A comprehensive review introduction

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Table 21: Commonly prescribed and abused psychoactive drugs.

Causes of drug dependence

The exact causes of illicit drug use is unclear, however, the genetic make up and innate psychoactive properties of the drug combined with peer pressure, emotional upheavals, anxiety, depression, and environmental stressors are all thought to play a role.

Among adolescents, peer pressure is a large contributing factor to drug abuse with 50 percent of those who become addicted eventually suffering from mental disorders such as depression, attention deficit disorder (ADD), and post-traumatic stress disorder (PTSD). Family behavior and habits also play a role in adolescent drug abuse. Children with parents who are drug abusers themselves are more likely to experiment with drugs and develop an addiction when they become adults.

Generally, there are 5 factors that are attributed to the development of drug dependence (158):


  • Existing mental illness such as depression, bipolar disorder, anxiety disorders, and schizophrenia

  • Accessibility to illicit drugs

  • Low self-confidence and poor family and social relationships

  • Stressful lifestyle

  • Cultural acceptance of drug use

Curiosity, an inherent human trait, is known to be a precipitating factor for both discoveries and disasters. Drug dependence proceeds through several stages from experimental use to downright addiction (see table 22). Age is a determining factor in the speed at which a person moves through the stages. Generally, the younger the person is, the faster he is likely to move quickly through the stages.

Stages


Description

Experimental use

Introduction by peers for recreational use

Regular use

Develop physical dependence, marked tolerance to drug; seek higher and frequent doses

Daily preoccupation

Deal drugs to support habit, social withdrawal, use of other drugs

Addiction

Psychological dependence, loss of control over drug use, legal and financial problems, denial of existing drug problem

Table 22: Stages leading to drug dependence

The table below lists the common psychoactive drugs and their street names (159).



Psychoactive drugs

Street names

Amobarbital

Yellow jackets

Butalbital

Blue devils

Secobarbital

Seconal

Phenobarbital

Downers, goofballs

Diazepam

Roofies, Vallies, blues

Amyl nitrate capsules

Poppers, snappers


Marijuana

Roach, weed, MJ, Mary Jane, grass

Amphetamine

Speed, crystal

Methadone

Dollies

Nitrous oxide

Laughing gas

Butyl nitrate

Locker room

Table 23: Street names of psychoactive drugs

Drug tests and screening

Illicit drug use can be detected using urine samples to test for the presence of the drug’s metabolites.

Marijuana



The drug is detected in urine for 48-72 hours after single use and up to 12 weeks after chronic use.

Barbiturates

Two of the most commonly detected tranquilizers are butalbital and phenobarbital (Luminal). Butalbital is prescribed for migraine while phenobarbital is primarily prescribed for seizure disorders. Their period of detection varies between the short acting to long acting drugs of this class, but generally, they are detected 2-10 after last use.

Benzodiazepines

Benzodiazepines such as diazepam (Valium) and alprazolam (Xanax) are found up to 7 days after the last chronic use, depending on its half-life.

Treatment

The first step in the treatment for drug abuse/dependence is its recognition as a problem. Recent research has found that addicts will less likely “deny” their drug abuse as a problem when confronted with empathy and respect.

Treatment, much like the process that resulted in full-blown drug addiction, occurs in a series of stages (158):

1) Cessation of drug use either gradually or abruptly. Since abrupt cessation can lead to severe withdrawal symptoms, professional detoxification in a controlled environment is encouraged along with peer support, and abstinence. Detoxification or “weaning off” sometimes require the administration of a drug with similar effects to reduce the side effects and risks of withdrawal. Depending on the severity of the dependence and health status of the patient, detoxification can be done on inpatient or outpatient basis.

2) Emergency treatment for acute toxicity due to overdose. Patients who overdosed usually present in the ED unconscious and on respiratory arrest. Antidotes are often used in these cases to bring down the toxic levels of the offending substance.

