Growth Hormone and Memory Endocrinology

Growth Hormone and Memory

Endocrinology

The Effect of Human Growth Hormone on Memory

The Effects of Growth Hormone on Memory

There is increasing evidence of a connection between levels of growth hormone in the body and cognitive functioning (Maruff & Faletti, 2005). Research studies on the topic have explored the role of growth hormone therapies on cognitive functioning. It has been indicated that growth hormone treatments are associated with cognitive improvements as well as a normalization of brain functioning and a return to appropriate growth hormone levels in the body (Maruff & Faletti, 2005). Growth hormone deficiencies can be congenital or acquired and most times will require treatment in order to normalize. In fact, 50% of children who have been diagnosed with idiopathic growth hormone deficiency will continue to exhibit these deficiencies into adulthood (Maruff & Faletti, 2005). The most common cause of adult onset growth hormone deficiencies are the direct result of damage to the pituitary gland including tumors, radiation, and surgeries.

Higher cerebral functions including learning and memory require the participation of brain structures such as the cerebral cortex, caudate nucleus, amygdale, and the hippocampus (Schneider-Rivas, Rivas-Arancibia, Vazquez-Pereyra, Vazquez-Sandoval and Borgonio-Perez, 1995). Neurotransmitters including dopamine, acetylcholine, and gamma-aminobutyric acid have also been identified as important contributors to the acquisition, transference, consolidation, and storage of memories (Schneider-Rivas et al., 1995).

Growth hormone is a protein hormone composed of amino acids that is produced by the anterior pituitary gland. It is responsible for childhood growth as well as the maintenance of many tissues and organs throughout the lifespan. Growth hormone is present in the brain tissues, central nervous system, and cerebral spinal fluid and is responsible for promoting growth in the body, as well as metabolizing carbohydrates, proteins, and lipids (Nieves-Martinez et al., 2009). Growth hormone has the ability to cross the blood-brain barrier with receptors found in the brain, pituitary, hippocampus, hypothalamus, putamen, and thalamus (Arwert, Deijen, Muller, & Drent, 2005). Deficiencies in HGH are correlated to the impairment of both long and short-term memory. In fact, cognitive tasks such as learning, memory, and intelligence are all linked to the availability of adequate growth hormone. Research has shown that early HGH therapies for those with growth hormone deficiency can prevent deficits in memory that may occur later in adulthood (Kinney, Coschigano, Kopchick, Steger, & Bartke, 20012001).

Growth hormone levels run a natural life cycle starting off slowly in childhood, peaking prior to puberty and then beginning to taper off as an individual reaches middle age. The pituitary gland naturally slows the production of growth hormone over time and it is believed that HGH production drops as much as 14% for each decade after 20 years of age (Kinney, et al., 2001). By the time an individual can be considered elderly, their growth hormone levels have dropped as much as 75% (Kinney et al., 2001). This natural decrease in the production of growth hormone in the body has led many individuals and researchers to explore the use of synthetic human growth hormone (HGH) to counteract the effects of decreased growth hormone in the body due to both the normal aging process as well as HGH deficiencies. As the body ages and produces less growth hormone one can expect to see changes in body composition that are comparable to the symptoms experienced by a person with growth hormone deficiency. These symptoms include a reduction in lean body mass, a rise in the percentage of body fat, and a decline in bone mineral density (Baum et al., 1998).

In addition to these physical changes in the body, growth hormone has also been linked to psychological and cognitive functioning. Studies in elder populations have identified a link between growth hormone levels and scores on short-term memory and cognitive flexibility tasks (Arwert et al., 2005). In fact this natural decrease in HGH secretion throughout the aging process may be a causal link to the reduction in the ability to learn and retain information as one grows older (Kinney et al., 2001). Studies have demonstrated that the number of growth hormone receptors in the brain also decrease throughout the lifespan (Arwert et al., 2005). These differences in age-related changes in those with HGH deficiency can be useful in determining if there is a factor in HGH replacement that promotes better long-term memory during the aging process (Kinney et al., 2001).

Many products now claim to be able to combat the natural aging process through the use of growth hormone. Despite the increasing interest in products of this nature, there is little evidence to suggest that HGH has the capability of reversing the aging process in otherwise healthy adults. The quest for the fountain of youth should not involve the use of this powerful substance due to the potential negative side effects are related to its use. However, synthetic HGH has been successfully utilized to address issues related to pituitary functioning in both children and adults. Growth hormone deficiencies can present themselves throughout the lifespan starting soon after birth and continuing through adulthood as the result of a variety of disorders of the pituitary gland (Nieves-Martinez et al., 2009).

