Is ED A Psychogenic (Mind) Or An Organic (Body) Problem?
What does it really mean to describe Erectile Dysfunction as Psychogenic or Organic?
Benjamin D Sachs of the University of Connecticut has questioned whether or not the distinction that we tend to make between the psychogenic, i.e. psychological, origin of erectile dysfunction and the organic, i.e. physical, origin of erectile dysfunction is genuine and meaningful.
He observes that the traditional distinction into the two categories was maintained in a recent report of the International Society for Sexual and Impotence Research (admittedly this report was written in 2002.) However, he says that the major problem with this distinction is that the traditional view of mind / body separation may be obsolete, and certainly does not take into account the neurobiology of psychological disorders. In essence, he claims, such a distinction disregards the fundamental meaning of psychosomatic. One consequence of this distinction, Sachs maintains, is that patients may often be told that their erectile dysfunction is "all in the mind". He claims that the distinction is now counter-productive in the diagnosis, the classification, and indeed in the treatment of erectile dysfunction, and that it can obfuscate research into the causes of ED.
An alternative classification of erectile dysfunction is based on a proposal that reclassifies as organic several of the etiologies of ED that are currently considered to be psychological, whilst others will be classified as situational (this is a particular class of ED defined for episodic occurrences of ED which are due to certain characteristics of an individual sexual experience).
Sachs makes it clear in his paper, published in the International Journal of Impotence Research, that his goal is to bring to an end the artificial distinction between organic and psychogenic ED, as he sees it. This is a response to the International Society For Sexual and Impotence Research's attempt to maintain the traditional distinction between organic and psychogenic ED, a classification which he claims has not been adopted by the membership of the organization.
In his attempt to argue against the traditional distinction, Sachs raises several problems with the concept of psychogenic erectile dysfunction:
1) Psychogenic ED is based on an obsolete view of mind body distinctions
What he means by this is that modern physiological research produces evidence that runs counter to the traditional separation of mind and body, a separation that takes no account of the principle that all psychological processes have a somatic basis. The essence of this view is expressed by the philosopher JR Searle, who has observed that once we have the vision to see that consciousness is indeed a biological phenomenon like any others, then it can obviously be investigated neurobiologically. If one maintains that consciousness is entirely caused by neurobiological processes which can be inferred from the activity of certain brain structures, and if one assumes that all psychological processes are in fact regulated by brain functions, the logical conclusion is that there can be no psychogenic dysfunction that does not involve an organic process.
Obviously this means that erectile dysfunction (ED) cannot be "all in the mind." Certainly it is true that some brain function is essential to the stimulation and the inhibition of a man's erection, and once again this process is mediated by functions of the brain.
2) Psychogenic erectile dysfunction disregards knowledge of the neurobiology of psychological disorders
Sachs discusses the example of depression which is referred to as a negative mood state in the classification mentioned above; in which situational ED is included as a psychological distress or adjustment related condition. The validity of such a classification can be questioned in the light of the progress that has been made by neurobiologists in discovering the origin of emotions such as depression in the neural activity of the brain. Depression, stress and anxiety are in fact clearly associated with major neurochemical and neuroendocrinological changes in brain activity.
Obviously it's quite likely that some of these changes would have an impact on a man's erectile function. So to classify stress and depression as a psychogenic cause of erectile dysfunction without relating this to the neurobiological and neurochemical changes in the brain may be inappropriate. For example, psychogenic causes of ED may simply be related to the organic (physical) issue of impaired release of nitric oxide in the penis as part of an underlying pathophysiology.
Sachs goes on to say that these neurochemical discoveries have led to drug treatments which have had a major impact on negative mood states; accordingly these treatments most likely have the capacity to reduce erectile dysfunction associated with these conditions; in other cases drugs will alter the neurochemical balance of the nervous system in such a way that they actually impair sexual function, causing side effects such as ED, delayed ejaculation, or lowered sexual desire.
All of this means that if psychogenic erectile dysfunction is viewed as a kind of brain ED whose origin lies within the neural activity of the brain, then psychotropic drugs would be expected to increase or increase or reduce this brain related erectile dysfunction.
To put this more simply, the neuroendocrinological and neurochemical basis of anxiety and depression are in effect acting as organic causes of ED. Further illustration of the problems in classifying ED as psychogenic comes from the committee's decision to include age-related decline in sexual arousability as a psychogenic cause of erection problems. Sachs observes that many aspects of sexual functioning decline in men as they age, and for many, varied reasons: degenerative changes in the vascular system of the penis, or degenerative changes in penile collagen, or degenerative changes in the peripheral nerves -- all of these would have traditionally been categorized as organic rather than psychogenic causes of ED, ones that develop with advancing age. However, some of these changes can clearly contribute to an age-related decline in sexual arousability, and some of the loss of that sexual arousability may be the result of various age-related neurochemical changes in the brain and nervous system.
