Anxiety and depression today: what is your personal experience?






Juan J. LÓPEZ-IBOR, MD, PhD
Institute of Psychiatry and Mental Health, WHO Collaborating
Centre for Research and Training in Mental Health and Health Research Institute (IdISSC)
Hospital Clínico San Carlos
CIBERSAM (Center for Biomedical Research Network on Mental Health), Department of Psychiatry
Faculty of Medicine Universidad Complutense
Madrid, SPAIN

Anxiety and depression today: what is your personal experience?


Interview wi th J. J. López-Ibor, Spain



Anxiety and depression are prominent symptoms in clinical practice and are the basis for the two diagnostic categories, anxiety disorder and depressive disorder, that are sometimes combined in a third: mixed anxiety and depressive disorder. Indeed, the main problem for the clinician and researcher is the somewhat blurred boundary between normal and morbid psychological experience, on the one hand, and between anxiety and depression, on the other. Comorbidity is high in anxiety and depressive disorders, and higher still when viewed long-term, with anxiety tending to predominate at younger ages and depression and somatization developing later. The distinctive quality of the affect is important in differentiating normal experience from anxiety and depressive disorders. Morbid anxiety and morbid sadness are “vital feelings”; as described by Scheler, Schneider, and López Ibor Sr, they are characterized by “embodiment” and non-dependence on external circumstance. Evolutionary theory offers useful insights into the possible adaptive value of the feelings of anxiety and sadness. Feelings may aid clinicians in classifying certain states of mood as “normal” or “pathological” and guide them to more appropriate decisions.

Medicographia. 2012;34:334-338 (see French abstract on page 338)


Prof López-Ibor, as one of the major figures in psychiatry in Spain, could you tell us the highlights of your career?

Just as my father followed his two elder brothers into medicine, so I followed my father into psychiatry, in which, I suppose you could say, we have formed a mini dynasty in the Spanish setting. We even have the same initials, which complicates life for bibliographers! My father was born in 1908, and completed his specialist training in Zurich, Berlin, Paris, and Tübingen. This background enabled him to bring Spanish psychiatry firmly into the European loop, via the Spanish Psychiatric Society and the journal Actas Luso-Españolas de Neurología, Psiquiatría y Ciencias Afines, both of which he cofounded. Intellectually, I would describe myself as his successor. I have approached psychiatric illness in the same tradition, with particular respect to anxiety and depression disorders. My father was at pains to emphasize a biological and evolutionary interpretation of the common syndromes, distancing himself from Freud in that regard, despite the initial attraction that had first drawn him to the specialty. For example, I believe that his description of vital anguish, published in his book of the same title, remains largely valid today, despite dating from 1950.

How do you view the relationship between anxiety and depression?

It’s extremely close. These are among the two most common complaints encountered at both the primary care and specialist levels. They are the backbone of two diagnostic categories, anxiety disorder and depressive disorder, that we frequently find combined in a third: mixed anxiety and depressive disorder, enshrined in the tenth revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10), and most probably in the forthcoming fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

Anxiety is the feeling prompted by an as yet unidentified threat or danger.1 It consists of increased alertness and exploratory attention, and an emotional readiness for fight or flight. Depression is the feeling that arises from the experience of loss.

Since a threat, such as severe disease in a beloved person, may be followed by actual loss (such as death), it is quite common for depression to follow an anxiety state. But the reverse also happens, as when a patient may feel hopeless, helpless, and hapless during a depressive episode, with the result that minor circumstances become highly threatening.

The lifetime combination of anxiety and depressive disorders is also common. We conducted a near 50-year follow-up study of 370 patients diagnosed with anxiety disorder between 1950 and 1961. Two-thirds were rediagnosed according to DSM-III-R (DSM, third edition, revised) criteria as suffering from panic disorder and the rest from generalized anxiety.2 On the whole, there is a common natural history starting with school phobia in childhood (more prevalent in panic disorder patients), followed by anxiety in the 20s and 30s, depression in the 40s and 50s, and somatization disorders thereafter. Interestingly enough, this is the same pattern as presented by one of Freud’s most celebrated patients, the Wolf Man.

The promotion of these two feelings, anxiety and depression, to the rank of diagnostic categories raises the issue of the frontier between normal and pathological psychological experience. Their frequent coexistence raises a second problem: that of the exact differences between anxiety and depression.

What are the clinical implications of these two problems?

That there are clinical implications is beyond doubt. Neither problem has a straightforward solution, despite the importance of each in determining whether and how a given individual should be treated, with particular respect to the rich armamentarium of anxiolytics and antidepressants and other therapeutic resources at the contemporary clinician’s disposal. A wrong decision may have negative consequences such as medicalizing normal suffering, interfering with normal psychological processes, and creating dependence on prescription drugs, the health system and/or on the physician him/herself. Clinicians should also be at pains to avoid cosmetic psychopharmacology, by which I mean dealing with health as if it were just another consumer item.

