Wasted on the Young

Having graduated by stages from the turbulent sexual vectors of youth to the detachment of old age, I currently survey the world of puberty from 30,000 feet. From this vantage point the terrain looks challenging, to say the least. Gender dysmorphia is rife (ie 1), locked in an uncomfortable four-way with reduced impulse control (2-6), increased depression and anxiety (7, 8), and accelerated pubescence. 

This post focusses on the last of these, the complicated transition into sexuality that has long been a substrate for lycanthropy (9-11).

Accelerated onset of puberty predominantly affects females / people with uteruses / the current thing – I am neither a biologist nor a SCOTUS candidate (12) – and is becoming increasingly common.

The age at which girls start to develop breasts, one of the first physical signs of puberty, has declined among white girls from 11 in the 1980’s to 10 in the mid-90’s, with black girls showing a year earlier, at age 9 (13). In fact, the age of puberty in girls has dropped by about three months per decade since the 1970s (ie 14), and parallel but less extreme shifts have occurred in boys (15).

These changes are so extensive that the diagnostic criteria for central precocious puberty, a rare hormonal syndrome triggered by lesions in the central nervous system, may have to be re-drawn. It has been suggested, for example, that the age threshold between normal and precocious puberty, previously set at 8, should be lowered to ages 7 and 6 in white and black girls respectively (16).

That is a problem for the medical profession to decide on. But does it matter to early pubers?

Probably, yes.

Girls who go through puberty early are at greater risk of depression, anxiety, substance abuse and other psychological problems (17). They are also likely be at a higher risk of breast (18) and uterine (19) cancer in later life, and are more at risk of early death (20); as are boys (21), likely for evolutionary reasons which are explored below. 

Re-setting the endocrine clock back to circa 1950 would make sense, and there are at least four interacting factors which could be manipulated to achieve this re-setting. Childhood obesity, which is obviously increasing (ie 22), is one factor which predisposes to early puberty (23, 24). Exposure to endocrine disruptors, which is also increasing (25) may be another (26-28). Neuroinflammation and gut dysbiosis, both of which are rife, are the third and fourth. 

The estrobolome (the aggregate effect of bacteria in the gut capable of metabolizing estrogens and thereby modifying estrogen levels in the blood) is known to affect inter alia the risk of breast cancer risk (29). More recently, it has been implicated in affecting the age of puberty (ie 30); both early antibiotic use and the lack of fiber in the modern diet appear to bring puberty forward. 

Prebiotic fibers up-regulate saccharolytic gram-positive species, which down-regulate various gram-negative species expressing beta-glucuronidase (31, 32) and thereby reduce circulating estrogen (33, 34). Thanks to the ultra-processed diet our intakes of prebiotic fibers have greatly declined, which pushes estrogen levels up. This opens up the prospect of reducing the risk of breast cancer, and delaying puberty, by restoring traditional foods and traditional amounts of prebiotic fibers to our children’s plates.

As a traditional diet also mitigates against neuroinflammation (35, 36) and obesity (37), this will cut down on three of the four known risk factors for advanced puberty. And as endocrine disrupters are also linked to an increased risk of obesity and metabolic disorders (38, 39), dietary strategies designed to reduce exposure to such compounds are likely to further improve our offspring’s sexual health and body composition. 

Such strategies include encouraging our children to avoid fast foods such as hamburgers, fries and chicken nuggets (40), and the excessive use of plastic packaging. Having said that, the effects of endocrine disruptors on pubertal timing are compound specific and vary according to the window of exposure (41), making them unlikely to be a major factor in pubertal acceleration as a whole (41, 42).

However, you should avoid ultra-processed foods in general because they promote obesity (43), infertility (44), generally worse health (45) and, probably, gender dysphoria (1). They affect at least two generations; mothers who consume these foods during pregnancy and breast-feeding put their children at increased risk of the same problems (46, 47), via acculturation and epigenetic shift.

It is all about living in the Goldilocks zone. Under-nutrition and over-nutrition both impair fertility. 

This bi-phasic response occurs in many species. Under-nourished birds lay few eggs, and many of the hatchlings die. When well-nourished, they exhibit advancement in laying, larger clutches, shorter incubation and greater hatching success. When they are chronically over-fed fertility falls, clutches shrink and hatching success declines (48).

