The term somatopsychics is derived from the Greek terms soma, meaning body, and psyche, which has become an English term as well. Somatopsychics refers to psychological effects engendered by somatic conditions. Such psychological states range from normal, to mild mood alterations (like irritability due to low blood sugar), to major psychiatric conditions.
Somatopsychics needs to be contrasted with psychoso-matics. Psychosomatic mechanisms operate when psychological conditions produce physical symptoms, such as dry mouth and nervous sweating as a result of stress. The distinction between psychosomatic and somatopsychic is clear in most cases and in theory, but in reality, when phenomena of both kinds become intertwined and feed on each other, causes and effects are difficult to disentangle. When somatic and psychological causes successively bring about effects that begin to serve as the cause for the next level of effects, an etiological spiral evolves, making it difficult to identify the degrees to which psychosomatic or somatopsy-chic factors contributed to the final outcome. For example, stress leads to tachycardia (psychosomatic effect), which in turn causes uneasiness and anxiety (somatopsychic outcome), resulting in a headache (psychosomatic effect), which may trigger irritability (somatopsychic effect).
Neither the concept nor the term is new, but not all researchers are using the term somatopsychics correctly, which has created some confusion. Many have used the popular term psychosomatic in lieu of somatopsychic when referring to a body-mind connection, regardless of the direction in which the cause and effect arrow points.
Linguistics attests to the recognition of somatopsychic connections. For example, the thymus gland, considered to be the seat of emotions, was named after the Greek word for mood, thymos, while hysteria, formerly believed to be related to the uterus, was labeled after the Greek term for uterus, hyster.
Somatopsychic connections were understood by Hippocrates, Aristotle, and Galen. In the 1700s Lammetrie's "L'homme machine" functioned on a somatopsychic basis. Cabanis perceived the mind as a function of the brain. Gall's phrenology led to Lombroso's somatically based theory about the criminal mind. Fechner's theory of psycho-physical parallelism asserted that every physical event has a psychological correlate and vice versa. Lotze, Ribot, and Galton prominently emphasized the somatic basis of psychological processes. Among prominent promoters of somatic hypotheses of mental illness, in the second half of the 19th and at the beginning of the 20th century, were Broca (localization of brain functions), Taine (nerve reflexes), Müller, Weber, Wundt, Jakobi, Griesinger, Westphal, Meyn-ert, Kraepelin, Bleuler, and Wernicke, who used the specific term somatopsychic. Meynert, for example, not only argued for an etiology of mental illness rooted in brain pathology but also supported it with specific observations concerning destruction of fibers, blood flow to the brain, and so on. Kretschmer connected body build and personality and proposed a corresponding affinity toward a specific mental illness. Sheldon's body based theories about temperament followed. .Around 1900 Pavlov established scientific proof for four personality types based on distinguishable patterns of nervous system reactivity.
In 1913/1973 Karl Jaspers presented several etiologies of mental illness, among them the somatopsychic etiology, which is divided into three parts: (1) brain pathology (trauma, tumors, infection, vascular system-related pathology, genetic deficits, deterioration due to aging, etc.),
(2) physical illness producing symptomatic psychoses (infectious diseases, endocrine disorders, uremia, etc.), and
(3) effects of toxic substances (morphine, cocaine, carbon monoxide, alcohol, etc.).
With the rapid expansion of biomedical research in the twentieth century, evidence for a somatic basis of many psychological disturbances mounted and in the 1970s lent credence to orthomolecular psychiatry. The theories of Pauling, Kety, Rimland, Pfeiffer, Osmond, and others identified specific mental disorders as somatopsychic effects of biological etiology. They countered adverse genetic, biochemical, nutritional, and environmental conditions with megavitamin and/or mineral therapy to treat and prevent mental illness.
Richard C. W. Hall's landmark 1980 book brought the concept of somatopsychics into focus. With his colleagues he documented and cataloged psychological presentations of physical illness as well as psychological side effects of pharmacological agents. Additional somatopsychic outcomes were reported to be related to genetic factors, to normal physical changes such as hormonally induced biorhythms or life phase changes, as well as to toxic substances, including gases, and to ambient environmental conditions.
