The Prostate Gland—is it ‘badly designed’?1
Countering design critics
The following brief web article was adapted from the section on alleged ‘bad designs’ in Dr Sarfati’s new book By Design, which is subtitled, Evidence for nature’s Intelligent Designer—the God of the Bible.
The prostate is a walnut-sized gland in male mammals that secretes a clear, slightly alkaline liquid that comprises about 10–30% of the volume of semen. Thus it is a vital musculoglandular organ for reproduction. Some critics of creation/intelligent design complain that it is badly designed because the urethra (the tube through which urine flows out) passes through it, so if the prostate enlarges, it restricts urine flow.
However, the positioning makes a great deal of sense. Rather than the urethra going through the prostate, it is more accurate to consider the prostate as a thickening of the urethral wall. It produces a major component of semen (other than the sperm, which come from the testicles; the testicles have to be outside the body for cooling purposes; much of the liquid is produced by the seminal vesicles). The prostate’s secretions have to be injected into the urethra at the right time to join up with the spermatozoa from the testicles. The prostate arrangement means that its 30–50 glands secrete into 16–32 ducts that open independently into the urethra. The whole prostate contracts during ejaculation, and its smooth muscle quickly empties its contents and forces the semen along. The prostate also contains nerve plexuses, and is responsible for much of the pleasure of male sexual activity.
So why did the designer not simply place the prostate alongside the urethra? Presumably because it would require a new duct system, and extra systems to propel its secretions and propel the semen along.
The prostate also acts as a spacer between the bladder and the urogenital diaphragm. This provides a support for the bladder, and prevents the urethra kinking when the bladder is full. Otherwise extra ligaments and attachment structures would be required. This positioning could also be necessary to shut off urine flow during ejaculation. Indeed, one potential problem with prostate removal is incontinence.
As for the problems with enlargement, they are not normal features but pathological ones, so in a biblical framework they would be regarded as post-Fall. In any case, even by age 80, only about half of men actually have significant enlargement of the gland, and only a quarter have any urinary symptoms. In many men, the prostate actually shrinks as they get older.2 If this was a design problem, all men would suffer from it. Factors involved in prostate problems include hormone imbalance, obesity, infections, medicinal side effects, and mutations.
Japanese men living in Japan have much less problem, whereas Japanese men living in America develop the same level of problems as Americans from other ethnic backgrounds. The reason for this is thought to be differences in diet. The Japanese diet comprises a lot of fish, which is rich in omega-3 fatty acids, which are anti-inflammatory, and zinc, which inhibits an enzyme involved in conversion of testosterone (male hormone) to dihydrotestosterone, which stimulates hypertrophy (enlargement) of the gland. The traditional Japanese diet also includes regular portions of tofu, which has mild oestrogenic effects that counter the deleterious effects of sometimes excessive dihydrotestosterone on prostate hypertrophy. Inadequate vegetable consumption quadrupled the risk of prostate problems in one study. Clearly, a defective diet could be a large factor in the men who suffer from prostate enlargement.3
Overall then, the prostate normally functions extremely well throughout a man’s life. Other mammals have a similar design. In any case, if it were as bad as evolutionary critics say, then surely natural selection would have eliminated this design.
- Thanks to Dr Don Batten for much of the information in this article, as well as Dr Jerry Bergman, Was the prostate poorly designed? Creation Research Society Quarterly 44(3):230–235, 2008. Return to text.
- Isaacs J.T., Etiology of benign prostatic hyperplasia. Eur. Urology. 25(suppl 1):6–9, 1994. Return to text.
- Araki, H., et al., High-risk group for benign prostatic hypertrophy, Prostate 4:253–64, 1983. Return to text.
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