Depression and anxiety: Introduction to quality of life

I'm conducting a little seo experiment and since my favorite niche is health I have decided to focus on "depression and anxiety" and the treatment thereof seeing this is something that has affected my life for many years, so its something I can be passionate about because not very many people actually understand exactly how this illness affects the life of the person suffering with it. Honestly I wouldn't wish it upon my meanest enemy because with depression whether or not it is coupled with anxiety it affects every single aspect of your life, I can describe it as something like having a thorn in the side that just cannot be removed. Since I just happened to do a test for depression and anxiety online a few minutes ago, I thought I'd post some of the findings I've discovered regarding keywords so in other words...what people searching for information concerning the above treatment are looking for specifically. Oh before I forget my stress and anxiety levels fell under the green (safe) level but my depression fell under the alarming red hot part of the graph so yes it was pretty high. Though I can attest that to a medication I've been giving for the past year in treatment of uterine fibroids. Anyways its always interesting to see how many people are looking for info and help concerning specific problems like depression and anxiety so have a look at these keywords. Try The Coolest Keyword Research Tool Today! Enter your keyword. Results may take a couple seconds to display. Anxiety depression G Trends Submit Export Keywords to CSV Keyword US Monthly Daily Google Bing+Y! CPC Traffic Value UK Monthly Daily CPC UK Value depression anxiety stress test 11,000 367 330 37 Y! $4.9 $48,510 0 0 £0 £0 depression and anxiety 7,333 244 220 24 Y! $5.39 $35,574 2,667 89 £2.29 £5,496 anxiety and depression 7,333 244 220 24 Y! $4.99 $32,934 2,111 70 £2.62 £4,978 anxiety vs depression 1,111 37 33 4 Y! $11.72 $11,720 44 1 £0 £0 adjustment disorder with mixed anxiety and depressed mood 978 33 29 3 Y! $13.22 $11,634 11 0 £0 £0 anxiety depression 2,111 70 63 7 Y! $5.08 $9,652 533 18 £1.98 £950 anxiety and depression medication 800 27 24 3 Y! $6.9 $4,968 56 2 £0 £0 depression anxiety stress scale 978 33 29 3 Y! $5.18 $4,558 122 4 £2.58 £284 dating someone with depression and anxiety 356 12 11 1 Y! $14.23 $4,554 11 0 £0 £0 depression and anxiety symptoms 656 22 20 2 Y! $7.54 $4,449 233 8 £2 £420 depression anxiety 1,111 37 33 4 Y! $4.44 $4,440 0 0 £0 £0 anxiety depression medication 533 18 16 2 Y! $8.89 $4,267 33 1 £0 £0 depression and anxiety medication 656 22 20 2 Y! $7.22 $4,260 33 1 £0 £0 depression anxiety and stress test 1,778 59 53 6 Y! $2.57 $4,112 56 2 £0.99 £50 depression stress anxiety test 1,111 37 33 4 Y! $3.99 $3,990 22 1 £1.02 £20 anxiety and depression association of america 978 33 29 3 Y! $4.13 $3,634 11 0 £0 £0 medication for depression and anxiety 656 22 20 2 Y! $5.69 $3,357 100 3 £2.02 £182 medications for anxiety and depression 433 14 13 1 Y! $8.44 $3,292 11 0 £2.93 £29 bayridge anxiety and depression treatment center 44 1 1 0 Y! $82.02 $3,281 11 0 £0 £0 anxiety and depression treatment 356 12 11 1 Y! $9.77 $3,126 33 1 £0 £0 medication for anxiety and depression 800 27 24 3 Y! $4.3 $3,096 122 4 £1.88 £207 treatment for anxiety and depression 189 6 6 1 Y! $17.91 $3,045 78 3 £2.78 £195 anxiety and depression treatment center newport beach california 78 3 2 0 Y! $42.49 $2,974 11 0 £0 £0 connecticut anxiety and depression treatment center 100 3 3 0 Y! $31.12 $2,801 11 0 £0 £0 anxiety and depression symptoms 533 18 16 2 Y! $5.17 $2,482 433 14 £1.91 £745 natural remedies for anxiety and depression 656 22 20 2 Y! $4.01 $2,366 56 2 £1.3 £65 medications for depression and anxiety 289 10 9 1 Y! $8.98 $2,335 11 0 £1.28 £13 dealing with depression and anxiety 356 12 11 1 Y! $6.87 $2,198 78 3 £3.04 £213 treatment for depression and anxiety 289 10 9 1 Y! $8.3 $2,158 100 3 £2.33 £210 meds for depression and anxiety 233 8 7 1 Y! $9.74 $2,045 0 0 £0 £0 symptoms of depression and anxiety 433 14 13 1 Y! $5.22 $2,036 233 8 £1.24 £260 dealing with anxiety and depression 233 8 7 1 Y! $9.36 $1,966 122 4 £1.72 £189 depression anxiety medication 289 10 9 1 Y! $6.85 $1,781 11 0 £0 £0 best medication for anxiety and depression 289 10 9 1 Y! $6.7 $1,742 33 1 £2.27 £68 how to deal with anxiety and depression 356 12 11 1 Y! $5.4 $1,728 44 1 £1.5 £60 depression anxiety and stress scale 189 6 6 1 Y! $10.08 $1,714 33 1 £0 £0 severe depression and anxiety 289 10 9 1 Y! $6.58 $1,711 100 3 £0.12 £11 help for depression and anxiety 189 6 6 1 Y! $9.59 $1,630 44 1 £2.46 £98 PS : Pls do excuse the copy and pasted keyword data above but this was merely to illustrate the extent to which health issues are big business not to mention the cancer industry but that's a whole other article.