Research into the somatic etiology of mental disorders is growing rapidly, forecasting a more accurate understanding of mental illness and leading to a new, largely so-matopsychically based systematization and to new codification of mental illness.
Everyday life is full of experiences illustrating etiology and effects of somatopsychic mechanisms. Parents are familiar with the mood changes that occur in children when they are hot, tired, or hungry. But people of all ages get irritable because of low blood sugar, heat, and fatigue. Effects of sensory overload, such as noise or heat, and many forms of sensory extremes, including sensory deprivation, are reflected in psychological sequelae. Total sensory deprivation as used in some prisons can lead to psychotic states and hallucinations. On the other hand, enjoyable sensations trigger psychological effects as well. Scents can evoke pleasant feelings that may include seductive messages. Music can be stimulating or calming, depending on tone, volume, and rhythm.
Diminished alertness and reactivity are well documented in fatigued drivers of motor vehicles. Fatigue is a generally recognized factor in diminished capacity to function mentally, particularly in learning. In fact, one of the earliest psychological tests was developed by Ebbinghaus (1897) to study fatigue in school children. Limitations of reasoning ability are easily accepted as an effect of a not-yet matured brain in young children but cause concern when they are the result of a deteriorating brain in an aging person.
Hormones are known to cause emotional changes in adolescence and in pregnancy and menopause and are related to mood swings in premenstrual syndrome. Postpartum depression is attributed to the birth-related sudden disruption of the hormone levels accompanying pregnancy.
Somatopsychic effects of common-use substances are well recognized: the stimulating effects of caffeine and nicotine, as well as the initially relaxing but later depressing and judgment-impairing effects of alcohol. Many toxic substances have more than a somatic impact. Lawsuits alleging lead poisoning cite outcomes of learning disabilities, lethargy, and so forth. Carbon monoxide exposure (car exhaust, cooking gas) can lead to memory deficits, apathy, and depression. Brain trauma due to insults from various causes like forceps birth, domestic abuse, accidents, or brain surgery may result in mental deficiencies, adverse emotional reactions, and personality changes. In rare cases trauma has caused a state of euphoria.
Sports-related somatopsychic phenomena include the runner's high, attributed to endorphins, and the SCUBA divers'rapture of the deep, a state of nitrogen narcosis that expresses itself in a euphoric, drunk-like state accompanied by cognitive impairment and poor judgment. High altitude exposure affects mountain climbers and skiers along with inactive sightseers. Apart from physical distress it may cause irritability, impaired judgment, and in extreme cases panic attacks, delirium, and hallucinations.
Light availability affects mood. Diminished presence of daylight in the northern and southern regions, as in Alaska and Scandinavia, causes depression in many people. Wetterfühligkeit, more readily acknowledged in Europe, refers to weather sensitivity. It implies that a person's vascular system is affected by weather conditions, particularly changes in barometric pressure affecting the emotional state. The Föhn, the oppressive, warm alpine winds, are blamed for migraine headaches as well as for bringing on depression and even suicide in susceptible individuals.
Disruption of circadian rhythm, especially when resulting in sleep deprivation, reduces optimal physical and mental performance and also appears to play a major role in depression. Leading causes are jet lag and shift work, particularly when shift cycles alternate as soon as the body has begun to adjust.
Medical Illness Producing Psychological/Psychiatric Symptoms
The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, fourth edition recognizes the existence of somatopsychic conditions as long as a general medical condition or a specific substance caused the mental disorder, but it does not explicitly label the mechanism involved as somatopsychic. Such recognized medical conditions likely to generate psychological or psychiatric effects include brain tumors, head trauma, neoplasms, neurological, endocrine, and cardiovascular conditions, specific infections, autoimmune disorders, hepatic and renal disease, and fluid or electrolyte imbalance. Several researchers have pointed out that side effects of medical illness or substance impact may lead to a misdiagnosis of mental illness, which most likely preempts the needed treatment of the underlying condition. Missed early interventions due to missed diagnoses can endanger the patients' life, as in brain tumors. Misleading symptoms depending on tumor site can include personality, affective and cognitive changes, altered perceptions, anxiety and depression, tactile or visual hallucinations, and depression.
