Concretism in Biological Suicide Research - Are We Eating the Menu Instead of the Meal?

• Introduction
• Are ‘suicidality’ and ‘suicidal behaviour’ really meaningful classifiers?
• Suicidality, impulsivity and aggression
• Suicidal behaviour and depression
• Central and peripheral serotonergic parameters
• References

Research into serotonergic parameters associated with suicidal behaviour has resulted in many inconsistent and ambiguous findings. In this mini-review, we have tried to name some examples of methodological and conceptual vagueness and pitfalls in biological suicide research. The existing literature indicates various critical issues considered when interpreting existing data in this area:

• The ‘suicidality’ construct is not useful in biological suicide research. Autodestructive tendencies mostly occur in suicide completers and are probably not found in many suicide attempters and individuals with suicidal thoughts. No consistent association has been found between suicide intent and injury, suicide intent and suicide risk, choice of suicide method (violent vs. non-violent) and suicide risk, suicidal thoughts or attempted suicide. No close relationship between different degrees and different forms of suicidal behaviour has yet been demonstrated with any degree of consistency. According to many studies, serotonergic markers do not correlate with the various qualities and intensities of suicidal behaviour.

• The association between suicidality and impulsivity or aggression is weak. There probably is a disturbance in impulse and aggression control, but only in a subgroup of ‘suicidal’ patients.

• It might be misleading to use nosological constructs of depression in order to characterize suicidal individuals in biological suicide research. Biological variables might be associated with specific depressive symptoms, but not with some nosological construct or the sum score of a depression rating scale.

• The alleged association between peripheral and central serotonergic parameters is based on assumptions for which there is insufficient proof. Several studies indicate that there is no correlation between changes in central and peripheral serotonergic parameters. The mechanism of changes of peripheral serotonergic parameters is not sufficiently understood.

Introduction

Central and peripheral biological markers have been studied extensively in many groups of psychiatric patients to gain a better understanding of suicidal behaviour, depression, impulsivity and aggression. However, the pathogenesis of suicidal behaviour and depression has remained obscure. Several factors might be responsible in the failure to classify suicidal and depressive individuals adequately in biochemical and/or psychological terms. On the one hand, there are complex methodological problems and discrepancies in biological studies on suicidal behaviour and depression. Some of these problems will be outlined elsewhere (Müller-Oerlinghausen et al.; in preparation). Another important factor that slows down progress in suicide research is that the constructs of suicidal behaviour, depression, impulsivity and aggression used are mostly not well validated.

Obviously, many constructs used in suicide research have been given somewhat capricious definitions. These constructs are used to classify suicidal individuals in artificially created populations that often have rather a limited predictive value for the outcome of a suicide attempt or for repetition of suicidal behaviour. Unfortunately, whenever some kind of behaviour is defined and a term is created for it, the term is often taken to refer to an existing clinical condition or manifestation with its own specific biological parameters. Sometimes, our conceptual approach in biological psychiatry makes us look like a schizophrenic patient sitting in a restaurant who eats the menu instead of the meal because he cannot distinguish between the description of a meal and the meal itself. In the following, we will show that some of the constructs of suicidal behaviour and depression are probably the ‘menu’ and not the ‘meal.’

Are ‘suicidality’ and ‘suicidal behaviour’ really meaningful classifiers?