3) Behavior modification through counseling. Many rehabilitation facilities have long after-care plans in place (when the user is released from the medical facility) for both the patient and the family.

4) Psychosocial support after overcoming addiction. The treatment of drug addiction does not stop when the patient leaves the clinic facility. Friends and family are needed to help the person establish some level of normalcy after a long period of social withdrawal.

Ethical Issues

If the truth, the whole truth and nothing but the truth were told, psychopharmacology does not cure mental illness any more than aspirin cures an infection.

Pharmaceutical companies are powerful players in the field of psychopharmacology. They protect and continue to advocate past hypotheses based on monoamine deficiency that initially influenced the widespread use and acceptance of psychoactive drugs more than 50 years ago. A lot has happened since then, but these hypotheses (serotonin and norepinephrine hypotheses) are actively used to justify and promote expensive psychoactive medications. In fact, these companies exert great influence on the prescribing habits of clinicians, sometimes more than patient history and evidence-based studies. What’s more, these hypotheses are wrought with limitations and dubious integrity (160).

Selective serotonin reuptake inhibitors

SSRIs treat depression by inhibiting the breakdown or reuptake of serotonin from the synapse, thus keeping the serotonin bound to the postsynaptic receptor and active for a longer period. The selectivity of SSRIs is misleading because the drug affects other neurotransmitters, not just serotonin. For instance, fluoxetine and paroxetine, also indirectly affect the activity of another neurotransmitter, norepinephrine. The indirect effect is clearly seen in the aggression tendencies of patients prescribed with these drugs.

The neurochemical mechanisms of the brain are poorly understood let alone the specific effects of serotonin in the brains of depressed individuals. Consistent evidence-based research has not been established yet, even after all these years. Although there is little doubt that SSRIs do act on the serotonin system, what is still questionable is the role of serotonin deficiency in depression. Even one of the leading scientists of initial serotonin research, George Ashcroft, did not pursue further studies on the idea of lowered serotonin levels being the cause of depression in the 1970s. Ashcroft pointed out that, “what we believed was that 5-Hydroxyindoleacetic acid (5-HIAA) levels were probably a measure of functional activity of the systems and not a cause. It could just as well have been that people with depression had low activity in their system and that 5-HIAA was mirroring that and then when they got better it didn't necessarily go up.” (161) 

SSRIs improve depressive moods by targeting the serotonin system but as Ashcroft implied, clearly there are factors other than neurochemical balance at play in the etiology, course and outcome of depression. The serotonin hypotheses clearly advanced the psychopharmacological treatment aspect of depression but the way that pharmaceutical companies have held onto it, despite its insufficient and inconsistent evidence, to make a solid marketing case to the public is also clearly unethical and most often, unchallenged. The therapeutic significance of SSRIs in depression is akin to aspirin in pain and fever. Just like aspirin that does not treat the cause of fever (e.g. infection); SSRIs do not treat the root cause of depression, and they merely elevate serotonin levels. It merely demonstrates a causal relationship between the symptom (depression) and serotonin levels. Symptomatic control of the disease is not treatment of the disease itself.

Another problem with the serotonin hypotheses is that there are other agents such as reserpine that cause depletion of serotonin levels in the brain; yet do not cause depression (160).

But perhaps the blame is not entirely on the pharmaceutical companies alone. The Food and Drug Authority (FDA) has played a hand in it too. They only require two positive clinical trials to demonstrate that an investigational antidepressant is better than placebo in order to approve it. Now all pharmaceutical companies need to do is conduct numerous studies until they come up with at least two that show positive results. This takes on the appearance of the FDA setting a minimum standard for the pharmaceutical companies; and, in so many words stating: show us two evidences that make it better than nothing and we’ll give you the green light.