Selected Examples of Somatopsychic Effects Substance-Related Somatopsychics
Somatopsychic effects may be related to a substance of abuse or to withdrawal from it. They also occur when a person incurs a deficit or accumulates a toxic amount of a needed substance, such as a vitamin or mineral. Psychotic, mood, and anxiety disorders, for instance, may be associated with intoxication with and/or withdrawal from many substances. Phencyclidine (PCP), for example, causes a sense of emotional numbing, detachment and isolation, and change in body and spatial images. If it triggers a psychotic episode, the symptoms may be indistinguishable from those of schizophrenia.
Common-use substances like alcohol, caffeine, and nicotine have their somatopsychic effects: Caffeine increases energy and alertness and acts as a mood elevator, but anxiety, fatigue, and depression are bound to follow at abstinence. Somatopsychic effects of alcohol consumption vary, ranging from elevated mood, impaired judgment, anger, rage, and violence to fatigue, or may lead to dysphoria and depression. Memory deficits are common after heavy drinking. Excessive, long-term use can lead to amnestic disorder, dementia, and delirium. Nicotine use increases arousal, vigilance, and concentration and reduces stress and irritability. Severe irritability follows withdrawal.
Malnutrition alters emotional reactivity and cognitive efficacy (starvation, poverty, dieting). Somatopsychic effects due to nutritional deficiencies, though present in the general population, have been noted prominently in the elderly due to both insufficient intake and diminished absorption capacity. Incorrect diagnoses of organic brain syndrome, paranoia, or depression have been made in patients suffering from nutritional deficits. Vitamin and mineral deficiencies can lead to irritability, confusion, mental deterioration, dementia, delusions, disorientation, apathy, hallucinations, depression, anxiety, and so on. Accumulation of toxic amounts of vitamins and minerals can generate similar outcomes. Toxic levels of copper may even mimic psychosis indistinguishable from bipolar disorder or schizophrenia.
Somatopsychics of Mental Disorders and Other Psychological Conditions
Some mental conditions are exclusively of somatic etiology. Most types of mental retardation and autism fit this category. Not as clear-cut are the etiologies of schizophrenia, mood, and anxiety disorders. These disorders, depending on type and severity, are believed to arise from psychogenic and/or so-matogenic conditions. Stress can interact with genetic predisposition. In addition, psychological factors can precipitate a psychosomatic outcome. Depending on the resulting somatic condition, it may become the somatic basis for a mental disorder. A selection of recognized etiologies follows. The samples provided are not intended to be all-inclusive.
1. Mental retardation. Most cases of mental retardation are somatically based.
a. Mental retardation related to the prenatal period includes chromosomal disorders, inborn errors of metabolism, disorders of the urea cycle, developmental disorders of brain formation such as hydro-
and microcephalus, maternal malnutrition, and substance abuse or illness (measles, diabetes).
b. Perinatal phase. Ahealthy fetus can develop into a child with mental retardation due to unfavorable birth-related events, such as maternal sepsis, and birth delays, umbilical cord accidents, head trauma, and so on. Other etiologies are neonatal disorders, such as infections or intracranial hemorrhage.
c. Severe malnutrition in the postnatal phase is a leading cause of mental retardation. Other damaging factors are head injuries, lead and mercury poisoning, aspirin-related Reye syndrome, childhood onset of metabolic disorders, infections, postimmu-nization disorders, parasitic infestations such as malaria, seizure disorders, and so on.
2. Autism. This has been related to bilateral brain damage in early life, genetic roots, neurochemical and im-munological factors, deficient oxygen delivery to the brain, in utero insults, and so forth.
