Many general practitioners as well as psychiatrists have begun to use off label prescribing for psychotropic drugs with little regard for impact on childrens health, mental or otherwise. [1] Only gradually are scientists beginning to explore the neurological, endocrine, metabolic and social effects of psychotropic drugs prescribed to children and adolescents. Drugs never intended for youth–especially as a cocktails containing several different types– have begun to interact with children’s brain chemistry, sometimes causing irreversible damage. [2] By treating what society deems psychiatrically “abnormal” children with psychotropic drugs, we must consider the possibility that we are creating four additional types of abnormalities: metabolic, endocrine, kinetic, and social. These unintended abnormalities or side effects are leading psychiatrists and physicians to add additional drug therapies in order to treat co-morbidities related to original drug intake. [3]
Metabolic Side Effects:
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Drugs will always play a role in the chemical composition of the brain and the signals it sends forthwith to the body. Neurotransmitters are chemicals that control and are capable of altering brain function in the broadest sense. They can be found in both pre- and post synapses. The way they affect functions, however, differ significantly. Presynaptic effects are seen through the enhancement or suppression of reuptake of neurotransmitters to the presynaptic receptor, whereas, postsynaptic effects are known to modify transmission by acting as an agonist or antagonist to the postsynaptic receptor. In layman’s terms modification of the presynapses by inhibiting the reabsorption of neurotransmitters, the signal senders, helps continue the excitation between the synapse for an extended period, whereas in the case of postsynaptic effects the flow of neurotransmitters is inhibited across the synapse to their postsynaptic receptor therefore the signal is not as strong or non-existent. Antidepressants generally work on the presynaptic receptors while antipsychotics work on postsynaptic receptors. [4]
The release of hormones and the way drugs effect the secretion of several key developmental hormones have potentially dangerous effects on children’s metabolic function. Some psychotropic drugs (second generation atypical anti psychotics and some classes of antidepressants) have high binding affinity to Muscarinic Ma‚? receptors on pancreatic Beta (I?) cells. [5] The Vegas Nerve X, originating in the brain and affected by psychotropic drugs, releases Acetocholene (Ach) to stimulate the Pancreas. In turn the Pancreas excretes numerous hormones through parasympathetic stimulation such as Glucagon, Epinephrine, Corticosteroid and Growth Hormone all of which induce a hypoglycemic state in excess. It also controls the hormone Insulin, which in surplus will contribute to hyperglycemia. Robinson et al. suggests that the Ma‚? receptors on the I? cells which are stimulated through parasympathetic control from Vegas Nerve are affected by the neurotransmitters (Ach) of the brain which is in turn manipulated by the drugs ingested.
As we explore the effects of drugs on the brain and in turn on the body, let us concentrate on insulin and the detrimental effects it has on the body when there is a surplus or a deficiency. One of the most lethal and debilitating problems our youth face today is obesity. Prescription drugs are increasingly contributing to effects on metabolic functioning resulting in Type 2 Diabetes Mellitus (T2DM). One class of drugs that contributes to significantly to these findings is Second Generation Antipsychotics as well as specific types of Antidepressants. T2DM is encountered when body becomes unable to remove glucose from the blood due to down regulation or a decrease of insulin receptors. [6] Generally an increase in glucose triggers an increase in insulin that will initiate the liver and muscles to cycle glucose out of the blood by storing it as glycogen and eventually fat; however, long term exposure to increased amounts of insulin causes cells to become “insulin resistant” through the down regulation of receptor cells. The results of this is glucose intolerance and diabetes are expedited unfortunately studies show that symptoms progress more rapidly in the case of children. Foggarty et al. have noted that T2DM carries an increased risk of early complication for micro- and macrovascular, atherosclerosis and myocardial infarction, renal insufficiency and failure, vasculopathy, neuropathy, retinopathy, and ketoacidosis in the case of children as opposed to adults. [7] Although there are a plethora of negative metabolic side effects for children while taking psychotropic medication, T2DM has attracted the most attention of the scientific community due to its rapid progression, and connection to multiple life threatening diseases.
Many drugs that have seen significant testing and are proven to negatively affect metabolic function but none are so severe as Second Generation Atypical Antipsychotics as well as specific classes of Antidepressants. Second Generation Atypical Antipsychotics are used to treat mood and psychotic conditions in schizophrenic patients and bipolar (BD) patients. Arizona Health, a well regarded publishing, lists positives and negatives associated with the medicated child. They claim that these drugs work to alleviate aggressive behavior in many cases but some side effects such as, weight gain, sedation, dizziness, insulin resistance, and muscle rigidity, are many times severe and should be taken into account. [8] Correll et al. write in depth pertaining to how exactly Atypical Antipsychotics block Insulin secretion by mediating Muscarinic receptor activation by acting as an agonist. [9] In other words the impulse to release Insulin is halted because the Muscarinic receptor is unable to be excited and pass on the signal. Diabetes and glucose intolerance are consequences of these drugs.