The most common construct in suicide research is the notion of suicidality. The generalization of suicidal thoughts, suicide attempts and completed suicide as ‘suicidality’ implies that a close relationship exists between these three facets of human experience and behaviour. However, this assumed underlying relationship is unproven, denying many obvious differences between these descriptions. Based on this assumption, what would seem obvious to anyone at first blush has been elevated to the general notion that there is a hierarchical continuum between individuals with suicidal thoughts, suicide attempters and suicide completers. Also, different degrees of ‘suicidality’ have been defined for suicide attempters according to the intensity of various behavioural dimensions such as intention to die, extent of injury arising from the suicide attempt, and degree of planning or ‘violence’ of the suicide attempt. A high expression of these dimensions has been assumed to be closely associated with completed suicides [34]. Biological suicide research in many of its facets is based on this concept. The usual rationalisation normally ends up something like this: A deficient serotonin system, such as reduced serotonin turnover, is associated with suicidal behaviour. The higher the ‘degree’ of suicide attempt - high level of planning, serious injury involved, violence of suicide attempt, high intent to die - the more ‘deficient’ the serotonin system. In some studies, it was shown that the number of platelet 5HT_2A-receptors and CSF 5-HIAA concentrations are correlated with the medical damage of a suicide attempt [33] [34] [36], while other studies observed lower CSF-HIAA concentrations indicating a reduced serotonin turnover in patients using violent suicide methods [4] [57] [58]. Thus, there is a widely held belief that the choice of the suicide method is an expression of a disturbed aggression control, and that suicidal behaviour can be interpreted as autoaggressive behaviour [5] [18] [19] [41] [60]. Assuming that this concept is basically true, the inevitable conclusion would be that suicide completers in the USA must suffer from greater ‘autoaggression’ than European suicide completers, as a higher rate of violent suicides is inflicted by shooting in the USA. However, various studies strongly indicate that the choice of a suicide method is mostly dependent on the availability of methods. ‘Autoaggressive’ behaviour is a construct, and a ‘violent’ suicide attempt is not necessarily associated with a higher degree of autoaggression or aggression than a non-violent suicide attempt. The labelling of individual suicidal behaviour as ‘violent’ or ‘non-violent’ does not necessarily imply that ‘violent’ suicide attempters are more aggressive than others. The association of violent suicide attempts with a high degree of autoaggression neglects important aspects; van Praag et al. [62] demonstrated that violent suicide attempts are associated with certain types of depression (melancholic type of depression), suggesting that it is hardly possible to define whether violent suicide attempts are associated with certain depressive symptoms or ‘autoaggression.’ Important factors influencing the choice of suicide method definitely include cultural background and availability of suicide methods. Several authors demonstrated the association between availability of suicide methods and suicide rates [25] [37] [65].

Looking for potential biological markers of ‘suicidality,’ either suicide attempters or suicide completers can be examined in clinical research projects. Significant changes in serotonergic parameters observed in some of these studies carry the risk of being generalized as an association of serotonergic markers with ‘suicidality.’ However, apparently similar changes in serotonergic parameters observed in suicide completers and suicide attempters allow neither the conclusion that suicide attempters and completers suffer from the same biological disturbance, nor that both behaviours are two sides of the same coin. Most likely, suicide attempters and completers do not have that much in common, even though they exhibit apparently identical behaviour patterns.

What, then, are the differences between suicide attempters and completers?

First of all, suicide attempts occur far more often than completed suicides. It has been postulated that the number of suicide attempts is 10 to 20 times higher than the number of completed suicides [11] [12] [13]. Secondly, there are impressive differences in age at which most of the suicide attempts and suicides occur. Suicide attempts occur mostly between the age of 20 and 30 years, whereas completed suicides mostly occur in older populations [11] [12] [46] [47] [49]. Women usually attempt suicide more often than men, while men complete suicide more often than women. Felber [16] and Duckworth & McBride [14] reported that a prior failed suicide attempt was found in only 15 % of all suicide completers. Thus, it can be concluded that only a very small fraction of all suicide attempters actually die by suicide. Most suicide completers succeed on their first attempt. On the other hand, suicide attempters often have a long history of suicide attempts. Why do some attempters repeat their attempts several times and always fail to kill themselves? It would probably not be cynical to conclude that a large proportion of ‘suicide attempters’ have no, or only a very diffuse actual intent to die [11]. A suicide attempt is an established way to communicate where there are interpersonal conflicts with the partner or social network [30]. The appealing character of many suicide attempts cannot be neglected. The self-destructive tendencies in most suicide attempters obviously cannot be described as weak. However, the high rate of successfully completed suicides at the first attempt in suicide completers indicates the high intention to die in this group. If suicide attempters and completers do have some psychological dysfunctions in common that could be reflected by a deficient serotonin system on a biological level, they probably do not share the dysfunction of ‘suicidality’ or self-destructive behaviour. Also, if suicide attempters and completers differ in degree of self-destructive behaviour, one might paradoxically be forced to conclude that a reduced serotonin turnover is not associated with self-destructive behaviour, assuming that suicide completers and attempters share the same changes in the serotonergic system.