3. Schizophrenia. While the evidence for somatic etiologies of SCH is increasing, no singular somatic cause of schizophrenia has been identified. The following are some of the more widely recognized somatopsy-chic etiologies of SCH. They center on (1) genetic factors; (2) environmental factors, including maternal malnutrition and effects of infectious agents or antibodies operating prenatally; (3) lipid dysfunction; (4) abnormal brain lateralization and/or abnormal hemispheric communications, brain damage occurring as a result of abnormal prenatal brain development, head injury, hypoxia, and so forth; (5) neuro-developmental errors and neurological malfunction; (6) extreme prematurity at birth; and (7) biochemical deficiencies or imbalances. The broad variety of etiologies producing schizophrenic symptoms calls for a new, somatopsychically based understanding of the disorder.
4. Depression. While there is psychogenic depression in response to negative life events, depression also has undisputed somatopsychic etiologies. They include genetics, biorhythms (circadian rhythms, sleep length, and quality), and environmental (sunlight deprivation) and biochemical factors, like activity of monoaminergic neurons, norepinephrine, serotonin-and thyrotropin-releasing hormones (TRH), dopa-mine deficiency, reuptake of norepinephrine, serotonin and dopamine, and others. In women, hormone-related depression has been associated with premenstrual syndrome, pregnancy, the postpartum period, and menopause.
5. Mania. In addition to genetics, mania has been related to various somatic etiologies, such as excess ep-inephrine and serotonin production, cerebral trauma, left hemisphere injury, sleep disruption, and CD4 count in HIV-infected patients.
a. Research has found that a single dominant gene causes a predisposition to panic disorder. A panic experience can be triggered when the autonomic nervous system is activated by agents like caffeine, yohimbine, lactic acid, increased CO inhalation, and so on. One hypothesis theorizes that patients with panic disorder may chronically be in a higher state of arousal.
b. Obsessive compulsive disorder is classified as an anxiety disorder, and its somatopsychic etiology is increasingly recognized. Among such etiologies are genetics, abnormal brain structures, and a dysfunction of the serotonergic system.
The rapidly expanding body of scientific findings has broadened knowledge about the role of somatic factors in the etiology of psychological and psychiatric presentations. Unless a condition is strictly psychogenic, symptoms are less significant in defining a disorder than their somatic origin is. Identical symptoms of psychopathology can result from vastly different somatic etiology. Somatopsychic research calls for a reassessment of the historically evolved understanding of so-called mental illness, which needs to be redefined in biological-medical terms, accepting etiology as the defining category, no matter how serious the side effects of mental and emotional disturbance are. Many of the old categories, based on symptoms, cannot adequately accommodate disorders that are now understood etiologically and diagnosed with the help of innovative scientific methods and defined by new and different standards. Expected new terminology portraying mental illness largely as a side effect of somatic conditions can remove stigmatization of mental patients and will encourage them to seek timely treatment. More accurate diagnoses invite more precisely targeted interventions, which will improve the efficacy of treatment.
Bleuler, E. (1995). Lehrbuch der Psychiatrie (5th ed.). Berlin:
Spinger. (Original work published 1911) Broca, P. (1876). Sur la topographie cranio-cerebral. Paris: Leroux. Cabanis, P. J. G. (1802). Rapport du physique et du morale de l'homme.
Ebbinghaus, H. (1897). Grundzüge der Psychologie. Leipzig: Veit. Fechner, G. T. (1860). Elemente der Psychophysik. Leipzig: Breitkopf & Härtel.
Fechner, G. T. (1882). Revision der Hauptpunkte der Psychophysik.
Leipzig: Breitkopf & Härtel. Gall, J. F. (1925). Sur les fonctions du cerveau et sur celles des chacune des ces parties. Paris: Bailliere. Galton, F. (1907). Antechamber of consciousness. London: Dent. Griesinger, W. (1845). Pathologie und Therapie der physischen Krankheiten. Stuttgart: Adolph Krabbe.