Arizona Health lays out very simply the dynamics and function of antidepressants showing how they work on several different neurotransmitters: serotonin, dopamine, and norepinephrine. In general they inhibit the reuptake process of specific neurotransmitters causing an increase in the specified chemical in the brain. [10] Antidepressants are used for a plethora of mental disorders including: anxiety, depression, Obsessive Compulsive Disorder (OCD), Post Traumatic Stress Syndrome (PTSD), child enuresis and BD as well as other numerous off label uses. There are several different classes of antidepressants: Selective Serotonin Reuptake Inhibitor (SSRI), Serotonin Norepinephrine Reuptake Inhibitor (SNRI), Tricyclic Antidepressant (TCA), Monoamine Oxidase Inhibitor (MAOI), Others. Each produces collectively similar side effects such as nausea, headache, insomnia, agitation, and sexual problems as well as carrying issues specific to each class. All cause a change in weight whether it is a gain or loss, however, only SSRI’s and SNRI’s are associated with hypoglycemia. [11]
Endocrine/Sexual Development:
It has also been shown through various researches that endocrine function is impacted in children treated with psychotropic medication. The role that atypical antipsychotics play in their binding affinity and ability to act as an agonist or antagonist for the dopamine receptors within the Hypothalamus exerts significant control over the Anterior Pituitary. Remembering the function of an agonist is important as it pertains to the dopamine (neurotransmitter) receptors. Literally, this means that the function the organs are meant to perform are slowed or even blocked. It is significant as the organs affected is a part of the brain that oversees the organ, Anterior Pituary, that is mainly in control the hormones associated with the management of growth functions. One such hormone is prolactin. Correll et al. has researched the affects that Atypical Antipsychotics have on the hormones and realized there is an incredible correlation to children who take these drugs and certain types of hormaonal disorders. He writes about how Atypical Antipsychotics raise prolactin levels severely possibly causing hyperprolactimeia. [12] This may have several effects on the body such as suppressing gonadatropin releasing hormone secretion which consequently will inhibit secretion of lutenizing hormone and follicle stimulating hormone leading to hypogonadism. Other effects are: suppression of penile erection, stimulate secretion of adrenal androgens and delay puberty.
This is a difficult topic to research due to its controversial nature and complexity the number of variables inherently associated with the study of sexual development in children and young adults. For instance, variables in young women may include: the onset of menstruation, which varies for a assortment of reasons, the multiplicity of reasons young women experience an increase in BMI during these years, and the fact that puberty is inherently a time of flux, which can lead to embarrassment and confusion in adolescents may lead to distortions in the reports of young patients. [13] I realize all of these are considerations that make data collection exceptionally difficult as each case is grouped according to norms and not explored on an individual basis.
Neurological Discrepancies:
The changes to a human’s brain chemistry are most profound and impressionable during their youth. The term commonly used for the developing brain during this period of development is pliability. The environment that is given for maturity must be carefully monitored and protected. It has been shown through more recent studies by Anderson et al. that long term exposure to psychotropic drugs can have not just detrimental but many times delayed effects on the neurological framework of the brain. [14] This in turn interrupts future growth and psychological functioning. The psychological functioning is not just seen through school but is physically apparent through the development of Tardive Dyskinesia (TD). The long standing effects of these drugs are called neuronal imprinting. Unfortunately, children because they are at a more vulnerable state have a compounded effect, which adults seem to escape due to the fact that they have a more fixed neurological framework.
Multiple studies by Anderson et al. were done on baby rats which have proven the hypothesis of the extended effects on childhood development after significant exposure to psychotropic drugs. It was recognized by Greenhill that the due to the decreased ability of children to metabolize drugs they were essentially slowly poisoning them. [15] Unable to cycle the toxins out of their system children had residual buildup that sometimes did not present until later.
One of the many detrimental effects seen with taking children off of psychotropic medications is tardive dyskinesia (TD). TD is syndrome entailing multiple mixtures of hyperkinetic involuntary movements such as orofacial dyskinesia, chorea, athetosis, dystonia and tics. Basically this means children suffer from muscle rigidity and uncontrolled movements of not just the body but the face. The repercussions of the physical sadly are perpetuated and become highlighted by social stigmatization.
