Written before translating the article:
This controversy began in 2022. A research team from the University of London conducted an “Umbrella Review” study and published it in the journal “Molecular Psychiatry” under Nature——The serotonin theory of depression: a systematic umbrella review of the evidence. This article brings together all the different areas of evidence to comprehensively identify and organize the existing evidence in the most important areas of research on serotonin and depression. The article concluded that these studies did not provide consistent evidence of a link between serotonin and depression, nor did they support the hypothesis that depression is caused by reduced serotonin activity or concentration.
Because for a long time, the psychiatric community has often used the statement that “the cause of depression comes from insufficient serotonin concentration” to persuade patients to take antidepressants, and this study may make patients unwilling to take antidepressants anymore, because this article Articles published in high-scoring journals make patients feel “cheated”.
However, the first thing that needs to be emphasized is that antidepressants can actually improve the symptoms of patients with depression in a very high proportion, and even reach the level of remission. Therefore, the problem is not that antidepressants are useless, but that we don’t really know why antidepressants can treat depression.
As for why the psychiatric community still uses this statement? The reason may be that it’s easier to explain. But in fact, psychiatrists themselves know that the real cause is still unclear.And the author of this translated articleNikolas Rosethis sociologist who is famous for his research on psychiatry wants to explain that the contemporary medical community already has an understanding of depression, so that the current discussion of the serotonin controversy may actually be very outdated and oversimplified. issue.
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original:
Articles on pyschological medicineNikolas Rose’s Blog(The article is titled: The Serotonin Wars)
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Commentary: The latest controversy over serotonin’s role in depression
Commentary: Recent disputes on the role of serotonin in depression
Published online by Cambridge University Press: September 12, 2023
Nicholas Ross (Nicholas Rose）1,2
Research School of Social Sciences and School of Sociology, Australian National University, Canberra, Australia; Institute of Advanced Studies, University College London, London, UK , London, UK
The recent debate in scientific journals about the role of serotonin in depression (Jauhar et al., 2023; Moncrieff et al., 2022) has made its way into print and social media, which has left me both confused and offended. Allow me to enumerate some of the key issues that seem to me to have been ignored or avoided in this debate.
What we call “depression” is of course not a single thing, but encompasses a variety of states of existence.The word itself has “looping effects” (Hacking, 1995) because it brings together these multiple states into an apparent coherence and puts in some states – feeling sad, losing motivation , lack of pleasure, etc. – this has been described before or elsewhere, and experienced in different ways. We have no reason to believe that these different states or the persons in these different states form a unity in any other way—in the permutations of causes, justifications, emotions, and thoughts—let alone in the states of the brain or body On the aspect.
Psychiatric medicine assesses depression through various scales or symptom summaries in diagnostic manuals and is used in research, such as recruiting cases to participate in clinical trials. The range of symptom items included reflects this heterogeneity. . Therefore, in the Hans Depression Scale (HAM-D), clinicians will rate a person’s mood, whether they have feelings of guilt, insomnia, weight loss, sense of illness, etc., and attach numbers and symbols indicating depression. Cutoff Score – The same score can be obtained by summing many different scores for individual symptom items. As Goldberg points out, in the DSM, “a patient with psychomotor retardation, somnolence, and weight gain is rated exactly the same as another patient with agitation, poor sleep quality, and weight loss. It seems like a magical idea to claim that all patients who meet the DSM diagnostic criteria for major depression suffer from the same disorder” (Goldberg, 2011, p. 226).The illusion of the additivity of ratings and the equivalence of numbers merges them into a single “diagnosis.” But there is no reason to think that the psychiatric diagnosis of major depression is specific to a single physical or neurobiological state; there is every reason to think that such a mixed set of states is highly heterogeneous.
The idea that every diagnosis of mental illness may be related to an abnormality in a single neurotransmitter system—too much or too little neurotransmitters in a specific synaptic cleft—dates back to the 1960s and was originally an intuitive inference. heuristic device (Schildkraut, 1965), one then assigned different biogenic amines—catecholamines and indolamines—to specific diagnoses—dopamine abnormalities were assigned In “schizophrenia”, serotonin is assigned to depression and so on. Of course, this was initially thought to be an oversimplification of intuitive reasoning, when it was generally thought that there were about seven key neurotransmitters—dopamine, epinephrine, serotonin, oxytocin, acetylcholine, gluten, and so on. Amino acids, GABA (gamma-aminobutyric acid).However, it is now thought that there are dozens, if not more, substances that play a role in the transmission and regulation of neural circuits in the mammalian brain; at least60 substances play an active role in brain processes, cooperating with each other in complex ways in the transmission of neural signals. therefore,Taking into account the heterogeneity of diagnostic categories and the heterogeneity of the actions and interactions of multiple neurotransmitters, assigning one transmitter to one function and one diagnosis, and subsequently to one (or even two ) treatment goals, there seems to be a dual problem.
Serotonin receptors are not only expressed in the brain, but are also involved in a variety of other physiological functions, including “eating, reward, temperature regulation, cardiovascular regulation, movement, pain, reproduction, sleep-wake cycle, memory, cognition, aggression, Reactions, emotions, and moods to stressors” (Charnay & Léger, 2022). There are at least 15 subtypes of serotonin receptors, generally divided into three broad categories. Within an organism, as with all of these functions, regulation of serotonin production and uptake varies greatly over minutes, hours, and days, and is subject to multiple other “inputs” to the organism and its physiological systems (including diet, (exercise, stress, etc.), and the regulation of serotonin receptor production and attenuation is intertwined with a variety of other neurotransmitter systems – the most commonly mentioned is the norepinephrinergic system (norepinephrinergic system), but people understand each other The complexity of the action and its temporality are not well understood.