There are probably substantial differences between suicide attempters and suicide completers, and psychological dysfunctions that have been associated with a deficient serotonin system cannot necessarily be attributed to suicide completers and suicide attempters in general. Suicidal behaviour in suicide attempters might be interpreted as an analogy to suicidal behaviour in suicide completers. An intriguing question is how to interpret the same changes of serotonergic parameters observed in brains of suicide victims and on platelets of suicide attempters. These changes might not be simply due to this so-called ‘suicidality,’ attributed to suicide attempters and suicide completers. In her review, Linehan [27] concluded that there is no proven relationship between suicide intention and medical damage. Plutchik et al. could not observe any association between the intent to commit suicide and the lethality of a suicide attempt [44], and van Praag postulated that the risk of success from a violent suicide attempt is no higher than that of a non-violent suicide attempt [62]. We were able to confirm this observation in a recent study on suicide attempters (Müller-Oerlinghausen et al.; in preparation). Mann & Arango [31] reported that suicidal thoughts are not good predictors for any increased risk of attempting suicide. All these studies suggest that suicidal behaviour can be classified in many ways, but these have only a poor predicting value for repeated suicidal behaviour and for the outcome of a suicidal act.

Still, many authors have tried to find a linear or hierarchical relationship between changes of serotonergic parameters and qualities of suicidality. However, many studies have searched in vain for an association between various serotonergic parameters and degree of suicidality, when the authors examined:

• Patients with a suicide attempt and patients with suicidal thoughts [6] [43] [56]

• Patients with more than one suicide attempt and patients examined at their first attempt [48] [58]

• Patients with violent suicide attempts and patients with non-violent suicide attempts [9] [29] [34] [38] [43] [48] [50]

• Patients with suicidal relatives and patients with relatives where no suicidal behaviour was reported [53]

• Suicidal patients that differed in their degree of medical damage [32,33 for CSF 5-HIAA].

Suicidality, impulsivity and aggression

Suicidal behaviour has been mostly associated with disturbances in impulse and aggression control [2] [5] [9] [10] [23] [35] [45] [47]. This apparently self-evident association neglects the fact that ‘suicidality’ is commonly diagnosed in an extremely inhomogeneous group of individuals. It is possible that many of these individuals do not suffer from any impulse or aggression-control disturbance. Since completed suicides are mostly carefully planned, it appears unlikely that a planned suicide is an expression of poor impulse control. The assumption that an impulse/aggression control disturbance is associated with ‘suicidality’ might be valid for a large subpopulation of suicide attempters, but completed suicides are commonly planned (and not impulsive) acts, and suicidal patients with a high intention to die have been found to be less aggressive than suicidal patients with a low intention to die [39] [30]. Thus, ‘parasuicides’ are often performed impulsively, but not the completed suicides [39] [30] [21] [31].