Whilst these changes are not yet understood, nor have they been clearly demonstrated, they do indicate the difficulty of continuing to draw a distinction between psychogenic and organic ED. More recent research by John Bancroft and Eric Janssen has indicated that there are three independent underlying processes in sexual arousal: there is one process associated with sexual arousal, and two associated with sexual inhibition, and the relative balance of these three factors is predictive of a man's erectile problems. Bancroft and Janssen allude in their analysis to the neurobiological regulation of sexual function and ask, possibly rhetorically, if psychogenic factors are regulated by orgasmic factors, why maintain a distinction?
However, they don't completely discard the distinction but suggest there is a balance between central brain and peripheral nervous system inhibition (organic) on the one hand and external problems (psychogenic / situational) on the other hand; this balance may determine whether a man is prone to erection problems in a particular sexual encounter. Even so, Bancroft and Janssen note that the processing of external problems is itself neurobiologically mediated. They observe that men with high propensity for brain inhibition of sexual response are more likely to lose sexual interest and erectile responsiveness when depressed or anxious. This may not depend primarily on cognitive processing, but on the related biochemical changes in the brain which are relevant to both mood and sexual arousability.
In response to this Sachs asks why, if psychogenic factors are regulated by organic factors, they should be maintained as separate classes. Even when some kind of cognitive function is involved, that processing is itself no less mediated by neurochemical changes in the brain than any other process.
3) The term "Psychogenic Erectile Dysfunction" disregards the fundamental meaning of psychosomatic
Two recently established branches of psychosomatics are psychoneuroendocrinology and psychoneuroimmunology. These subdivisions of the science of somatics emphasize the interaction of their parts and not their separation, which may be a metaphor for not taking psychological processes to be separate from organic processes, even where erectile function and dysfunction are concerned.
A general statement made by Wolff in 1961 to the effect that the human nervous system is implicated in all types of disease applies just as much to ED as it does to any other condition. But one clear area where the psychological and somatic do interact in a man's erection problems is when a man has fears about the adequacy of his sexual performance -- fears that may be provoked by the response of his body to the situation he is in.
Bancroft and Janssen, among many others, including almost every man who has ever had sex, have observed that even relatively slight and occasional impairments in erectile capacity can come from many different causes, whether those be medical, such as vascular problems and peripheral neuropathy, or situational, such as excessive drinking. In any event, when a man worries about a mild impairment of his erectile function, it is almost certain that some additional deficit will result. In other words, cognitive feedback from a slight failure of erection can lead to performance anxiety, which can reinforce other conditions to further impair his erectile function.
While performance anxiety is clearly a psychological state, anxiety is in no small measure an organic or physiological condition which is amenable to treatment with anxiolytic drugs. It is therefore not surprising that administration of these drugs can interrupt the feedback cycle that aggravates a man's erection problems: this is no different than the traditional consumption of alcohol for increasing sexual desire and reducing performance anxiety.
A study by Cranston-Cuebas et al compared a number of men, both sexually functional and dysfunctional, as they viewed erotica. The men were given three placebo pills in turn: these purported to enhance erection, to impair erection, or to act as a placebo. It's not surprising to learn that dysfunctional men had less erectile capacity when they took the pills that were supposed to be erection impairing; unexpectedly, though, sexually functional men developed stronger erections with the tablet that was supposed to impair their erection. Whatever this means, it's a clear indication that situational erectile dysfunction and situational erectile function vary according to the beliefs that a man has about the circumstances in which he is becoming aroused.
4) Psychogenic erectile dysfunction is often diagnosed by exclusion
Sachs observed that diagnosing ED's etiology generally involves a thorough medical examination and a psychological history as well. It's not uncommon for a penile tumescence test to be taken as the man sleeps: if his capacity to get a sleep-related erection is normal, and there is no evidence of any organic cause for his erectile dysfunction, then a diagnosis of psychogenic ED would most likely be made.
However, Sachs points out that this conclusion is unreliable because conditions like depression can themselves impair sleep related elections. (Also, recent research has demonstrated that the area of the brain that is responsible for erections during the night is different from the area of the brain that is responsible for erections during sexual arousal.) Sachs lists a number of examples which demonstrate that while the neuroendocrinological varies with the sexual contexts, the organic basis of erection in one situation may or may not be predictive of erectile dysfunction in a different one.
5) Psychogenic ED is not all in the mind
It's certainly true that many people regard medical problems and psychological problems differently, and psychological problems tend to be more stigmatized. It's therefore not surprising that medical problems with psychosomatic features have been described as "all in the mind", and have developed a negative association. Sachs makes the observation that describing a man's condition as psychogenic ED may be no less demoralizing and demeaning for the individual concerned than describing his condition as impotence (a term which has long since fallen out of use in most contexts because it is regarded as disparaging).