These symptoms have an increased frequency among patients treated with antipsychotic drugs. Neuroleptics, generally used for their sedative or tranquilizing nature, act on dopamine receptors in different capacities to produce desired behavior or effect. A link has been reported between patients treated long term with antipsychotics as well as those treated for any length and who develop TD, Acute Extrapyramidal Symptoms (EPS) and with drawl emergent symptoms (WES).
What is unclear is the distinction and separation, if there is one, between TD and with drawl dyskinesias. Unfortunately it is an ambiguous line and an obvious delineation cannot be made. Ordinarily movements that emerge as nueroleptic withdrawl are tics, stereotypies, nervous mannerisms, imitative gesturing and psychotic posture. Some will argue that these movements are associated with the original diagnosis and the medication contributed in no way. This seems to hold some truth as various diseases maintain choreiform movements as a symptom; however, not all diseases treated through antipsychotics are associated with movement disorders or hyperkinetic movements. In fact it must be noted that in some cases neuroleptics may suppress stereotyped movements. Discontinuation of the drugs can lead to reemergence of the stereotypy movements. It is up to researchers and individual physicians to do thorough intakes to assess the validity and type of abnormal movement.
It is theorized that there are two types of dopamine receptors in the basal ganglia: excitatory and inhibitory. Studies also indicate that they develop at different stages so that the effects of neuroleptic medications have effects that are almost impossible to trace and make systematic research tremendously difficult. For this reason, clinical manifestations differ for children as opposed to adults. In children, and adolescence dyskinetic movements generally reported to be facial tics and grimaces, choreathoid and myoclonic movements of the extremities and body, abnormal posturing, generalized motor restlessness and ataxia [16] .
The above theory is supported by two generalized groups with TD. Group one appears to do worse when the drug is withdrawn and do better with the reinstatement which would indicate a dopamine dominance and acetocholine deficiency. This group also seems to worsen with the introduction of anticholinergenics. Group two’s indicates a dopamine deficiency and acetocholine dominance as we see their symptoms improve when the drug is decreased or stopped. [17] Anticholinergenics are seen to either agitate or alleviate the symptoms according to the time of supplementation. [18] In the end TD is thought to generally arise from postsynaptic dopamine receptor sensitivity, whether it be an excitatory or inhibitory synaptic sensitivity, an increase or a decrease in dopamine is hypothesized to be at least partially effected by development. To quote the Journal of American Academy of Child Psychiatry, “The notion that dopamine receptors might demonstrate different patterns of vulnerability to the noxious effects of neuroleptic drugs at different developmental stages might ultimately shed some light on the changing clinical manifestations of drug-induced dyskinesias in patients of different ages.” [19]
The Socially Abnormal Child:
The vast majority of psychotropic drugs prescribed to children and adolescence is done through off-label prescription. As Minde stated at a Toronto conference it should be noted the prescribing physician is generally not a psychiatrist and these children have not been through a proper psychiatric evaluation. [20] What is more, he agrees with recent efforts to increase regulations of the practice parameters and set standards for the psychiatric treatment of youth and the continued trial testing on drugs.
Childhood and adolescence, a time of flux and uncertainty, simultaneously becomes a time in which there is increased pressure to conform to peer group norms. Consequently, the impact of stigmatization of abnormal can lead to social withdrawl and noncompliance, creating new social abnormalities. Doing this can unintentionally foster a condition that a doctor would consider co morbidity, and in turn, increase the need for supplemental medication which can create a vicious self-fulfilling cycle as most drugs are not tested in combination because it is too difficult and lengthy a process. [21]
Due to many significant factors physicians need to exercise caution when administering “a life sentence.” These diagnoses are not just a simple fix. These are life-long stigmas that children begin to identify themselves as if they are not careful. [22] It is unfortunate that physicians dispense diagnoses so callously. These children are not only identifying themselves as their illness but are suffering psychological side effects from the drugs- loss of identity as an individual, losing self-esteem, isolating themselves. [23] With these effects, the chance of a normal childhood is gone. The damage can be irreversible.
Conclusion:
Drugs are a necessity in some cases and do enhance the lives of some children, however, the question of what is “abnormal” and who is truly benefiting from the treatment of these children has yet to be fully explored. The drugs administered create significant side effects that make it difficult to determine their utility thus raising questions regarding the motives of drug companies and even possibly the new “hands off” parenting that seems increasingly popular. [24] If the trend towards medicating children continues, we risk eliminating the “normal” pediatric population as a result of our ever-narrowing definition of normal. Through the creation of new diagnosis, and consequential medicating of the pediatric population, abnormalities within metabolic, endocrine, neurological and psychological systems may have devastating effects not just our pediatric patients but on our entire community in the long term.