Please note that the following article is published by Daniel Wildlocher at Cairn.info‌‌ In France, the arrival in the therapeutic field of antidepressant and "anxiolytic" drugs coincided with the development of psychoanalytical practices. A generation of young psychiatrists was thus confronted, in the mid-1950s, with care practices and psychopathological theories that were difficult to reconcile. It took several decades for a certain coherence in practices to emerge, without however an integrative view of the modes of action of the treatments being really found. Therapeutic indications will not be discussed here, but we will draw certain milestones to develop this integrative view of the theory, a necessary condition for establishing our practices. PSYCHOGENESIS OF DEPRESSION AND MEDICINE 2 The high effectiveness of antidepressants should not overshadow the interest of psychotherapy. The opposition between a depression of organic origin and a psychological depression accessible to psychotherapy can be considered as a hypothesis definitely refuted. But, too often, the unicist theory of depression served as a clash between an organicist explanation and a psychological interpretation. A resolutely unicist perspective, which takes into account these two modes of explanation, should imperatively distinguish between the problem of the mechanism and that of the cause. In terms of mechanism, being depressed, that is to say acting depressed, is both reacting to the environment and to oneself, and having a brain that produces this reaction. In terms of cause, being depressed will result either from a particularly "depressogenic" environment or personality, or from a brain particularly capable of producing the depressive response. In terms of mechanism, psychotherapy finds logical application in all forms of depression; in terms of cause, it is especially indicated in the forms where the psychosocial factors play a decisive role. 3 If psychotherapy is thus justified in principle, it does not mean that it is practically feasible. Without going back on the nature of the mental operations which characterize the depression, it is necessary to emphasize the rigidity of this system of thought. All argumentation comes up against a narrow but flawless logic. Any interpretation, and in general any reference to another way of thinking, encounters a stubborn refusal. But there is no psychotherapy without a relative working alliance, that is to say, a certain intention to change and an ability to adopt certain thoughts of the therapist. This psychorigidity of depressive thought is obviously more marked in serious forms. Gold, we are completely ignorant of how the persistence of a pathogenic biological mechanism maintains this "psychological" resistance to change. It is always surprising to observe how a system of thought so inaccessible to all argumentation and interpretation is transformed in a few days under the effect of well-conducted chemotherapy. This obviously reduces the practical role of psychotherapy, whose applications are especially envisaged in moderate or mild forms, in forms resistant to drug treatment, often with subacute evolution, and in the intermediate periods. The first two indications, however, remain debatable. The failure of chemotherapy is not a guarantee of accessibility to psychotherapeutic work, and one must be wary of a defeatist attitude of resigning too quickly to a failure of chemotherapy. Moderate and minor forms are often rapidly corrected by chemotherapy. In other words, the problem of indicating psychotherapy as an alternative to chemotherapy should not be questioned. Both questions must remain completely independent. Especially since, as we shall see, empirical studies seem to show that the effects of these two therapeutic approaches are of a different nature. Both questions must remain completely independent. Especially since, as we shall see, empirical studies seem to show that the effects of these two therapeutic approaches are of a different nature. Both questions must remain completely independent. Especially since, as we shall see, empirical studies seem to show that the effects of these two therapeutic approaches are of a different nature. 4 The only question that we have to ask ourselves is therefore, independently of the prescription of drugs, if a given patient, at this moment of its evolution, is accessible or not to a psychotherapeutic intervention, and to define this mode of intervention. It is necessary, for that, to specify the objectives and the means of the psychotherapeutic interventions which we have. 5 How do we reconcile what we know about the psychogenesis of the melancholic state with the effect of antidepressant drugs? 