The average age of onset of puberty, when girls physically become women, has been decreasing since 1850. The earlier puberty begins, the earlier menstruation occurs, there being about a two-year period between appearance of the breasts and onset of the menstrual periods. In general, the reason for this is thought to be better health for girls, ie, less disease and improved nutrition. Less disease is linked to a cleaner environment, less child labour and immunisations. Better nutrition means not necessarily a better class of food but more calories and, most importantly, a more regular and continuous supply of calories. The earliest sign of puberty is breast development. One hundred and fifty years ago, this used to start around age 15 to 16. It is now considered normal if it begins at eight in girls. When I was in training 35 years ago, the lower limit of normalcy was nine years. Like everything else in medicine, onset of puberty depends on the two major factors that affect our health: genetics and the environment. These are not separate since various environmental factors can turn on or turn off genes so that their expression does not take place. Genetic factors account for half of the variation of pubertal timing and this is clearly seen between mothers and daughters. Environment factors are clearly important as well. For example, puberty occurs later in children raised at higher altitudes. Young girls who spend lots of time in the company of adult men have an earlier onset of puberty, something most adult women seem to know instinctively but which seems, in many instances, not to be acted upon in the Caribbean.
The most important of the environmental influences is nutrition. This explains how the difference in onset of puberty seen at one time between Afro-American girls (early average onset) and Japanese-American girls (late average onset) disappears after one or two generations of a western diet. Of late, however, environmental pollutants are being implicated more and more, despite the resistance and wonderful advertising of the chemical corporations and their spin-doctors. For example, bisphenol (BPA) is a chemical frequently used to coat the interior of baby bottles and food and beverage cans. BPA mimics the action of the female hormone estrogen and theoretically can lead to the early onset of puberty, although this has not yet been proven. It leaches out of plastic into liquids and foods, especially when warmed, as occurs when baby bottles or food is warmed up in the microwave, and has been found in over 90 per cent of Ame-ricans. One of the problems with early onset of puberty, quite apart from the apparent ones of children menstruating, early sexual activity, unwanted pregnancies, abortion, venereal disease, sexual abuse, mental illness ("madness" usually starts during puberty) etc, you know, the usual bacchanal that we daily grapple with in these sun-blessed isles, is that in girls it is associated with higher prevalence of disease in later life, especially breast cancer. So there is justifiably lots of interest in the medical community about chemicals and their effects on human health and two news reports attracted attention this week.
For some time now there has been a massive worldwide decline in bee colonies ("colony collapse disorder"), so bad that the decrease in bee population has began to threaten agriculture. Bees not only produce honey but they are the pollinators for many crops including almonds, apples, avocados, cantaloupes, cucumbers and a host of others. Two studies, one from France the other from the UK, strongly suggest that the reason for the decline is a new pesticide, a nerve agent, called neonicotinoid. The compound has already been banned in France and Italy and a host of other countries. Of interest is that the American Government's own chief bee researcher, Dr Jeffrey Pettis of the US Department of Agriculture, had conducted a study two years ago, showing that bees exposed to microscopic doses of neonicotinoids were much more vulnerable to disease-but his study had not been published until two months ago, when it was described by The Economist as "a plausible hypothesis for the cause of colony collapse disorder."
It is wondrous strange how studies that implicate toxicity from chemicals have a habit of not being published for years until the weight of evidence overcomes the natural propensity of chemical corporations to not release data affecting their profits.
The second study is quaintly described in medical jargon as "a prospective study that observed the female offspring of exposed and unexposed women who worked in a greenhouse during pregnancy and were exposed to pesticides in the first trimester and examined the breast development of their offspring at six to 11-years-old." In prenatally exposed girls, mean onset of breast budding was 8.9 years compared with 10.4 years in the unexposed girls. After checking that the girls in both groups, exposed and unexposed, were similar in all aspects, the conclusion of the Danish authors that "maternal exposure to pesticides in early pregnancy is associated with earlier breast development among the female offspring" can hardly be faulted.
Poor bees. Poorer children.