Overtime memory deficits in growth hormone deficient individuals were believed to be caused by disturbances in neural cell metabolism that could eventually be reversed (Arwert et al., 2006). This belief came as a result of variations in the cerebrospinal fluid absorption of the dopamine as the result of the introduction of synthetic growth hormone. Since high levels of dopamine are concentrated in the hippocampus, the part of the brain that influences learning and memory, this increase in dopamine in the cerebral spinal fluid was believed to be capable of altering the memory processes (Arwert et al., 2006). Since it has been established that HGH can cross the blood-brain barrier it is able to access receptors for growth hormone that are located in the choroid plexus, hypothalamus, putamen, thalamus, and hippocampus all of which play a substantial role in memory processes (Arwert et al., 2005). HGH replacement therapies of two years or greater have been related to long-term increases in synaptic efficacy in the hippocampus (Arwert et al., 2005). The increases in short-term memory that are found after one year of HGH replacement therapies are the result of the activation of NMDA receptors in the basal forebrain (Arwert et al., 2005). Results are also seen in the executive functions, such as attention and working memory, which are controlled by the prefrontal cortex.

The first controlled studies of HGH replacement in growth hormone deficient adults took place in 1989. Overtime studies have attempted to address the effect of HGH replacement on symptoms of growth hormone deficiency. Findings have suggested that adults with growth hormone deficiency are less psychologically and physically healthy than their same age peers (Carroll et al. 1998). Further these studies indicated the emergence of substantial clinical benefits through the use of HGH supplemental therapy in growth hormone deficient adults and children. Recent studies have also begun to indicate that HGH replacement may result in improved memory functioning in adults with growth hormone deficiency (Carroll et al., 1998).

There are several factors that can lead to growth hormone deficiencies in individuals. Growth hormone deficiencies can be seen at any point in the lifespan and may manifest different symptoms in each life phase. For example, growth hormone deficiency in an adult with adult onset of symptoms is most often the result of pituitary tumors and their remediation (Carroll et al., 1998). The incidence of adult onset growth hormone deficiency has yet to be identified but it is estimated that 10 million persons annually experience pituitary tumors (Carroll et al., 1998). On the other hand, childhood onset of growth hormone deficiency does not demonstrate the same linkage and is often believed to be idiopathic (Carroll et al., 1998).

Individuals with growth hormone deficiencies experience significant cognitive deficits, particularly in the area of memory function, when compared to their healthy same age peers. This is evidenced by performance on ionic memory, short-term, and long-term memory tasks (Arwert et al. 2005). Cognitive function and IQ have been observed to be impacted in persons with growth hormone deficiency. These include lapses of attention, difficulty concentrating, and issues with long and short-term memory task completion. The connection between cognitive functions and growth hormone can be explained by the existence of many growth hormone receptor sites in the hippocampus (Huisman et al., 2008). The hippocampus is a part of the brain that is responsible for learning and memory structures. This explains how some researchers have drawn the connection between HGH supplementation and increased cognitive function, particularly memory and learning, in adults (Huisman et al., 2008). Nieves-Martinez et al. (2009) also found that growth hormone deficiency during adolescence negatively impacted learning and memory by middle age unless treated through the use of HGH supplementation.

In childhood, growth hormone deficiency has been associated with academic difficulties and behavioral problems consistent with attention deficit disorder (ADD) (Baum et al., 1998). These children are not observed to have a decrease in intelligence quotient (IQ) yet cognitive functional impairments do exist (Baum et al., 1998). Cognitive functioning, particularly memory performance has been found to be impaired in patients with childhood onset of growth hormone deficiency and HGH replacement therapies have been found to offset this memory impairment (Arwert et al., 2005). Studies have identified a link between improved attention and increases in memory performance in children with growth hormone deficiency (Arwert et al., 2005; Arwert et al., 2006). This is due to the connection between memory capacity and attentional resources.