6 A remark, almost incidental, poses in "Mourning and melancholy" the existence of a general economic factor that could play a role in certain melancholic states: "The melancholic complex behaves like an open wound, attracts on all sides to him investment energies (which we have named in the neuroses of transfer "counter-investments") and empties the self to total impoverishment: it can be easily resistant to the wish to sleep self. A presumably somatic factor, not elucidable by psychogenesis, is manifested in the regular sedation of the state in the evening. To these considerations is connected the question of whether a loss of the ego, without the object being taken into account (attack of the ego, purely narcissistic) is not enough to generate the picture of melancholy, and if a directly toxic depletion of the self-libido can not produce certain forms of the affection. A few years later, in "Inhibition, Symptom and Anxiety", the principle of global inhibition is also retained and its role in melancholy clarified: "The more general inhibitions of the ego follow another mechanism which is simple. When the ego is involved in a psychic task of a particular difficulty, such as a mourning, a huge repression of affect, the obligation to hold in subjection sexual fantasies that go back constantly, he knows such an impoverishment of the energy available to him that he is forced to restrict his spending in many places at once, as a speculator who has immobilized his funds in his companies. I have seen an instructive example of such an intense and short-term general inhibition in someone with a condition of constraint, which fell into a paralyzing fatigue lasting from one to several days, sometimes which should have obviously caused an explosion of fury. From there, a path must be found that leads to the understanding of the general inhibition by which states of depression are characterized, and the most serious of these, melancholy. The comparison between the two texts is interesting because if in "Mourning and melancholy" it is a factor that would intervene only in certain states and whose origin would be of a toxic nature, in "Inhibition, symptom and anguish "it is a more general mechanism that we would find in different pathological states and whose psychogenic nature can not be doubted. At the opposition between psychogenic and toxic depressions, in the first text, the idea of ​​a common mechanism, of an "energetic" response to psychogenic factors, is substituted. Should we admit two forms of depression, one psychogenic, the other organic (so-called toxic), or recognize the entanglement in any depression of mechanisms related to the intentional experience and others related to an undifferentiated psychic energy? 7 When the biological therapies of the depressions were discovered, the same question was posed with renewed acuteness. Already in the 1940s and early 1950s, electro-convulsive therapy was questioned as to whether a positive response to this therapy was evidence of the organic origin of the disease. Some thought they could contrast even more clearly than before endogenous depression (curable by ECT) and reaction and neurotic depression, likely to be treated by psychotherapy. It had to be recognized, however, that depressions that seemed frankly reactive to life events (such as pathological mourning, for example) nevertheless responded favorably to biological treatment. This became even clearer when antidepressant drugs (imipramines and MAOIs) were discovered. Indeed, drugs being much easier to handle than "electroshock", they were widely used in depressive states where psychic factors played an obvious role. The opposition between organic and psychogenic depressions was no longer acceptable. It had to be admitted that all the depressions that could be treated by medication were of organic origin, otherwise it was necessary to wonder by what mechanism the drug acted in clearly psychogenic states. The opposition between organic and psychogenic depressions was no longer acceptable. It had to be admitted that all the depressions that could be treated by medication were of organic origin, otherwise it was necessary to wonder by what mechanism the drug acted in clearly psychogenic states. The opposition between organic and psychogenic depressions was no longer acceptable. It had to be admitted that all the depressions that could be treated by medication were of organic origin, otherwise it was necessary to wonder by what mechanism the drug acted in clearly psychogenic states. 8 Psychoanalysts who were interested in this question had the choice between two answers. The first was to see in the effect of the drug only a purely symptomatic action. But this hypothesis hardly holds; antidepressants are not psycho-stimulants, many of them are rather sedative. It is clear that the specific effect of these drugs on depressive states and certain obsessive states requires another explanation. 9 The thesis I have been defending for about twenty years is that of the general inhibition proposed by Freud and repeated by various authors under the term "basic depressive response". It poses the existence, in the depressive states, of an inhibition of the implementation of the action, inhibition which would be corrected by antidepressant drugs and which would make depression a real psychosomatic disease. 