Many of the clinical trials concerning the effectiveness of SSRIs that were approved by the FDA show time and again that they do not offer a clinically significant advantage over placebo in the treatment of depression. According to recent global data on antidepressant studies, there is a less than 10% difference in the effect of FDA approved antidepressants versus placebo (162). And as for the small number of studies that did provide positive results, they catch the public’s eye through numerous publications in well-respected and peer-reviewed journals and FDA databases. But the remainder majority that provided negative and less than promising results were obscured and never mentioned. Sometimes, these trials are stopped even before they could be completed because of the alarming side effects found, which do not make it to the journals either (163).

Manipulation of the release of clinical data on antidepressants makes them less of a threat than the mental disorder that they were studied to treat. The hidden dangers are ugly and when do they become known, are often blamed on the underlying disorder rather than caused by the drug treatment. A good example is the increased risk of suicidal tendencies in patients on SSRIs. Because SSRIs were initially developed to study the serotonin levels of suicide victims, this particular finding is a tough pill to swallow by the very same companies who spearheaded the studies. After all, these drugs were studied to treat depressed individuals who were at risk of harming themselves and others. To protect the company’s interests, they’ve assigned the blame on the disorder, a practice known as “defending the molecule”. Other scientists are catching up on this practice and have released studies that undermine it such as those that emerged in the early 1990s showing healthy and non-depressed volunteers increased likelihood to develop suicidal thoughts after treatment with SSRIs for other indications (164, 165).

Another ethical dilemma to be considered in the administration of psychopharmacological treatment is the unethical manipulation of the mentally ill. Despite their refusal to treatment, the law sometimes forces them to sign up for one anyway. As mentioned in the previous section, such an action is the result of the law acting on behalf of the public’s best interests at the expense of the patient’s personal freedom.


Patient advocacy

Unlike antihypertensive treatments with a well-defined and measurable outcome, psychopharmacologic treatments are hard to measure let alone quantify in a patient’s chart. There’s simply so much subjective data to sort out and make sense of. There isn’t a consistent measuring tool that tells both clinicians and patients that full mental stability has been regained that is in keeping with practice guidelines. Even mental illness is a poorly understood disorder. Moreover, treatment costs money, even with Medicare in place. These facts plus the risks that the treatment present to the well being of the patient are serious considerations that must be weighed in by the patient themselves before committing to it.


CONCLUSION

Mental disorders, despite various attempts at understanding them throughout human history, remain a poorly defined group of illnesses. There is a large gray area that research has not yet uncovered. As a result, experts in the field such as psychiatrists, therapists, clinicians and other healthcare professionals are left with the daunting task of “making do” with what medical literature and training has taught them – symptomatic control. Since the root causes are unknown, trying to treat them is next to impossible. What’s left in the cards for these healthcare professionals are three things; alleviate the symptoms and establish some degree of normalcy, protect the safety of the patient and the public, and improve the patient’s overall quality of life.

Various interventions, both clinical and nonclinical, have been introduced in the last 50 years. Freud’s groundbreaking research in psychology put forward the use of somatic treatments in mental illness. The acceptance of somatic treatment introduced to the world the use of psychotropic medications to correct biochemical disturbances in the brain, Freud’s proposed pathology of mental illness.

Modern psychopharmacology has its roots in the 1960s revolution where drug use became a normal part of life for Americans. The era saw the entry of antidepressants and antipsychotics into the pharmaceutical market. Research in the following decades brought to light many of the adverse effects of these older medications, prompting pharmaceutical companies to develop novel therapeutic agents that are safer, though not necessarily more efficacious. The past two decades have seen the trend of “medicalization” of almost, if not all known mental disturbances, grow and spread. The DSM-IV even added normal human psychological responses to their expanding list of diagnosed disorders.

Psychopharmacologic interventions have undoubtedly made the lives of the mentally ill better and their presence in society not just tolerable but acceptable. However, like many medical advances, it came with several pitfalls too; namely studies that failed to demonstrate their efficacy being superior to placebos, ethical issues regarding their administration, and their propensity to cause fatal adverse effects (e.g. suicide tendencies and cerebrovascular events).

Appendix A






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