The point is that if there is actually an organic basis for what appears to be chronic psychogenic erectile dysfunction, then it's possible that the stigma associated with the condition could be reduced and men would be more likely to seek appropriate treatment.
Sachs observes that recent evidence has emerged that seems to show that psychotherapy can be responsible for changes in brain physiology; maybe psychotherapy for ED acts by changing the underlying physiology of the brain.
In conclusion, Sachs observes that it's possible classification of erectile dysfunction will never be as clear as classification for other medical conditions, but one alternative to the traditional classification of ED might be to associate the term organic erectile dysfunction with "peripheral" or "central" problems, meaning "outside" or "within" the brain and spinal column, respectively.
This means that central problems would include ED caused by neurobiological and neuroendocrinological examination, as well as ED resulting from conditions such as stress or depression, since these are clearly mediated through brain activity. This group would also include factors related to ageing when things such as age-related peripheral pathology have been ruled out as a cause.
Furthermore, a classification such as this would allow a distinction to be drawn between peripheral problems such as primary hypogonadism and androgen receptor insensitivity in the genital tissues, and central problems such as those of brain origin, for example inadequate gonadotropin releasing hormone or other issues that relate to hormone metabolism in the brain.
And finally the term "situational erectile dysfunction" would be only applied to clear cases of ED arising in the context of certain partners, events or environments, or situations where a man perceives that his performance may be impaired by the expectations placed on him.
Sachs does admit that his proposed classification retains some dichotomies, notably organic versus situational, and peripheral versus central. However, he makes the point that separating situational ED from organic ED does not imply there is no clear organic basis for situational ED; and this may well still be treatable with drugs such as anxiolytics or Viagra. However, limiting situational ED as a term to refer to the more transient occurrences of ED that depend on circumstance rather than any long-term cause implies no chronic pathology of the central nervous system and would not warrant a man's erectile dysfunction being diagnosed as organic.
In conclusion, Sachs observes that most pathologies include central and peripheral factors, and the expression of those would be affected by a man's perception of his partner, his environment and his sexual performance. In other words, diagnosing the causes of erectile dysfunction might in fact end up being a matter of assigning priority, seeking out the thing that is most likely to cause the problem, and treating that before others. It's also interesting to note that even if there is no organic cause identifiable there may still be an organic cure -- and he draws the parallel of treating premature ejaculation with Dapoxetine. he mentions the possibility that men who have difficulty in delaying ejaculation and men who frequently have erectile dysfunction in certain situations may lie outside of normal ranges of neurotransmitters or receptor density or sensitivity. This might allow a physician to prescribe drugs which would interfere with brain chemistry and provide a solution to a man's ED.
International Journal of Impotence Research
2.Silberstein SD, Lipton RB, Dalessio DJ (eds). Wolffs Headache and Other Head Pain, 7th edn. Oxford University Press: New York, 2001.
3.Lizza EF, Rosen RC. Definition and classification of erectile dysfunction: report of the Nomenclature Committee of the International Society for Impotence Research. Int J Impot Res 1999; 11: 141–143.
4.Rosen RC, personal communication, October 2000.
5.Symposium on Taxonomy of Erectile Dysfunction. 9th World Meeting on Impotence Research, Perth, Australia. November 26–30, 2000.
6.Searle JR. Consciousness. Annu Rev Neurosci 2000; 23: 557–578.
7.Stuss DT, Levine B. Adult clinical neuropsychology: lessons from studies of the frontal lobes. Annu Rev Psychol 2002; 53: 401–433.
8.Bancroft J. Central inhibition of sexual response in the male: a theoretical perspective. Neurosci Biobehav Rev 1999; 23: 321–330.
9.Giuliano F, Rampin O. Central neural regulation of penile erection. Neurosci Biobehav Rev 2000; 24: 517–533.
10.Heaton JPW. Central neuropharmacological agents and mechanisms in erectile dysfunction: the role of dopamine. Neurosci Biobehav Rev 2000; 24: 561–569.
11.Sachs BD. Contextual approaches to the physiology and classification of erectile function, erectile dysfunction, and sexual arousal. Neurosci Biobehav Rev 2000; 24: 541–560.
12.Davidson RJ, Abercrombie H, Nitschke JB, Putnam K. Regional brain function, emotion and disorders of emotion. Curr Opin Neurobiol 1999; 9: 228–234.
13.Cowan WM, Harter DH, Kandel ER. The emergence of modern neuroscience: some implications for neurology and psychiatry. Annu Rev Neurosci 2000; 23: 343–391.
