Aging of the

Male Reproductive System

Spring 2007
PS Timiras
Dr. Brown Sequard (Physiologist,
Univ. Sorbonne, Paris) introduced
the idea that some glands secrete
internally (in the blood) potent
substances that affect the whole
organism.
In 1905, these substances were
called “hormones” by the British
physiologist E.H. Starling.
Comparison between the relative simplicity of the male reproductive
system and the complexity of the female reproductive system.
Anatomy of the Male Reproductive Tract
In humans the principal reproductive organ is the brain
In addition to the brain, the male reproductive system consists of the:
TESTIS
Primary sex organ suspended outside of
the body in the scrotum

Secondary male sex organs include:

EPIDIDYMIS,
VAS DEFERENS,
EJACULATORY DUCTS
which carry sperm to the urethra

SEMINAL VESISCLES, PROSTATE, &

BULBOURETHRAL GLANDS
which secrete seminal fluid

PENIS with URETHRA

through which flow both urine and semen
 A simplified version of
the male reproductive
endocrinology:

The hypothalamus releases

GnRH into the circulatory
system and, through blood,
directly into the pituitary.
GnRH triggers the release of
the pituitary LH and FSH that
stimulate the testes to
testosterone secretion and
sperm production.
The testis, the male primary reproductive
organ, contains three types of cells, all
necessary for reproduction:
the GERM CELLS or GAMETES,
involved in fertilization.

the INTERSTITIAL CELLS of LEYDIG

that secrete testosterone, the major androgen

the SERTOLI CELLS

with secretory and reproductive functions
 With Age:
• On the average, the male reproductive function
remains normal (or only slightly diminished in some
individuals) until advanced old age (80+ years)
when it decreases
• Subtle changes include:
GnRH
Sensitivity of androgen secretion to LH
Sensitivity of negative feedback between
GnRH and LH
Young Old Figure 12.2
Differences in levels
(total, bioavailable, and
percentage)
of free/bioavailable
Young Old testosterone

Young Old
 Young Older
Young Older

Serum LH concentration Serum testosterone concentration

With aging, loss of high- With aging, decreased
amplitude LH pulses despite responsiveness of testis
normal or increased pituitary LH androgen secretion to LH
stores
 TABLE 12-2
SELECTED NEUROENDOCRINE MODELING ISSUES IN THE
AGING MALE REPRODUCTIVE AXIS

1. How does the timing of GnRH pulse-generator change with

age?

2. Which alterations in the aging male reproductive axis reflect

pathophysiology versus secondary adaptations?

3. What mechanisms account for greater inter-subject

heterogeneity in aging of GnRH-LH testosterone secretion?
Aging of the Prostate
Figure 19.7
 Table 19-12
The Prostate and Testosterone

The healthy prostate is dependent on androgens for growth

In the prostate: testosterone  dihydrotestosterone (DHT)

The enzyme catalyzing this reaction is 5--reductase

DHT stimulates growth of the prostate

 Table 19-13
Normal Aging of the Prostate

After age 40:

Outer regions:
Atrophy of smooth muscle and proliferation of
connective tissue
Flattening of secretory epithelium
Inner region:
Increase in the number of cells present (hyperplasia)

After age 60:

Slower, but more uniform atrophy of the prostate
Accumulation of prostate concretions
Figure 19.8
 Table 1 9- 14 Synopsis of Benign Prostat ic Hyperplasia ( BPH)
Charact eristics

 Caused by g rowt h of th e pro st at e f ro m about age 40 un t il deat h

 Af f ect s 50 % of m en > 5 0 ye ars o ld
 Af f ect s 95 % of m en > 7 0 ye ars o ld
 Clinical sympt oms d ue t o obstru cti on of th e ur eth ra are present up to
2 5 % of me n w it h histo logic e videnc e of BPH
 BPH t issue resembles no rmal prosta t e t issue w it h inc re ased am ount s
of smoot h muscle, g land ular, and / or str omal c ompon ent s
 An enlarg ed prost at e can str angle th e ur eth ra
 BPH is not f ound in men who have been castr at ed or m en who lack 5 -
-reducta se
 Table 1 9- 15 Possible Risk Factor s for Benign Prostat ic
Hyperplasia ( BPH) and Prostat e Cancer

Possible Risk Factor s f or BPH Possible Risk Factor s f or Prost at e Cancer

 Aging
 Use of a nabolic st ero ids
 Dieta ry f act ors
 Genet ic pre disposit ion
 Env ironm ent al to xins
 No oth er m ajor risk fa cto rs
 Genet ic pre disposit ion
 To bacco exp osure
 Cadmium expos ure
 Vit amin A def iciency
 Vasecto my
 Sexually t ransmit t ed d iseases
 Muta genic hor monal f acto rs
 Dieta ry f act ors ( part icularly h igh le vel of
animal fa t)
Treatment of Prostate Cancer
Depends on
Life expectancy
Overall health status
Personal preferences
Size of the prostate
State of disease
Treatments include:
Watchful waiting
Surgery
Radiation Therapy
Hormonal Therapy
Cryotherapy

**PSA controversy pp. 353, 354**