Amerika

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DDT May Have Doomed Us After All

History will record that humanity died of too much humanity: individualism, technology, money, and of course voting and peer pressure — both are popularity contests for illusions — most of all.

When one wonders what went wrong with the Boomers, consider the influence of the pesticide DDT (Dichlorodiphenyltrichloroethane), which prevented malaria and other horrific diseases from the 1940s-1970s but may have de-masculinized the children of parents exposed to it:

We measured p,p’-DDT and p,p’-DDE in preserved maternal serum samples drawn 1-3 days after delivery between 1960 and 1963. We recorded time to pregnancy in 289 eldest daughters 28-31 years later. Daughters’ probability of pregnancy fell by 32% per 10 microg/L p,p’-DDT in maternal serum (95% CI 11-48). By contrast, the probability of pregnancy increased 16% per 10 microg/L p,p’-DDE (6-27). The decreased fecundability associated with prenatal p,p’-DDT remains unexplained. We speculate that the antiandrogenic activity of p,p’-DDE may mitigate harmful androgen effects on the ovary during gestation or early life.

In other words, DDT less increases estrogen than suppresses androgens including testosterone.

Anti-androgenic activity limits testosterone, meaning that male babies had less exposure to it in the womb and were likely to produce less of it during their lives. This is consistent with the damage done to wildlife by DDT (“it turned the frogs gay”):

The increase in the number of reports of abnormalities in male sex development in wildlife and humans coincided with the introduction of ‘oestrogenic’ chemicals such as DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane) into the environment. Although these phenotypic alterations are thought to be mediated by the oestrogen receptor, they are also consistent with inhibition of androgen receptor-mediated events. Here we report that the major and persistent DDT metabolite, p,p’-DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene), has little ability to bind the oestrogen receptor, but inhibits androgen binding to the androgen receptor, androgen-induced transcriptional activity, and androgen action in developing, pubertal and adult male rats. The results suggest that abnormalities in male sex development induced by p,p’-DDE and related environmental chemicals may be mediated at the level of the androgen receptor.

To make matters worse, this hits during the menstrual cycle, ensuring that only low-testosterone-compatible fetuses will be formed:

These results support the potential for DDT to be associated with decrements in estrogen and progesterone levels at times during the menstrual cycle that are critical for ovulation and early pregnancy maintenance.

DDT ended the awful scourge of malaria and probably saved the lives of many troops, but as is the case with all magic, there was a sacrificial cost, and it may have been the hormonal health of future generations.

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