In other words, failure to give due consideration to the above two problems can lead the clinician to take important decisions on the basis of inaccurate diagnosis. The danger is urgent and real: mood (affective) disorders attract the lowest inter-rater reliability scores in ICD-10 field trials. It is important to go beyond purely symptomatic aspects into a more comprehensive approach to the understanding of anxiety and depression. This goal may be achieved by integrating insights from the spiritual, philosophical, and neurobiological literature.3

Can you illustrate the dangers of a purely symptom-based approach?

Current classification systems in psychiatry can lead to confusion if clinicians fail to realize that classifications are not treatises of psychopathology, defining what illnesses are. Nor must diagnostic criteria be confused with symptoms, or symptoms with illnesses. For instance, two patients displaying identical symptoms (eg, depressive mood during most of the day and most days; marked reduction of their ability to show interest or enjoyment of all or almost all activitiesmost times of the day andmost days; significant weight loss; insomnia, and psychomotor inhibition) attract different diagnoses— major depressive episode or bereavement—according to DSM-IV-TR (DSM, fourth edition, text revision) depending on whether or not they are associated with the loss of a beloved relative or friend.

DSM-5 is considering dropping the exclusion criterion of grief for diagnosing major depression, a step wrongly interpreted by some as converting (normal) bereavement into a clinical disorder: as a member of the DSM-5 Mood Disorder Work Group has recently argued, the diagnosis of major depression requires the presence of a set of clinical manifestations, regardless of whether the patient has or has not recently lost a beloved relative.4




Comparative psychopathology appears to have been one of your abiding interests

Indeed. One consequence of the difficulty in clarifying the significance of anxiety and depression is the variable worldwide prevalence of the clinical disorders concerned. Take the example of depressive disorder, which shows large and unexplained international differences. The prevalence of major depressive episode oscillates between over 3500 per 100 000 inhabitants per year among women in the World Health Organization (WHO) region of the Americas, to under 1500 among Western Pacific Region men.

In primary health care, the differences are even more striking: depression accounts for around 30%of consultations in Santiago de Chile, but under 3% in Nagasaki. The differences reported by the WHO between cities such as Buenos Aires and Santiago de Chile or between London and Padua are, strictly speaking, inexplicable.5

In a more general sense, the steady increase in the incidence and prevalence of mental disorders conveys the impression that psychiatry is ineffective at the public health level. When dealing with such widely prevalent disorders, I think an alternative approach could be important. Rather than investigating the causes of depressive disorder, it might be more useful to determine instead why certain individuals are spared.

The prevalence of negative affect appears disproportionate: 15% of the US population has had an episode of severe depression, while many others simply have frequent bad days when they are too worried, sad, or angry to function, or at least nowhere near being full of energy and loving well-being. Most attempts to understand this state of affairs seek explanations in individual differences, often based on the assumption that there is something wrong with those affected.

Is this where we come back to the difference between normal and pathological anxiety and depression?

The first systematic attempt todifferentiate (normal, everyday) sadness from depression took place 100 years ago in continental Europe when the sadness present in depression was shown to have a distinct quality that could be identified in clinical settings and used as a basis for diagnosing (morbid) depression. This distinctness has been variously characterized as a lack of subjective response (blunting, affect anesthesia), behavioral withdrawal (inhibition), and altered vitality (vital sadness), associated with the presence of somatic symptoms, absence of motivation, and anhedonia. It is also interesting to note that observers are able to perceive this distinct quality despite patients often having considerable difficulty in verbalizing differences from normal sadness (a semantic factor that can be a source of diagnostic error).6

The psychiatrist Kurt Schneider (1887-1967) introduced the concept of vital sadness7 as a disturbance of vital feelings, based on the description by the philosopher Max Scheler (1874-1928)8,9 of four types of feelings:

i) Sensory feelings (sinnliche Gefühle) or emotional or sensation feelings (Empfindungsgefühle) involving specific parts of the body, such as pain, a knot in the stomach from hunger, or spine-chilling fear.

ii) Vital feelings (Lebensgefühle) or body feelings (Leibgefühle) involving body experience as a whole, such as distress or wellbeing.

iii) Psychic feelings (seelische Gefühle) or pure ego feelings (reine Ichgefühle), corresponding to the environment and external world. They are reactive to external circumstances such as joyfulness, enjoyment, sadness, or despair.

iv) Spiritual feelings (geistige Gefühle) or personality feelings (Persönlichkeitsgefühle), such as ecstasy or agony that are spontaneous and absolutely beyond specific values.

In summary, vital sadness is experienced independently of external circumstance as a negative subjective experience of one’s body, which is felt as weighty, slow, unpleasant, or painful, while normal (reactive) sadness is directly related to negative circumstance.

Similarly, López Ibor Sr concluded that the anxiety characterizing neurotic disorders was a vital rather than psychic or reactive feeling.10 This introduced the concept of “vital anxiety,” thereby paving the way for the biologic treatment of this group of disorders (ie, monoamine oxidase inhibitors for anxiety, and clomipramine for obsessive neurosis, as I proposed in the early ’70s).

