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Male Fertility’s Two-Front War, Plus Sneaky HFCS

Today’s edition of Monday Musings is a quick account of two recent studies that highlight actual, literal threats to the fruitfulness and productivity of the human male loin. For years, the average male sperm count has been decreasing [1], especially in Western industrialized nations, by about 1% to 2% per year. Globally, of course, populations have been increasing, so sperm is successful by playing the numbers game, but we’re worried about the individual. We’re concerned with per capita sperm count. And it’s been dropping.

But why?

For candidate number one, let’s look to the bones. Bones, as you know, are active, living organs rather than passive inert structures. They grow (in response to a complex soup of hormonal messaging), they densify (in response to weight-bearing activity), they even atrophy (in response to a lack of weight-bearing activity and/or gravity). The primary regulators of bone growth and function are the sexual organs, which manufacture testosterone [2] and estrogen [3], the hormones with a big effect on bone structure, but new mouse research is showing that it’s a two-way street: osteocalcin, a hormone produced by bone osteoblasts, induces the testicles to produce testosterone [4]. Male mice dads with low osteocalcin levels produced smaller, less frequent litters than male mice with normal levels of osteocalcin, who had larger litters and more of them. The tiny mice testicles actually carried a heretofore undiscovered osteocalcin receptor; we human males carry the same receptor in our testicles, so it’s likely that osteocalcin plays a similar role in human male fertility. You’d better take your osteocalcin supplements, fellas!

Of course, by “osteocalcin supplements,” I mean resistance training and protein, both of which¬†help raise osteocalcin [5] levels in human males. People probably get enough protein [6] (just make sure it’s mostly animal-based), but they generally don’t lift enough heavy stuff to stimulate osteocalcin and increase bone density, and this may be reflected in the lowered sperm counts (and osteoporosis rates).

Candidate(s) number two are agricultural pesticides and their effects on the endocrine system [7]. Drawing upon a pool of 134 chemicals, a trio of scientists from University of London’s Toxicology Center ran a thorough analysis [8] of the anti-androgenic (blocks or mimics testosterone and other male androgen hormones) potential of 37 popular pesticides, fungicides, and herbicides in use across Europe. Of the 37, 30 were found to interact with the androgen receptors. Of the 30, 14 were previously known, but 9 were newly identified as anti-androgens, while 7 were identified as androgens (bodybuilders, don’t get any ideas).

Take a look at the group’s supplementary PDF [9] for some troubling data. The most widely-used pesticide tested negative for androgen antagonism, but the next four most prevalent pesticides all tested positive, including two – cyprodinil and pirimiphos-methyl – which were previously unknown to affect the androgen receptors. Critics rightly point out that the tests were in vitro and, thus, inconclusive. The authors agree. In fact, due to “estimated anti-androgenic potency, current use, estimated exposure, and lack of previous data,” the authors “strongly recommend that dimethomorph [used on potato crops, squash, melons, tomatoes], fludioxonil [used on strawberries, tomatoes, and wine and table grapes], fenhexamid [grapes and strawberries], imazalil [citrus], ortho-phenylphenol [mainly used on post-harvest citrus, but it’s also found in general surface disinfectants] and pirimiphos-methyl [stored grains] be tested for anti-androgenic effects in vivo” using lab animals.

That seems like a reasonable request. A free market requires the full availability of relevant information to all parties involved. Given the preliminary in vitro results of these early tests, I think whether or not a relatively novel pesticide in wide use across the industrialized world interferes with human sperm count, motility, and other androgenic hormones is highly relevant information.

One more quick bit: all that high fructose corn syrup [10] you aren’t guzzling might have even more fructose than previously assumed. See, we all like to throw around that 55/45 fructose/glucose number as proof that HFCS isn’t that much worse than plain old white sugar [11], but a study from late last year [12] examining various HFCS-sweetened commercial products [13] arrived at a different number. The mean fructose content for all HFCS tested was 59%, with several popular products from major brands coming in at 65% fructose! I wasn’t able to find any brand or product names, but it’s safe to assume – and the authors agree – that people consuming popular products sweetened by HFCS are consuming more fructose than indicated by packages, producers, or previous assumptions. This doesn’t directly affect us, since, you know, we avoid the stuff altogether, but what about family, friends, or coworkers who eat it everyday? There’s no way to know. At least with sucrose, your liver can expect a certain proportion of fructose.