Little is known of the male climacteric.

When does it occur, if it develops? Is it a constant occurrence? What is the specific symptomatology? Should sex-steroid-replacement techniques be employed? What, if any, are the patterns of sexual responsivity engendered by these replacement techniques? So little is known of the male climacteric.

Now that these definitive laboratory studies can be done with some confidence, relative rapidity, and at not too staggering a cost, much more will be known of the male climacteric within the next few years.

There will be more basic information of the effects of steroid replacement not only upon the aging male's sexual response cycle per se but also, and infinitely more important, upon the total metabolic function of the climacteric male.

Without the gross advantage of fully supportive laboratory data, tentative clinical conclusions have been drawn with reference to the influence of steroid-replacement techniques upon the aging male's sexual functioning.

These conclusions may have to be restated or even possibly abandoned in the not-too-distant future as more definitive information is accrued from the healthy combination of clinical and laboratory evaluations.

When the male notices alteration of his orgasmic response pattern from the usual two-stage to a one-stage process, when he consistently responds during orgasmic experience with loss of seminal fluid volume without significant ejaculatory pressure, when average ejaculatory volume is cut at least in half, and when none of these reactions develop under the extenuating circumstances of a long continued plateau phase of voluntary ejaculatory control, he may be experiencing the physiological expression of reduced production of male sex-steroid to metabolically dysfunctional levels.

Occasionally prostatic pain develops from spastic contractions of the organ during the ejaculatory process.

These spastic contractions create a continuing sense of ejaculatory urgency that may last through the entire orgasmic experience until full expulsion of the seminal-fluid bolus has occurred.

With the subjectively painful evidence of physiological prostatic spasm recurring with most ejaculatory experiences and no obvious pathology of the prostate gland demonstrable to adequate urological examination, sex-steroid replacement also may be indicated.

Until there is a more reliable laboratory definition of a general metabolic need for testosterone replacement and until the clinical existence of the male climacteric can be defined with security during treatment of older men for sexual dysfunction, individual eases must be treated empirically.

If the sexually dysfunctional male describes a physiological or psychological symptomatology that appears to indicate clinical need for sex-steroid replacement and if the general physical and laboratory evaluations are negative, there is no professional hesitancy to institute such replacement techniques.

However, sex-steroid-replacement techniques are not employed routinely for the 50 to 70 year age group man referred for therapy.

Steroid replacement concepts and specific techniques, together with indications and contraindications for the aging male will be presented in more complete form by the Foundation in monograph format in the future.