You have also drawn attention to more recent Spanish contributions on this topic

Ramos Brieva et al carried out a series of controlled studies over two decades. Using discriminant analysis to determine how patients define pathological sadness, they developed a Pathological Sadness Index with a sensitivity of 0.94, specificity of 0.96, and total misclassification rate of 5% (κw=0.90).11 They found two factors that accounted for 55% of total variance (construct validity): “distinct quality” and “embodiment.” The presence of “distinct quality” was independent of the presence or absence of a life event and more frequent in melancholic subjects.12 The Pathological Sadness Index showed “distinct quality” in 83% of cases without subjective experience of sadness.

The same authors reanalyzed the Newcastle data of Kiloh and Garside13 and Carney et al.14 They studied the influence of the “distinct quality” item on core depressive symptoms. Removal of the influence of this item deprived the depressive syndrome of its original cohesion, suggesting that the “distinct quality” could be the agglutinative component of core depressive symptomatology.15 In other studies Ramos Brieva et al addressed the issue of vital anxiety.16 Discriminant analysis of the description of the anxiety experienced by subjects with panic attacks and control subjects with common fear showed the existence of qualitative differences between both experiences. The difference was also present in the sadness reported by patients with anxiety disorders.

How does evolutionary theory help in understanding emotion?

Experience and emotional behavior are so varied and omnipresent in human beings and animals that they must play an important role in individual and species survival. The philosopher Sartre considered emotion as an instance of the replacement behavior (Ersatzpsychologie) that appears when objectively guided behavior is not possible.17 Given the impossibility of facing too rational a world, as after the loss of a significant other, emotion establishes a new relationship with the world in which the apparently non-adaptive withdrawal reaction makes sense. Affective reactions have a significance that is not rational, but symbolic and magical.

The most appropriate strategy for differentiating normal from pathological mood states takes its inspiration from evolutionary theory by addressing the following two questions: i) what concerns a particular person visiting a psychiatrist?; andii) what are the public health consequences of defining a boundary between normal and pathological?

Evolutionary theory helps to explain why disease is so prevalent and difficult to prevent. Human genetic variations that increase resistance to disease often have costs, while some variations that increase vulnerability can have benefits. Take the classic example of sickle cell anemia. Is it “normal”? The answer is that it depends on where the person lives, given that those with sickle cell anemia are better able to resist malaria than those without.

Functionalists consider that emotions evolved for particular functions, such as to keep the subject safe.18 Natural selection has shaped emotions so that they adjust various aspects of the organismto provide selective advantage in particular kinds of situations. Emotions are designed tomaximize reproductive success rather than happiness. Negative emotions such as anxiety and low mood are defenses that have evolved from conflicts inherent in social life. Emotions are valenced because selection shapes special processes for situations that have influenced fitness in the past.19,20 In situations that decrease fitness, negative emotions are useful and positive emotions harmful.

An emotion that confers evolutionary advantage can hardly be described as abnormal

Just as there are positive aspects to (normal) anxiety, namely, the subjective experience of threat and the preparation for fight or flight, we should assume that depression also has adaptive value. Indeed, sadness has positive functions: it increases the ability to confront adaptive challenges when the effort to achieve an important goal may expose to danger, loss, harm, or the pointless expenditure of energy. Sadness also communicates a need for help. It shields the individual from hierarchical conflict by inhibiting aggression towards rivals and superiors. It promotes compromise in striving for unreachable goals, modulates interventions, and may lead to the recovery of lost relationships. Depressive feelings increase a person’s sensitivity to the suffering of others, thereby enhancing the survival of the kinship group and, by extension, that of the species. Just as negative emotions are an advantage in threatening situations, positive emotions aid in situations that offer opportunity or when progress toward a goal is faster than expected.We need to challenge the common notion that positive and negative emotional states are simple opposites.

One of my special interests is the mood disorder cyclothymia, with particular respect to creativity. The pursuit of romantic opportunities in cyclothymia suggests that this condition may have evolved as a mechanism for reproductive success. The cyclothymic creative bent as expressed in poetry, music, painting, cooking, and fashion design (among men, in particular) also appears useful for sexual seduction. Hyperthymic traits lend distinct advantage in leadership, exploration, territoriality, andmating. Selected aspects of this hypothesis have been tested using correlations between the constituent traits of the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego (TEMPS) scale and the Temperament and Character Inventory (TCI).21

A final word?

Anxiety and depression are feelings, that is, psychological experiences, but not only that. Feelings go together with somatic manifestations, specific gestures and expressions, and behaviors such as crying or shouting for help. The somatic manifestations of anxiety are stress reactions. They are neurohumoral reactions to stressors that are triggered as nonspecific mechanisms for confronting actual or threatened imbalance of the milieu intérieur or homeostasis.

Depressive reactions are more difficult to characterize, but go along with the findings of chronic stress. The neurobiology of depression resembles hibernation, in other words, a state of drowsy withdrawal in which key physiological and biochemical activities are suppressed and energy consumption turned down to its lowest setting, as a survival strategy under extreme environmental conditions. _


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Keywords: anxiety; depression; evolutionary theory; mood; normal and pathological psychological experience