As we mentioned above, many suicidal patients have a low intention to die. Suicidal acts are probably often abused to put pressure on the partner. They could thus be interpreted as an expression of outwardly directed aggression. Weissman et al. [64] studied non-suicidal depressed females and non-depressed suicidal females. They observed that the depressed women were not very aggressive, while the suicidal women had a high degree of outwardly directed aggression and a very demanding attitude. Brown et al. [7] reported that suicidal patients with a personality disorder were more aggressive than non-suicidal patients with a personality disorder. Verkes et al. [63] studied ‘multi-impulsive’ individuals (identified with the Emotionality Activity Sociability Impulsivity Temperament Survey III (EASI III) and the Personality Diagnostic Questionnaire (PDQ-R)) after a suicide attempt, and observed a low suicide intention and a low degree of planning. Thus, it seems more plausible that aggressive and impulsive suicide attempters have a rather low intention to die. On the other hand, we may speculate that suicide attempters with a high intention to die do not suffer from poor impulse or aggression control. There appears to be a contradiction when on the one hand, various studies report on reduced CSF-5HIAA concentrations in impulsive and aggressive individuals, and on the other, reduced CSF-5HIAA concentrations have also been observed in suicidal individuals with a high intention to die, serious resulting injury, high degree of planning, or in suicidal individuals that complete a suicide within one year after a suicide attempt.

Suicidal behaviour and depression

In their study, van Praag et al. [62] reported that many suicide attempters had many depressive symptoms before their suicide attempt and experienced a mood elevation afterwards. This reflects a general methodological problem in biological suicide research. Since most suicide attempters are admitted to hospital after a suicide attempt, it is almost impossible to assess the degree of depressive symptoms before their suicide attempt with sufficient validity. Thus, it might be hard to decide whether changes in the serotonin system are due to either suicidality or a pre-existing depression.

On the other hand, depressive symptoms of suicidal patients are often rated with depression rating scales such as the HAM-D. These rating scales might be useful for determining the severity of a depression but they might be of little use in biological suicide research. There is no reason to believe that there is any valid interface between the nosological construct of depression, underlying the construct of such rating scales as the HAM-D, and specific changes in serotonergic parameters. If the serotonin system is associated with ‘depression,’ such an association is probably restricted to selected symptoms of depression only. We agree with van Praag et al. [59] [61] and Apter et al. [2], who both suggested that serotonergic parameters should be related to single psychiatric symptoms, not to a global quantitative measure of a psychiatric syndrome as is the case with depression rating scales.

Central and peripheral serotonergic parameters

Since it has been shown that blood platelets have some biochemical characteristics in common with brain cells, platelets are regarded as an easily accessible model of the CNS [1] [8]. However, even though it has been shown that platelet 5HT-transporters and 5HT2A-receptors have the same genetic origin as brain cells [15] [24] [55], there is no convincing evidence that platelet serotonergic markers do reflect changes in the CNS. In fact, substantial differences of serotonin turnover and metabolism exist between platelets and central neurons. Platelets cannot synthesize serotonin themselves [42]. Blood serotonin is derived from the enterochromaffin cells of the intestine [54] and accumulated in platelets through a fast-uptake mechanism. Degradation of serotonin in platelets is performed by MAO-B only (brain cells contain both, MAO-A and B), for which serotonin is a poor substrate.

Andres et al. [1] examined the 5HT2-receptor in the brain and peripheral blood of epileptics undergoing neurosurgery [1]. They did not find any correlation between the number of central and peripheral 5HT2-receptor binding sites. Young et al. observed no association between central and peripheral MAO-activity [66]. Moret and Briley observed a reduction of central paroxetine binding sites by 55 % after creating lesions in central serotonergic neurons in rats, which was not accompanied by a modification of platelet paroxetine binding sites [40]. Franke et al. [17] and Karege et al. [20] have both reported that there is no correlation between platelet serotonin content and plasma tryptophan concentration. Assuming that the serotonin concentration in the brain is determined by peripheral tryptophan availability, it has to be concluded that platelet serotonin concentration does not provide any reliable information about serotonin availability in the brain since platelet serotonin availability appears to be determined by factors other than plasma tryptophan concentration.

What form could a possible relationship between peripheral platelet markers of the serotonin system and brain cells take? Also, are there any studies that confirm these possible relationships?