10 There are two forms of depressive inhibition. The first affects a sector of the subject's content of thought. It is the consequence of the dominant investment of certain contents of thought. Thus the inhibitory effect of the "aggressive" thought system or the experience of object loss on the other thought programs of the individual can be described. The latter, occupied by the theme of destruction or loss, can not be the place of activation of these other programs. Inhibition results from competition between systems of thought. From a semiological point of view, we will speak of painful mono-ideism, and we will discover the dominant contents of thought (loss of object, self or hetero-aggressiveness, loss of self-esteem, etc.). 11 This form of inhibition relates to representations that are easily expressible in words. It will be easy to describe the concrete and particular scenes that constitute the content of these representations (no longer seeing one's son, not being able to write to X, etc.) that can be grouped into more general classes (pessimism, feeling of incapacity). . However, these representations can be conscious or unconscious, in the psychoanalytic sense of the term. The subject may ignore his ambivalence or his narcissistic megalomania. They are mechanisms of repression, cleavage or projection that prevent these representations from being expressed in conscious language. But it is concrete and particular representations that are thus repressed. 12 The second form of observable inhibition in depression affects the whole activity of the subject. Variable according to the situations or the time of the day, it touches indifferently all the contents of thought and all the acts motor. From a semiological point of view, we will speak of psychomotor slowing down, cognitive impairments, especially concerning memory and attention, and subjective impressions interpreted according to the case as fatigue, a lack of will or a lack of concentration. These symptoms do not refer to thought content but to information processing and decision-making processes that relate to a more basic level of mental activity. 13 We must face the facts: depression expresses both a certain state of the central nervous system, on which chemical molecules act powerfully, and a mode of response to the world which testifies to a complex psychopathological structure. 14 A number of clinical arguments support these two realities. We are more and more acquainted with depressive states which are not accompanied by alterations of mood: states of non-organic fatigue, states masked by somatic symptomatology react remarkably well to antidepressant treatment. However, in these cases, the major importance of the slowdown, sedation under treatment, do not seem to be related to mood. Conversely, many states of sadness present almost all depressive symptomatology without this basic behavioral component. The experience of mourning, situations of frustration, big narcissistic wounds, the neurotic states dominated by the lack of libidinal satisfaction and the strength of the death drives resemble the depressive state but react only very imperfectly to antidepressants. This is why, in the very vague setting of so-called neurotic and reactive depressions, one should distinguish true depressive responses, with psychomotor retardation, sensitive to chemotherapy, and states of mental suffering without altering the tempo of the activity and not responding to the antidepressant action of drugs. This view is corroborated by two facts that have been underlined several times: among all the symptoms of depression, 15 Although it is well established that psychomotor retardation, in the broadest sense, is a fundamental component of depressive states and that this component is very much dependent on neuronal mechanisms sensitive to the action of drugs, it is obviously very tempting to try to deepen our understanding of its intimate mechanism. This is likely to be a very universal type of answer. It is present in the clinical pictures described under the term of "anaclitic depression of the infant". This answer may not be peculiar to man; it has been shown that the separation of pups from their mothers in other primates results in behavioral inhibitions that respond to antidepressant drugs. 