Hall, R. C. W. (1980). Psychiatric presentations of medical illness: Somatopsychic disorders. New York: Spectrum.
Hall, R. C. W., Gardner, E. R., Strickney, S. K., LeCann, A. F., & Popkin, M. K. (1980). Physical illness manifesting as psychiatric disease. Archives of General Psychiatry, 37, 989-995.
Hall, R. C. W., & Beresford, T. P. (1984). Handbook of psychiatric diagnostics (Vols. I & II). New York: Spectrum.
Hall, R. C. W., Beresford, T. P., & Blow, F. C. (1987). Depression and medical illness: An overview. In Oliver G. Cameron (Ed.), Presentations of depression: Depressive symptoms in medical and other psychiatric disorders. New York: Wiley.
Hawkins, D., & Pauling, L. (1973). Orthomolecular psychiatry— treatment of schizophrenia. San Francisco: Freeman.
Hoffer, A. (1962). Niacin therapy in psychiatry. Springfield, IL: Thomas.
Jakobi, M. (1830). Beobachtungen über die Pathologie und Therapie der mit Irresein verbundenen Krankheiten. Elberfeld: Schoenian'sche Buchhandlung.
Jaspers, K. (1913/1973). Allgemeine Psychopathologie (9th ed.). Berlin: Springer.
Kety, S. (1972). Toward hypotheses for a biochemical component in the vulnerability of schizophrenia. Seminars in Psychiatry, 4, 233-258.
Kety, S. (1976). Genetic aspects of schizophrenia. Psychiatric Annals, 6, 11-32.
Kraepelin, E. (1893) Psychiatrie (4th ed.). Leipzig: Meiner.
Kretschmer, E. (1967). Körperbau und Charakter (25th ed.). Berlin: Springer.
Lammetrie, J. (1748). L'homme machine. In Ouevres philosophiques. Hildesheim: Olms.
Lipps, G. F. (1899). Grundriss der Psychophysik.
Lombroso, C. (1896). L'uomo delinquente (5th ed.). Turin: Fratelli Bocca.
Lotze, R. H. (1852). Mezidinische Psychologie oder Physiologie der Seele. Leipzig: Weimann.
Meynert, R. (1889). Klinische vorlesungen über Psychiatrie auf wissenschaftlichen Grundlagen. Vienna: W. Braumüller.
Müller, G. E. (1879). Zur Grundlegung der Psychophysik. Göttingen: Vandenhoeck & Ruprecht.
Müller, G. E. (1882). Revision der Hauptpunkte der Psychophysik. Göttingen: Vandenhoeck & Ruprecht.
Osmond, H. (1973). Come home psychiatry! The megavitamin treatment and the medical model. Psychiatric Opinion, 10, 14-23
Pauling, L. (1968). Orthomolecular psychiatry. Science, 160, 265171.
Pauling, L. (1974). On the orthomolecular environment of the mind: Orthomolecular theory. American Journal of Psychiatry, 131, 1251-1257.
Pfeiffer, C. C. (1976). Psychiatric hospital versus brain biocenter. Journal of Orthomolecular Psychiatry, 5, 28-34.
Pavlov, I. P. (1966). Essential works of Pavlov. New York: Bantam.
Ribot, T. (1885). Les maladies de la memoire. Paris: Bailliere.
Ribot, T. (1888). Les maladies de lapersonalite. Paris: Alcan.
Rimland, B. (1974). Infantile autism. Status of research. Canadian Psychiatric Association Journal, 19, 130-133.
Sheldon, W. H. (1942). The varieties of temperament. New York: Harper.
Taine, H. (1870). De l'intelligence. Paris: Hachette. Wernicke, C. (1874). Der aphasische Symptomkomplex: eine psychologische Studie auf anatomischer Basis. Breslau: Cohn & Weigert.
Wundt, W. (1874). Grundzüge der physiologischen Psychologie. Leipzig: Engelmann.
St. John's University, New York
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