Nutrition is important for baby too. Breast-fed girls consume fewer calories than bottle-fed babies (49), grow more slowly in infancy (50), and arrive at puberty significantly later (51). The mechanism probably involves the adipocytokine leptin. Bottle-feeding leads to increased adipose tissue, increased leptin and thence earlier puberty. Conversely, food deprivation (as in anorexia nervosa) reduces fat deposits and thence leptin, delaying puberty (52).

According to life-history trade-off theory – and perhaps common sense – this is the natural order of things. When food is scarce animals tend to start breeding later and live slightly longer, whereas when food is plentiful animals start breeding earlier and live somewhat shorter lives (52, 54). Humans appear to show the same pattern (20, 21). 

In nature, chronic over-nutrition hardly exists. This is why we never developed defenses against the calorie-dense / nutrient-lite ultra-processed foods that dominate our landscape.

Back to baby. 

In humans, omega 6 and 3 fatty acids in breast milk are entirely derived from the maternal diet. Changing maternal lipid intakes during lactation can, therefore, if the homeostatic efforts of the mammary gland are overwhelmed, generate significant differences in the 6:3 ratio of the milk (55). The flood of omega-6’s into industrial foods has surely changed the composition of breast milk over the last few generations, and has likely changed babies’ brains in various ways, including making them more prone to chronic neuroinflammation.

If an infant starts life with a degree of chronic inflammation and continues in that vein, thanks to the ultra-processed diet, might this also affect pubertal timing?

The industrial high fat/high omega-6/high sugar diet causes inflammation in the hypothalamus, with microglial activation leading to hypothalamic dysregulation and, eventually, damage (ie 56). Obesity, dysbiosis and endocrine disruptors do the same thing (57-59). Hypothalamic neuroinflammation has been shown in preclinical studies to release GnRH (gonadotropin-releasing hormone) and related mediators, which would lead directly to early puberty (60). (This last paper, out of Athens Medical School, is a particularly interesting read).

One final possible caution. It has been known for some time that exposure to the blue light from LED’s and LED screens suppresses melatonin synthesis (ie 61), and re-sets the circadian clock in our brains (62). New data show that this kind of light exposure affects sex hormone levels too, and accelerates puberty – at least in rats (63); so here is another element in our dystopian world which may be damaging us.

In short, the answer to the problem of accelerated puberty in both sexes is likely to be the same as the answer to many of our other health problems, and the route to extending our health and life expectancy. Cut down on ultra-processed foods, learn how to cook with basic produce, stop neuroinflammation, avoid endocrine disruptors, take more exercise and spend less time on-line. Or at least switch your smartphone to amber light (64).

The industrial diet has harmed boys in other ways too.

During the 20th century industrialized countries experienced a decline in total fertility rates to well below 2.1, the rate considered necessary to sustain population size (65, 66). Female infertility has become common, and males are falling into line.  

Sperm counts have fallen by 50-60% over the last half century (67-69), and testosterone levels have also declined (70-72). Males are becoming less fertile, less masculine and less robust (73 74).

They are also plagued by increasing numbers of hypospadias (75), a congenital anomaly in males which affect the penis and urethra.  

Hypospadias can generally be surgically corrected, but there are more serious issues at play here. Pre-pubertal crypto-orchidism (failure of the testes to descend) seems to be increasing (76-78), and there has been a spectacular rise in testicular germ cell cancer (79-82).

Maternal diet appears to be an important factor behind the rise in germ cell cancer; a more industrial diet is associated with greater risk (82). The endocrine disruptors are implicated in hypospadias (83). Both diet and the endocrine disruptors seem to be involved in falling testosterone, sperm quality decline (84) and the shrinkage of pre-pubertal penis size (85), and the endocrine disruptors (again) are probable risk factors for the dreaded micropenis (86).

Accelerated puberty is just a fig leaf in the prevailing wind, but it adds yet another set of negative health indices to our already appalling public health. How much more damage must we and our children suffer before the food multinationals are finally brought to heel?

Next week: C-PAP and Star Wars.

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