16 Depressive slowing is, moreover, an exaggeration of what can be observed in humans in non-pathological conditions. The announcement of a great misfortune is often marked by a congestion of motor expression and activity. This reaction is most of the time only very transient. It is only when it persists and worsens that one speaks of depressive state. It is conceivable, moreover, that this answer depends on psychological and organic factors. What we call endogenous depression reflects the ability of certain nervous organisms to trigger this type of response, regardless of any psychological cause. Moreover, there are probably variations in the activity rate in each of us, corresponding to an endogenous or cyclical acceleration or slowing down. 17 If one tries now to get even more into the details of the mechanism, exciting questions arise. What is this change in the tempo of the activity? This is probably not an extension of the performance of the acts but more likely an increase in the break time in the succession of acts. Is this a loss of the incentive to implement the following act? And what does this loss of incentive consist of? It is striking to see that the manic state offers us exactly the opposite of the slowdown: the flight of ideas, hypersyntony, tachypsychie are the expressions of an acceleration of the tempo, a facilitation of the activation of the acts. It should be made clear that by act we mean here motor and speech acts as well as mental operations. 18 It may be thought that fine cognitive studies of the decision-making act, together with those on the rhythmicity of activity, perhaps related to that of sleep, may give us the key to the mechanism. We have constructed psychophysical-type tests that seek to specify this type of cognitive impairment, which is not observable by the usual clinical investigation methods but can be detected by experimental apparatus dealing with phenomena of the order of a hundredth of a second. 19 These last remarks allow us a general conclusion. It is necessary in psychopathology to give up the belief that we can analyze all mental processes at the same level of observation. What psychoanalytic inquiry brings into depressive states is an individual and general knowledge of the great structures of thought exploring the intentionality of representations. The quest for love, the narcissistic position, the aggression against the mental object define such plans of action revealed by the words of the subject. We have seen that depressive illness can be considered as the result, in many cases, of a disturbance of these plans of action and the domination of the psychic apparatus by these psychopathological structures. On the other hand, psychomotor retardation, which affects the whole of the activities of the subject, pertains to an infra-clinical perturbation altering elementary mechanisms of the associativity of the acts which escapes the "naked eye" of the clinician. Of course, both the systems of action and this fundamental cognitive disturbance express functional alterations of the central nervous system. But, if we know little about the neural wiring that comes into play in the basic cognitive regulation of mental activity, we know even less about the cabling that organizes the system of action that the clinician observes. Antidepressant drugs probably work on mono-aminergic neuronal systems that regulate basic cognitive operations. It is hard to imagine that they can intervene on the fine wiring that regulates this or that system of action. It is therefore not surprising that their action focuses on the slowdown in activity and acts only secondarily on these systems. 20 A second conclusion, of a therapeutic nature, can be proposed. The psychotherapeutic action is exerted on the systems of action. This type of intervention will be all the more desirable if the depressive response appears secondary to these high-level psychopathological disturbances; provided, however, that an elementary neuronal mechanism, partly irreversible, is not put in place which, creating an overall slowdown in activity, would limit or cancel the psychotherapeutic action. It is at this more elementary level that the action of antidepressants is exercised, both when the slowdown is secondary to complex psychopathological mechanisms and when endogenous, genetic or acquired factors predominate. 21 The theoretical advantage of this model is to make compatible the uniqueness of the mechanism of depression and the dualism of its causes. Its practical advantage is to provide a clear and, it seems to me, effective framework for articulating different therapeutic strategies. 22 During acute depressive attacks, two principles seem important to me. The first concerns the indications for long-term psychotherapy, the second is the priority given to drugs. 23 The decision to undertake long-term psychotherapy, especially in psychoanalysis, can not and should not be discussed during a depressive state. At first, it is very difficult to correctly assess the subject's personality. Depressive thinking masks certain traits and arbitrarily magnifies others. In particular, it is very difficult to study permanent intrapsychic conflicts and habitual defense mechanisms. On the other hand, the patient's intentions may change completely after the healing of the depressive state, either because the initial refusal follows a genuine request for help, or, on the contrary, because, after freed from the depressive experience, the patient, rightly or wrongly, no longer feels any reason to engage in such treatment. 