormone. In human puberty, LH-RF releases luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Collectively, these two hormones are called gonadotropins because they stimulate the development of testes in males and ovaries in females. As a result of this stimulation, the gonads secrete the sex hormones: testosterone from the testes and estrogen from the ovaries. The various morphological and behavioral changes of puberty are due to the actions of these hormones on the various target tissues. As in metamorphosis, there appears to be a maturation-inhibiting hormone whose activity decreases to permit the reactivation of development. In humans, this hormone is probably melatonin, whose serum concentration decreases as that of LH rises (Waldhauser and Dietzel, 1985).

Figure 1
Figure 1   Hypothalamus-pituitary-gonadal axis in mammalian sexual development.

Although the details concerning the initiation of puberty are not known, Grumbach and co-workers (1974) have proposed the following mechanism (Figure 2). Before puberty, the child secretes a small amount of LH-RF, so that the amounts of circulating LH and FSH are very small. Therefore, the gonad remains immature and secretes little estrogen or testosterone. Moreover, the hypothalamus is highly sensitive to these sex hormones and turns off LH-RF production when the circulating sex hormones rise anywhere above their very low levels. The onset of puberty is thought to involve the maturation of the hypothalamus. At this time, the hypothalamus becomes less responsive to the negative feedback of testosterone and estrogen. Thus, it takes more of these hormones to turn off LH-RF secretions. (This is analogous to giving a thermostat a higher set point.) Thus, the hypothalamus makes more LH-RF, ultimately causing the further differentiation of the gonads and the release of more testosterone or estrogen. This, in turn, causes the development of those secondary sexual characteristics. Read a recent review of work on the onset of puberty.

Figure 2
Figure 2   Proposed mechanism for the induction of puberty in humans. Before puberty, the hypothalamus is sensitive to very small concentrations of sex steroids and stops LRF production, thereby halting further steroid synthesis. Sex steroids are kept at low levels. At the onset of puberty, the hypothalamus becomes progressively less sensitive to the sex steroids, thereby allowing more of them to be synthesized, until finally the adult level of sex steroids is achieved. Relative widths of arrows indicate levels of hormone production. (After Grumbach et al., 1974.)

It can readily be seen, then, that puberty is a hormonally controlled reactivation of development leading to sexual maturity and changes in bodily form and physiology. As such, it has many parallels to the metamorphic changes seen elsewhere in the animal kingdom.

* The primary sex characteristic is the presence of ovaries or testes.

** LH-RF is also known as gonadotropin releasing factor (GnRF) since it acts to release both luteinizing hormone and follicle-stimulating hormone. The LH-RF-secreting neurons do not form in the brain but migrate from the olfactory placode in the developing nose. Defects in the migration pathway cause Kallmann syndrome, a condition causing both sterility and anosmia (lack of smell).

Literature Cited

Forbes, G. B. 1975. Puberty: Body composition. In S. R. Berenson (ed.) Puberty. Stenfert-Kroese, Leiden. pp. 132-145.

Grumbach, M. M. Roth, J. C., Kaplan, S. L., and Kelch, R. P. 1974. Hypothalamic regulation of puberty in man: Evidence and concepts arrived from clinical research. In M. M. Grumbach, G. D. Grave, and F. E. Meyer (eds.), Control of the Onset of Puberty. Wiley, New York. pp. 115-166.

Styne, D. M. and Grumbach, M. M. 1978. Puberty in the male and female: Its physiology and disorders. In S. S. C. Yen and R. B. Jaffe (eds.) Reproductive Endocrinology. Saunders, Philadelphia. pp. 189-240.

Waldhauser, F. and Dietzel, M. 1985. Daily and annual rhythms in human melatonin secretion. Role in puberty control. Ann. N.Y. Acad Sci. 453: 205: 214.

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