I answered a post on the IguanaMail List (thread: Picture of male breeding aggression) rather briefly yesterday, saying, basically, that the brain is as big as it needs to be (for animals with normal brain size for their species, living in their native habitat), thus leading to the probability of a behavioral trigger for the extreme aggression some iguanas display. I thought my further thoughts on the matter might be of interest to some folks here...

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I woke up this morning thinking about the situation of extreme breeding season aggression. Some of you may remember Bon's iguana, iZ, who became fiercely aggressive as a result, it was later found out, of pain caused by a tumor (see Tough Love, or Attigtude Adjustment.

So, might there be a physiological or biochemical reason for some of the cases of extreme breeding aggression seen in some males? Er, male iguanas? Assuming, of course, more obvious things like tumors and illness and other sources of pain have been ruled out by the vet.

Some of you through the years may have wandered through my Chronic Neuroimmune Diseases website and come across my articles on Estrogen Dominance and Glucuronidation (linked to the Environmental Estrogens/Xenoestrogens section of my Hormones page), or vaguely remember me talking about this.

The quick overview (see Glucuronidation for more complete info): the body produces an acid that binds with the body's used estrogen, keeping control of it as it is escorted out of the body. Thus, the body keeps producing estrogen, but also gets rid of the estrogen previously produced.

However, an enzyme may be created by, it is believed, one of the 500 or so cousins of E. coli that live quietly (and benignly or commensally) in our gut, that breaks this bond or otherwise prevents it from being formed. When that happens, the bound and should-have-been-bound estrogen is free to keep circulating through the body, wrecking havoc as it goes.

So, I started thinking: does the same thing happen with testosterone? Is there something that is supposed to be binding the 'used' testosterone? If so, could something cause this bond to be broken, or kept from being made in the first place.

Another possibility: Could some part of the conversion cascade that results in testosterone and its metabolites be faulty, thus increasing total testosterone (higher up the conversion cascade) or free testosterone (that which circulates in the blood at any given time)?

And then I went back to sleep.

When I got up and got online, however, I did google "binds testosterone" and found that, indeed, there are similar processes going on in males that can go wrong, just as they can in females. In fact, women will recognize many of the hormones, since they play roles in our own monthly cycling and cause problems as we progress through perimenopause.

The following is from a booklet on low testosterone, but it simply and clearly describes how things work properly and why they might become dysfunctional:

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Testosterone Production (page 4)
The body carefully controls the production of testosterone. Chemical signals from two locations - the pituitary gland at the base of the brain, and a part of the brain called the hypothalamus - tell the testes how much testosterone to produce.

The hypothalamus controls hormone production in the pituitary gland by means of gonadotropin-releasing hormone (GnRH). This hormone tells the pituitary gland to make follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH signals the testes to produce testosterone. If the testes begin producing too much testosterone, this is sensed by the brain which sends signals to the pituitary to make less LH. This, in turn, slows the production of testosterone. If the testes begin producing too little testosterone, the brain senses this and sends signals to the pituitary gland telling it to make more LH, which stimulates the testes to make more testosterone.
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The role of binding testosterone in males and females is played by a hormone cleverly called sex-binding hormone protein (SBHP). Needless to say, SBHP binds more testosterone in females than it does in males, once they reach puberty. Since both males and females produce testosterone and estrogens, it isn't surprising the SBHP production and function is a complicated one, resulting from the amounts of free estrogen and testosterone, which affect the body's production of SBHP--or lack of it.

A research paper, Sex Hormone Binding Globulin and the Assessment of Androgen Status, goes into this rather densely but might be useful in talking to your vet about getting your ig's hormones tested.

Now, true, this paper is written more from the perspective of women's diagnosis and health issues arising from increased levels of testosterone, but the male is the flip side of the female (physiologically if not socioemotionally and so, where there are dysfunctions and dysregulations that can cause a decrease in total and free testosterone in males and females, and increases in females, there are going to be things that cause increases in males.

(Here's another easier-to-read discussion of the free and bound testosterone, if you want to read a bit more.)

Excess testosterone can cause irritability, even rage. The steroids abused by body builders and athletes are synthetic testosterone; regular long-term use leads both to the irritability and rage (as well as severe acne and impotence, which probably does little to ameliorate the irritability and rage.).

The impotence, btw, is caused by the fact that excess testosterone is converted into estrogen, with the result that males become feminized, leading to weight gain and reproductive problems (which leads us back to Environmental Estrogens, for those who want to look at the long term effects of male feminization of a species and the sources of environmental--xeno--estrogens).

What I'm wondering is this: Could there be an excess testosterone situation occurring in breeding season male igs, perhaps due to a pituitary, hypothalamus, or adrenal problem, or a problem with the liver detox pathway associated with SHBP production/function, that is not leading to feminization because breeding season--and the cyclical increase in testosterone--occurs for only a relatively short period of time each year?

Remember: in the wild, males are in season for only 28-30 days, not months, as they are in captivity. A wild male iguana may have this type of problem, but he lives in a much bigger area and is only dealing with testosterone overdose for a month, if that, out of the entire year. In captivity, where breeding season for males lasts much longer (and may be triggered twice in one year), this ain't good for an iguana with a genetic or acquired hormone regulatory system.

So, perhaps a talk with the vet about testing to check out the androgen/testosterone cascade, including free and total testosterone, and SHBP, might start yielding clues. Ditto checking out the pituitary, hypothalamus, adrenals, and liver function.

The problem with the standard LFTs (liver function tests) is that they really don't tell you much - just whether enzymes are elevated or not, or whether the liver is cirrhotic or nearing failure. They don't tell you anything about what detox pathways are impaired. There is such a test for humans, but it involves ingesting caffeine and aspirin before the 24 hour saliva and urine collection, so I'm thinking it won't be particularly usable with igs.

Anyway, that's what I woke up thinking about.
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Melissa Kaplan
Anapsid.org
Lizards-in-Scarves Blog