24 The second principle concerns the necessity of drug treatment. The difficulty is to know to what extent a depressiogenic thought system is reversible spontaneously or under the influence of psychotherapy. We are sorely lacking comparative studies here. In the absence of objective data, it seems that irreversibility is to be feared, and therefore the drug treatment necessary whenever there is a stable alteration of the capacity to act, to speak and to think. In case of doubt, it is better to have a trial treatment than a therapeutic abstention. 25 These two principles do not go against the necessity or the opportunity to bring to the patient a psychotherapeutic help in acute period. In all cases, it seems necessary to help the patient become aware of the events that may have played a role in triggering acute access (mourning, disappointment, narcissistic injury, etc.). It also seems necessary for the patient to become aware of the condition in which he is. It is good to think of depression as a state of illness and to make a difference with the legitimate attitudes that some depressive thought systems may have. He must know that his personal efforts can only be limited, that any important life decisions must be postponed and that, as a general rule, it is not by suddenly modifying its living conditions that the difficulties will be overcome. "Healing" takes a while. You must know how to tolerate the presence of the drug, both for its troublesome side effects and for its generally negative symbolic value. To heal from depression is not to cancel or mask the suffering or hardships of life; it is to regain strength (by lifting the inhibition) to treat them actively instead of remaining frozen in a lethal position. 26 Beyond these minimum requirements, more ambitious strategies can be put in place. They depend on the severity of the depressive state, the interests of the patient and the competence of the clinician. A psychodynamic analysis of relationships with the entourage, or psychoanalytic-inspired focal psychotherapy may be used. This one can aim at the sadomasochistic dimension which is hidden behind the complaints, the narcissistic megalomania which is hidden behind the ideas of inferiority and the behaviors of failure, the unconscious mourning of an object whose symbolic or real loss is treated by repression, isolation or denial. 27 It is therefore only in the period of remission, drug treatment being completed or not, that the opportunity for long-term psychotherapy will be discussed. Objectives should also be discussed carefully (prevention of new episodes, improvement of living conditions, treatment of neurotic or permanent narcissistic disorders, borderline state or pathological organization of character, etc.). 28 What seems fundamental is, before any beginning of treatment, to relate the expected effects (life goals) with the modifications of the permanent mental functioning which would make it possible to obtain them. It is not psychotherapy that treats the symptoms or changes the life, it is the changes of the mental structures operated by the psychotherapy (goals of treatment). In the absence of this connection, the objectives will remain illusory and sometimes quite unrealistic. 29 The psychotherapist will then have to ask himself whether the means at his disposal (the psychotherapeutic techniques he uses, his personal availability) are in line with these treatment goals. Are there reasonable chances for the patient to truly experience the therapeutic process? And does this experience have a reasonable chance of causing a change in the expected mental functioning (technical goals)? THE ACTION DESINHIBITOR OF TRANQUILIZERS 30 Just as the antidepressant and the psychostimulant drug were too easily confused, the action of anti-anxiety medications was abusively covered by the term "tranquilizer". But there is an important difference between the two classes of medicine. Antidepressants only act on depressive states and have no stimulating or euphoric effect on non-depressed subjects (hence the absence of any addictive dependence); anxiolytics have favorable effects on any individual (hence their addictive effect). Like alcohol, of which they are pharmacologically fairly close, anxiolytics act on a common psychic state. But what does the term "tranquilizer" cover? 31 Experimental animal research has sought to apply stressful situations to the action of these products. The action of the tranquilizer medication in such situations may be considered a good example of the anti-anxiety effect. 