To answer this question, we would first have to decide whether platelet markers should be considered as state or trait markers. If platelet markers are trait markers, they might not reflect any actual psychological distress situation in the individual. In this case, changes in platelets could be found even if the individual is not suicidal, depressed or in any other acute state of distress. This hypothesis is preferred by several authors, who believe that suicidality and depression are genetically determined [28] [43] [52]. Observed changes of serotonergic markers would then be seen as vulnerability factors for depression and/or suicidality. These would, by necessity, not be associated with any observed acute psychopathological changes. However, we could not find any reliable longitudinal studies confirming this concept.

If platelet markers are state markers, there would be difficulties in explaining why peripheral serotonergic parameters should change in the same direction as central serotonergic parameters do. Changes in central serotonergic indices are, to a great extent, due to the interaction of several neurotransmitters affecting brain cells. However, this complex situation is not present in peripheral blood. It might be argued that changes in serotonergic parameters are controlled by serotonin availability. But this is unlikely - for example, Leysen & Pauwels [26] could not observe any change in central 5HT2A-receptor density after destruction of serotonergic neurons in rats. Furthermore, they observed a downregulation of 5HT2A-receptors after administration of 5HT2A-agonists as well as 5HT2A-antagonists. If the 5HT2A-receptor were controlled by serotonin availability, one would have expected an upregulation of 5HT2A-receptors under the influence of 5HT2A-receptor antagonists. However, this was not the case. Changes in central and peripheral serotonergic parameters, such as receptor density, are probably only partially due to serotonin availability. Since approximately 95 % of all peripheral serotonin is stored in platelets, it seems unlikely that peripheral serotonergic receptors experience a similar exposure to serotonin as serotonergic receptors on brain cells do. Further, if serotonergic receptor density were controlled by serotonin availability, it would be hard to explain how platelet serotonin receptor densities could correlate with central serotonin receptor densities, as central serotonin is derived from a different source than peripheral serotonin. Consequently, there could be a shortage of central serotonin while peripheral serotonin concentrations are normal and vice versa.

If changes of central and peripheral serotonergic parameters are not controlled in an analogous way by serotonin availability, we would be forced to hypothesize some form of communication between platelets and brain cells indeed takes place. What form this might take has not yet been elucidated.

In summary, it must be concluded that the concept to use platelet serotonin markers as model for brain cells is based on many speculative assumptions. So far, no study has demonstrated any reproducible relationship between central and peripheral serotonergic markers, save that some receptors and transporters share the same genetic origin. Even though the serotonin transporter or the 5HT2A receptor of platelets and brain cells is encoded by the same gene, substantial differences may exist between the regulation of central and peripheral receptors and the enzyme kinetics. The encoding of a protein is one part of the story. But how do we know that the expression of the same gene is similar in platelets and brain cells? Do some of the receptor and transporter proteins experience changes in their kinetics due to phosphorylisation by kinase-enzymes and/or glycolisation by Golgi vesicles? And if so, is it very likely that kinetic changes of platelet and brain cell receptors are identical? This would seem to be no more than a faint hope for 5HT researchers in psychiatry.

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• 56 Theodorou A E, Katona C LE, Davies S L, Hale A S, Kerry S M, Horton R W, Kelly J S, Paykel E S. ³H-imipramine binding to freshly prepared platelet membranes in depression.  Psychiatry Research. 1989;  29 87-103
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Univ.-Prof. Dr. med. B. Müller-Oerlinghausen

Jebensstr. 3

10623 Berlin

Phone: +49 (30) 310 01-361

Fax: +49 (30) 310 01-366

Email: bmoe@zedat.fu-berlin.de

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Univ.-Prof. Dr. med. B. Müller-Oerlinghausen

Jebensstr. 3

10623 Berlin

Phone: +49 (30) 310 01-361

Fax: +49 (30) 310 01-366

Email: bmoe@zedat.fu-berlin.de