In summary,While there may be a relationship between the constellation of states we call “melancholia” and changes in different aspects of the brain’s serotonin system, this will always only be a small part of the story, and its significance is not yet clear(e.g., Jesulola, Micalos, & Baguley, 2018).Therefore, we not only have research and hypotheses on the role of norepinephrine in depression (e.g., Maletic, Eramo, Gwin, Offord, & Duffy, 2017), but also on the key role of glutamate in depression. research and hypotheses (perhaps partly related to the microbiota [microbiome] and gut-brain axis [gut-brain axis] related) (Moriguchi et al., 2019), the role of dopamine in depression (e.g., Belujon & Grace, 2017), and undoubtedly many others, each of which is related to the role of neurotransmitters in regulating other neurotransmitters. and regulatory hypotheses related to the role of neural circuits in brain regions associated with different factors in the diagnosis of depression.
Broad awareness of these issues tells us that we certainly do not yet know enough to attribute causality, let alone primary causation, to serotonin metabolism or the serotonin circuit for any of the conditions we call melancholia a priori, inevitable and decisive changes in certain aspects. Suffice it to say that we found a correlation between this or that aspect of “melancholia” and changes in some aspect of serotonin metabolism—perhaps as a cause, as a consequence, or as some combination of the two—in It tells us nothing useful, either in explanation or in action. This connection is even less useful apart from an understanding of the general role of the serotonergic system in neural circuits and its relationships with other neurotransmitters and modulators of neural activity.
Furthermore, we need to understand thatThe brain is not a homeostatic system, but a homeodynamic system.Therefore, the key to understanding the neurobiological processes of depression and the effects of various medications is to understandneuroplasticity. For example, a temporary increase in one aspect of a neurotransmitter system, such as an increase or decrease in the availability of certain neurochemicals in certain parts of a neural circuit, will lead to subsequent upregulation or downregulation of other neuronal receptors (Carlson , Singh, Zarate, Drevets, & Manji, 2006; Liu, Liu, Wang, Zhang, & Li, 2017). In this highly networked and interactive dynamic system, we know very little about the effects of artificially altering neurotransmitter levels through drugs, except for very few short-term and local changes: we do not know to what extent these drugs triggers a cascade of further changes aimed at returning the system to its previous state; from a neurobiological perspective, we also do not know the consequences of long-term chronic use of these drugs, although we are beginning to distinguish withdrawal symptoms from relapse symptoms (Massabki & Abi – Jaoude, 2021; Murray et al., 2016).
Given that serotonin, like other neurotransmitters, plays an important role in numerous physiological functions, it is clear that disruption caused by taking drugs designed to modulate the serotonin system can have widespread effects on the human body. As for how to differentiate between these consequences—some of which are considered “effects” and others “side effects” or “adverse effects,” depending on the person making the distinction— Such as the perspective of researchers, clinicians, pharmacists, pharmaceutical companies or patients.
What we call depression involves thoughts, emotions, motivations, experiences, beliefs about ourselves and others, and more. In this sense, depression is not just hardwired into the brain (embrained) and is embodied (embodied), extended (extended) or placed (emplaced) (at a specific time and place), implemented (enacted) (not just a matter of experience, but a way of being and doing), embedded (embedded) a specific environment or way of existence, as well as conditioned (encultured) (shaped by the linguistic resources and belief systems of a particular culture).This is the so-called 5E approach to mental health.
Therefore, it is obvious thatNeural activity and changes in neural activity in the (human) brain are much more than just neurotransmitters!If we think of neural circuits as is now common—a metaphor widely used in popular debates about neurodiversity (“my brain is wired differently”[my brain is wired differently]) – We know very little about the complexity of the neural circuits involved in any “mental” process that we describe in normal language, whether cognition, memory, belief, emotion, feeling, intention, agency, etc., Not to mention issues of consciousness, or in general what are sometimes called “higher mental functions” arising from the “mere meat” of the brain.
We do know that neurons in the brain renew rapidly, not only during rapid periods of synaptic pruning and synaptic remodeling during childhood and adolescence, but also throughout a person’s lifetime. Now, while there is controversy, there is reason to believe that neurogenesis still occurs in adulthood and is exposed to exposures such as diet, stress, certain medications, practical learning, exercise, and other physical contact. ) to be highly responsive. In popular parlance, there is much evidence that the human brain is able to “rewire itself” in response to these exposures. In fact, humans can create new memories, learn new skills, and engage in new activities well into old age. , which proves the credibility of neuroplasticity neuroscience.
Our growing understanding of epigenetics suggests pathways by which these exposures can produce these effects. One key pathway is through regulation of gene expression in the brain. Approximately more than 75% of human gene sequences are expressed in brain tissue. Certain exposures regulate the expression of some or all of these gene sequences, making people pay more attention to the effects of gene activation and deactivation (gene activation and deactivation) in neural circuits. Factors related to the importance of plasticity of each and every element, common examples include through the stress response, through the microbiome or through inflammation. These are key neurobiological questions currently being investigated in the 5E approach to mental distress.
Taken together, we can’t help but feel that the current debate about the role of serotonin in depression and the effectiveness of drugs that act on the serotonin system is a naive and blind view of the brain, neurotransmitters, and neural circuits. , not to mention the embodied, emplaced, and encultured character of those states we call melancholia.
2023-09-18 06:50:56
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