32 What is the relationship between what experimentation shows in situations of response to danger and the chemical treatment of human anxiety? Can we talk about an anxiety that is not just such an answer? This example takes advantage of the fact that it is a chemotherapy of rapid action, temporary, certainly, but very specifically effective on a rather well identified emotional state. In reality, this identification is based more on the cognitive content of the experience than on the physical sensations and the purely affective characteristics. Waiting for imminent danger, fear without object, so-called neurotic anxiety is hardly distinguished from real fear by the illusory nature of danger. It is not surprising that E. Kandell (1983), based on his work on a model of fear learned in Aplysia, 33 Anxiety-fear is no longer held for the symptom of a disease. His existence in a very vast field of pathology did not permit it. Just enough to distinguish an isolated morbid anxiety (anxiety neurosis) and secondary anxieties observable in various states, as well in other forms of neurosis than in psychoses or various disorders of the personality. 34 It is these specific characteristics, due to its intentionality (the expectation of a real or illusory danger) and its absence of semiotic specificity, which made it possible to approach the study of anxiety in a psychophysiological perspective. It was thus possible to show the importance of the role played by the awakening reaction of the autonomic nervous system. This awakening reaction would, moreover, be common to all emotional states, but draw its cognitive content only from the cognitive treatment of the situation. 35 This neurovegetative response would be cognitively associated with an orientation reaction. This would be characterized by a fleeting effect to process and analyze the new information, an inhibition of current activity and an orientation towards future information, likely to reduce the degree of uncertainty. 36 Drugs with the ability to inhibit adrenergic excitation in the neurovegetative arousal reaction are known to have a clear anxiolytic effect (beta blockers). Likewise, benzodiazepines, like other sedatives, have been thought to have anxiolytic action because of the depressing effect on the orientation reaction. This explanation was questioned as we isolated molecules with strong anxiolytic effects without marked sedative action. 37 We then became interested in models of animal behavior different from that of the learned fear. It has been shown (M. H. Thiébot et al., 1986) that benzodiazepines decrease the holding capacity. If, for example, in a T-maze the rat is offered two food rewards of different importance, the animal learns quickly to move to the side where the reward is strongest. Through a system of doors in the two horizontal branches of the labyrinth, the animal is immobilized after it has chosen the route but before obtaining the reward. Two parameters can be varied: the waiting time and the importance of the reward. It can be observed that the length of the wait creates a powerful aversive effect that guides the choice of the animal towards a low reward. A benzodiazepine is then administered to the rat. If this molecule had the effect of reducing the orientation reaction, the animal should "accept" a greater expectation. It is the opposite effect that occurs, tolerance to waiting decreases. 38 These experimental data agree with a certain number of clinical data: the pleasure effect sought by subjects who have become dependent on benzodiazepines is not sedation, but the quest for disinhibition of behavior and activity. mental. This facilitating or disinhibiting action is also consistent with that sought in alcohol consumption, regardless of the sedative effect. As in some cases of acute alcoholic intoxication, fugue and violence behaviors accompanied by amnesia of the episode are sometimes observed under a single dose of benzodiazepines. 39 Thus, the study of the mode of action of so-called anxiolytic drugs prompts us to reconsider our general theory of anxiety, or rather to complete it by granting a determining role to the inhibition of the usual plans of action. This last hypothesis had already been put forward with regard to emotions in general, the difference between anxiety and all the other emotions then holding the impossibility in anxiety to develop a specific response appropriate to the situation. The anxiety state is in this sense different from fear, the latter involving the identification of a danger and the setting up of appropriate responses. 40 McReynolds (1976) already defined anxiety as resulting from a situation of cognitive incongruence that does not allow the mobilization of any relevant action plan. A new situation is thus generated that is not comparable to known patterns and which does not allow the use of an appropriate response mode. Thus would be constituted a cognitive debt (cognitive backlog) defined as the ratio between the unassimilated percepts and the sum of assimilated and non assimilated percepts. 