Body odor or body odour (BO) is present in all animals and its intensity can be influenced by many factors (behavioral patterns, survival strategies). Body odor has a strong genetic basis, but can also be strongly influenced by various diseases and physiological conditions. Though body odor has played an important role (and continues to do so in many life forms) in early humankind, it is generally considered to be an unpleasant odor amongst many human cultures. Causes
In humans, the formation of body odors is caused by factors such as diet, sex, health, and medication, but the major contribution comes from bacterial activity on skin gland secretions. Humans have three types of sweat glands: eccrine sweat glands, apocrine sweat glands and sebaceous glands. Eccrine sweat glands are present from birth, while the latter two become activated during puberty. Among the different types of human skin glands, body odor is primarily the result of the apocrine sweat glands, which secrete the majority of chemical compounds that the skin flora metabolize into odorant substances. This happens mostly in the axillary (armpit) region, although the gland can also be found in the areola, anogenital region, and around the navel. In humans, the armpit regions seem more important than the genital region for body odor, which may be related to human bipedalism.
Homeostatic mechanisms
Homeostatic control can change the PCO2 and hence the pH of the arterial plasma within a few seconds. The partial pressure of carbon dioxide in the arterial blood is monitored by the central chemoreceptors of the medulla oblongata. These chemoreceptors are sensitive to the levels of carbon dioxide and pH in the cerebrospinal fluid.The central chemoreceptors send their information to the respiratory centers in the medulla oblongata and pons of the brainstem. The respiratory centres then determine the average rate of ventilation of the alveoli of the lungs, to keep the PCO2 in the arterial blood constant. The respiratory center does so via motor neurons which activate the muscles of respiration (in particular, the diaphragm). A rise in the PCO2 in the arterial blood plasma above 5.3 kPa (40 mmHg) reflexly causes an increase in the rate and depth of breathing. Normal breathing is resumed when the partial pressure of carbon dioxide has returned to 5.3 kPa. The converse happens if the partial pressure of carbon dioxide falls below the normal range. Breathing may be temporally halted, or slowed down to allow carbon dioxide to accumulate once more in the lungs and arterial blood. The sensor for the plasma HCO−3 concentration is not known for certain. It is very probable that the renal tubular cells of the distal convoluted tubules are themselves sensitive to the pH of the plasma. The metabolism of these cells produces CO2, which is rapidly converted to H+ and HCO−3 through the action of carbonic anhydrase.