14.Davidson RJ, Pizzagalli D, Nitschke JB, Putnam K. Depression: perspectives from affective neuroscience. Annu Rev Psychol 2002; 53: 545–574.
15.Grasby PM. Imaging strategies in depression. J Psychopharmacol 1999; 13: 346–351.
16.McEwen BS. The neurobiology of stress: from serendipity to clinical relevance. Brain Res 2000; 886: 172–189.
17.Ninan PT. The functional anatomy, neurochemistry, and pharmacology of anxiety. J Clin Psychiatry 1999; 60(Suppl 22): 12–17.
18.Nutt DJ, Glue P, Lawson C. The neurochemistry of anxiety: an update. Prog Neuropsychopharmacol Biol Psychiatry 1990; 14: 737–752.
19.Lue TF. Erectile dysfunction. N Engl J Med 2000; 342: 1802–1813. | Article
20.Brock GB, Lue TF. Drug-induced male sexual dysfunction. An update. Drug Safety 1993; 8: 414–426.
21.Rowland DL, Greenleaf WJ, Dorfman LJ, Davidson JM. Aging and sexual function in men. Arch Sex Behav 1993; 22: 545–557.
22.Schiavi RC, Rehman J. Sexuality and aging. Urol Clin North Am 1995;
23.Wespes E. Erectile dysfunction in the ageing man. Curr Opin Urol 2000; 10: 625–628.
24.Stevens JC, Cain WS. Changes in taste and flavor in aging. Crit Rev Food Sci Nutr 1993; 33: 27–37.
25.Rolls BJ. Do chemosensory changes influence food intake in the elderly? Physiol Behav 1999; 66: 193–197.
26.Bancroft J. Central inhibition of sexual response in the male: a theoretical perspective. Neurosci Biobehav Rev 1999; 23: 763–784.
27.Bancroft J, Janssen E. The dual control model of male sexual response: a theoretical approach to centrally mediated erectile dysfunction. Neurosci Biobehav Rev 2000; 24: 571–579.
28.Bancroft J, Janssen E. Psychogenic erectile dysfunction in the era of pharmacotherapy: a theoretical approach. In: Mulcahy J (ed). Male Sexual Function: A Guide to Clinical Management. Totowa, NJ: Humana Press, 2001, pp 79–89.
29.Dalessio DJ. Remembrances of Dr. Harold G. Wolff. In: Silberstein SD, Lipton RB, Dalessio DJ (eds). Wolff's Headache and Other Head Pain, 7th Edition. Oxford University Press: New York, 2001, pp 3–5.
30.Cranston-Cuebas MA, Barlow DH, Mitchell W, Athanasiou R. Differential effects of a misattribution manipulation on sexually functional and dysfunctional men. J Abnorm Psychol 1993; 102: 525–533.
31.Bancroft J, Malone N. The clinical assessment of erectile dysfunction: a comparison of nocturnal penile tumescence and intracavernosal injections. Int J Impot Res 1995; 7: 123–130.
32.Broderick GA. Evidence based assessment of erectile dysfunction. Int J Impot Res 1998; 10(Suppl 2): S64–S73.
33.Thase ME, Reynolds CF, Jennings JR, Frank E, Howell JR, Houck PR, Berman S, Kupfer DJ. Nocturnal penile tumescence is diminished in depressed men. Biol Psychiatry 1998; 24: 33–46.
34.Meisler AW, Carey MP. A critical reevaluation of nocturnal penile tumescence monitoring in the diagnosis of erectile dysfunction. J Nerv Ment Dis 1990; 178: 78–89.
35.Schmidt MH, Valatx JL, Sakai K, Fort P, Jouvet M. Role of the lateral preoptic area in sleep-related erectile mechanisms and sleep generation in the rat. J Neurosci 2000; 20: 6640–6647.
36.Schwartz JM, Stoessel PW, Baxter Jr LR, Martin KM, Phelps ME. Systematic changes in central glucose metabolic rate after successful behavior modification treatment of obsessive-compulsive disorder. Arch Gen Psychiatry 1996; 53: 109–113.
37.Althof SE, Levine SB, Corty EW, Risen CB, Stern EB, Kurit DM. A double-blind crossover trial of clomipramine for rapid ejaculation in 15 couples. J Clin Psychiatry 1995; 56: 402–407.
38.Strassberg DS, de Gouveia Brazao CA, Rowland DL, Tan P, Slob AK. Clomipramine in the treatment of rapid (premature) ejaculation. J Sex Marital Ther 1999; 25: 89–101.
39.Carter CS, DeVries AC, Getz LL.
Physiological substrates of mammalian monogamy: the prairie vole model.
Neurosci Biobehav Rev 1995; 19: 303–314.
Other pages on this website about erectile dysfunction, erectile dysfunction and impotence