41 Anxiety, seen in terms of inhibition of the action plans, is therefore the result of a situation identical to any situation generating emotion (interruption of previous plans of action, state of cognitive awakening and neurovegetative), to the except that no appropriate course of action can be activated. We can say that she is the "failure" of emotional life rather than one emotion among others. The action of the anxiolytic drugs, at least of those currently known, would result less from a sedative effect on the orientation reaction than a disinhibition allowing the previous action plans to mobilize despite the new situation. 42 In view of the initial question, the model of anxiety is both instructive and disappointing. It is instructive for a variety of reasons. From a methodological point of view, it is a good example of what can be a process of experimental psychology in relation to a hypothesis on the mode of action of a drug. No more than learned fear, that of deferred reward is a model of anxiety; it is a model of the suspension of the execution of a plan of action, operation which enters in the composition of an anxiety state. The drug thus helps us break down into more basic operations what the clinic makes us see as isolated subjective events. It provides a form of dissociation between functions that seemed linked in a single structure. 43 Thus an observable variable is drawn which calls for a psychological interpretation. The ability to postpone the act was already known and had given rise to several experimental devices, but how to articulate it with the opposite one, which consists in impelling the act despite inhibitory constraints? Is this not a matter for defining a new object of study and for drawing experimental protocols for testing hypotheses within the framework of the new theoretical paradigm? 44 Here we come up against a difficulty justifying the "disappointing" epithet just mentioned. Indeed, the anxious state is not a permanent state. We already know the highly questionable character of experimental situations designed to provoke a state of anxiety. But the natural anxious state, unlike the depressive state, does not lend itself better to the experimental approach. Its permanence is only that of a predisposition to episodic access. The concept of generalized anxiety responds only to this provision: on a background of increased vigilance, it is the occurrence of anxious access that defines it. The spontaneous anxious state can not therefore be used as a field of experimentation. At best, one can select naturally anxious subjects to put them in experimental conditions of stress. 45 On a theoretical level, a new concept emerges: the ability to control the initiation of action no longer appears to depend solely on a field of motivations and cognitive and behavioral strategies, but on a more modulating function. General. It has little opportunity to manifest itself in the usual experimental situations. On the other hand, it can be seen as a source of variations in conditions observable in pathology. 46 One can venture to generalize this last remark. The joint use of observation and experimentation in psychopathology does not only make it possible to better understand the behavioral and cognitive mode of action of psychotropic drugs. It opens new avenues of research in the field of emotions and behavioral regulation, the drugs available to us being endowed with an action on very general modulatory functions of the control of the activity.‌ The reason why I decided to use the above data was to show the method that depression and anxiety are viewed by mainstream doctors. Its a very word for word, by the book approach to something that cannot be boxed by science. Do anti depressant medication such as SSRI's actually work and what if natural treatment or integrative medicine could better treat this malady without the side effects synthetic meds such as Prozac and tranquilizers cause as side effect. Of course all man made drugs have side effects and this is the reason I've written this article to shed light on what really works as depression and anxiety treatment for quality of life. Fact is there is really no living done where there is absent quality of life for people living with depression anxiety and such. Watch this space for updates on natural remedies that bring a soothing effect on depression and anxiety. Please take note that I am not entirely against allopathic medication and will disclose that there are in fact side effects of natural treatments for anxiety and depression that one has to keep in mind because there are special precautions with some of these too. The main idea behind this blogging space is for quality of life and ease of suffering. Please feel free to share your personal experience and knowledge of depression & anxiety treatments and what has been successful for you and what you will avoid in future. http://click.a-ads.com/965447/54869/