Growth hormone deficiency that begins in childhood is most often treated with growth hormone supplementation in order to increase body size during adolescence (Nieves-Martinez et al., 2009). Yet recent studies have demonstrated that this treatment directly correlates to improved memory in adulthood. In fact studies have suggested that treatment with growth hormone in child onset deficiencies can in fact prevent learning and memory deficits later in life (Nieves-Martinez, 2009). Childhood onset of growth hormone deficiency has been correlated to adult memory impairment. However, studies have shown that early supplementation of growth hormone in adolescence has been able to prevent age related deficiencies in learning and memory that are prominent in this population. In fact treatment of growth hormone deficiencies in adolescents was correlated with a cease in the impairment of spatial memory past adolescence (Nieves-Martinez et al., 2009). In fact, supplementing growth hormone during puberty thwarts the deterioration of brain functioning as the result of growth hormone deficiency. Adolescence is a period of maturation and HGH replacement assists the maturation of the brain which may have significant implications for the course of the illness (Nieves-Martinez, 2009).

Children who experience cognitive impairments in childhood as the result of growth hormone deficiencies are more likely to experience psychosocial problems later in life (Baum et al., 1998). Further, as adults these children have decreased employment and marriage rates. Persons who develop growth hormone deficiency as adults have been found to perceive their quality of life and overall health as poor (Baum et al., 1998). Therefore the cognitive changes of growth hormone deficiencies in adults also warrant exploration.

Growth hormone deficiency is the most common endocrine deficiency linked to pituitary disease in adults (Baum et al., 1998). During the aging process, there is a significant decrease in IGF-I protein levels in the body. There are also noticeable changes in the cerebrospinal fluid concentration of the dopamine, metabolite, and homonvanillic acids in the body (Arwert et al., 2005). Studies have shown that growth hormone replacement in adults with a deficiency has shown improvements in body composition as evidenced by an increase in bone density and lean muscle mass (Baum et al., 1998). Adults with acquired growth hormone deficiency who have undergone HGH treatments have reported improved mood, cognitive functioning, and overall sense of well being when measured on tasks of attention, memory, and perceptual motor skill (Baum et al., 1998). There has been concern that growth hormone deficiencies are correlated to learning disability and memory deficits that are commonly seen in adults who have experienced growth hormone deficiency in childhood.

As with any drug, HGH has potential negative side effects therefore one must weigh these against the potential gains associated with HGH treatment. Persons most at risk for experiencing negative side effects of HGH therapies are those that are older and out of shape. The most common side effects after HGH supplementation in adults who are growth hormone deficient include water retention, weight gain, symptoms of carpal tunnel syndrome all of which may be attributed to an increase in the sodium levels in the body (Baum et al., 1998).

However, despite these side effects, HGH treatment has been shown to improve the cognitive functions, particularly memory, in childhood onset growth deficient persons within the first year of treatment (Arwert et al., 2006). This includes improvement in short- and long-term memory tasks as well as iconic memory tasks. In adult onset growth hormone deficient patients significant improvements in memory occurred after one year with maximum benefits not being recognized until after two years of treatment (Arwert et al., 2006). In fact, after a year of treatment, memory shows significant signs of improvement and these gains could still be recognized after 10 years of treatment (Arwert et al., 2005).

The improvements in short-term memory after the first year of treatment and long-term memories after two years identify that in order to achieve increased cognitive functioning the course of treatment should be a minimum of two years in duration (Arwert et al., 2005). Individuals who experience an increase in memory function after six months may have higher IGF-I I (insulin like growth factor) levels. Persons who reported results after one year had an IGF-I level that was within normal range. At the one year mark, increases in cerebral blood flow increases as well as improvement in memory performance, including working memory. Working memory has been identified as the ability to keep information readily available should it be needed for immediate recall ad application (Arwert et al., 2005). Improved working memory can be evidenced by improved and faster memory performance as well as increased regional brain activity that can be measured with PET imaging (Arwert et al., 2005).

Researchers have found that memory processing for small memory loads is quicker in persons with higher IGH-I levels (Arwert et al., 2005). This suggests a direct link between the speed of information processing and IGF-I levels in adults. Recent studies have begun to incorporate imaging, particularly PET scans and MRI imaging, to show task-related activity in the areas of the brain associated with working memory and cognitive functioning. Images are taken to compare baseline vs. task activities and to observe changes as task load increases (Arwert et al., 2005). Arwert et al. (2005) identify that the anterior cingulated cortex is involved in response selection and error monitoring while postural parietal activity is responsible for the attentional processes and information storage. Imaging aids researchers in identifying baseline functioning in individuals so that differences in functioning between groups cannot be associated with differences in baseline. Brain activity can then be observed during task completion, while controlling for load associated activity (Arwert et al., 2005).