Endocrinology of Aging (Contemporary Endocrinology)

Endocrinology & Metabolism International Journal

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Coffee in Exhibit Hall. Clinical Aspects to the Management of Hypothyroidism. Thyroid Case Histories. Close of session.

Endocrinology, Diabetes, Metabolism, and Nutrition

Estrogen Dominance and its Clinical Implications. How to Assess and Improve Estrogen Detoxification. Personalizing BHRT. Male Hormones. Case Histories: Male Hormones. A Metabolic Approach to Hypocortisolism and Hypercortisolism. Fellows Breakfast. A Metabolic Approach to Insulin Resistance. Problem Solving through Contemporary Compounding. Lunch in Exhibit Hall with ticket. Mercedes Car Drawing in Exhibit Hall. She lectures nationally on preventive medicine and has appeared on national and local television. Landa just completed her first book with co-author Virginia Hopkins. Landa addresses with her patients every day.

Alison McAllister, ND. Alison McAllister is passionate about medical education and enjoys teaching both colleagues and patients. She is a clinical consultant at ZRT laboratory and also works in her own private practice. She has done advanced work in midwifery as well as doing a 3 year residency in integrative oncology.

On a nice summer day, Dr, McAllister can be found digging in her garden with her young daughter. Pamela W. Pamela Wartian Smith, M. She has been featured on CNN, PBS, and many other television networks, has been interviewed in numerous consumer magazines, and has hosted two of her own radio shows. She is a regular contributor for Fox News Radio. Sahar Swidan, PharmD. Sahar Swidan obtained her Doctor of Pharmacy degree from the University of Michigan and then she completed a 3 year research fellowship in Bio-Pharmaceutics at the University of Michigan.

This study is notable and refreshing because the authors evaluated gene expression in the animals after compensating for changes in GH. However, because of age-dependent changes in other hormones, such as sex steroids, and the difficulty of replacing hormones in a way that recaptures the physiology of a young animal, it is impossible to precisely differentiate hormone-dependent from hormone-independent age-related changes.

Despite this caveat, studies using DNA microarray analysis of brain tissue from rats that show improvements in memory following GH replacement should be particularly informative. It seems reasonable to speculate that restoration of GH release in a way that mimics the physiology of a young adult will provide functional benefits, not necessarily by increasing longevity, but by improving the quality of life.

This is based on observations in GH-deficient humans showing that GH increases bone density and improves body composition, cognitive function, cardiac function, and exercise tolerance.

One of the reasons is based on laboratory animal studies, where the data suggest that reducing GH, IGF-I, or insulin signaling increases longevity — However, these studies do not address quality of life in elderly subjects, which is more important than longevity. Indeed, although caloric restriction has also been shown to improve longevity in a variety of species, a recent, careful study and review of the literature shows that prolonged caloric restriction impairs cognitive function in rats All of these models exhibit dwarfism, reduced body temperature, and reduced fertility.

The reduced longevity was suggested to be a result of more stressful animal housing conditions, typical of 30 yr ago, and poor adaptation to stress , Indeed, it has been speculated that the negative effects of prolonged stress, which causes suppression of the immune system by glucocorticoids, are balanced in wild-type animals by the positive effects of GH, IGF-I, prolactin, and thyroid hormone , In addition to antagonizing the adverse effects of chronic stress on the immune system, GH and IGF-I may play a similarly protective role in the CNS, thereby potentially improving quality of life.

Indeed, Koo et al. They showed that when old mice are treated with an oral GH secretagogue, restoration of GH and IGF-I reversed the age-dependent shrinkage of the thymus and improved T-cell production. Treatment with a GHS-R agonist reduced the rate of tumor growth, inhibited metastasis, and increased longevity The characteristics and significance of GH binding in the human brain have been reviewed by Nyberg and Burman In addition to reduced GH release during aging, the concentration of GH receptors in the brain also declines.

The highest density of GH binding is in the choroid plexus, with significant binding in the hippocampus, hypothalamus, amygdala, putamen, and thalamus GH-deficient children have an increased incidence of anxiety, depression, and attention deficits, which may contribute to their observed learning disabilities in arithmetic, spelling, and reading compared with age-matched controls , GH deficiency in adults is reported to be associated with reduced energy, unfulfilled personal life, low self-esteem, problems controlling emotional reactions, social isolation, impaired social function, mental fatigue, impaired general and mental health, and deficits in cognitive function — Markedly reduced GH levels, particularly the integrated nocturnal levels, have also been associated with major depressive illness This may explain the increased incidence of depression and poor sleep quality in the elderly population.

The neuroprotective property of GH was documented in rats. Hypoxic-ischemic damage causes increased GH transport into the brain as manifested by an increase in the number of GH-immunopositive neurons To demonstrate GH binding by immunostaining, the authors went to extraordinary lengths to document specificity. The immunohistochemical evidence showing that GH migrates to the sites of injury following hypoxic-ischemic injury is most persuasive. The authors also demonstrated that icv administration of GH was neuroprotective in the cortex and hippocampus Table 1.

Thus, the decline in the amplitude of GH secretion during aging likely attenuates GH-mediated neuroprotection. Protective effect of icv injection of GH on cortical and hippocampal neurons following hypoxic-ischemia. Scheepens et al.

II. Complex Behavior of Neurons in Aging

However, between the ages of 11 and 32 months, IGF-I protein levels were reduced by When different age groups of rats were compared 6 months vs. Whether a causal relationship between age-associated deficiencies in cognitive function and declining brain IGF-I levels exists is the subject of continuing debate.

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However, an association is supported by the observation that when IGF-I is administered icv to rats for 28 d, the age-dependent decline in spatial reference and working memory is reversed Lower doses selected to provide physiological IGF-I concentrations in the blood improved memory function more slowly, but normal function was restored after 12 months of treatment. Reduced IGF-I levels are characteristic of aging 2 , , — Endogenous IGF-I plays a significant role in recovery from insults such as hypoxia-ischemia Neurons die within hours or days following initial injury because of activation of cell death pathways.

However, IGF-I with its binding proteins and receptors is induced within damaged areas following brain injury, which suggests that IGF-I plays a neuroprotective role. Administration of IGF-I within a few hours after brain injury confers protection on gray and white matter; by contrast, IGF-I pretreatment is ineffective, probably because of limited intracerebral penetration into the uninjured brain. It has been suggested that IGF-I deficiency could be involved in cognitive deficits seen with aging.

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To investigate this observation in more detail, cognitive functions known to decline during aging were compared with those insensitive to aging. The outcome was consistent with a protective effect of IGF-I on the onset of age-dependent cognitive deficiencies, particularly in speed of information processing , Similarly, Dik et al. Although cross-sectionally IGF-I was directly related to information processing speed, memory, fluid intelligence, and Mini Mental State Examination score, these statistics were not significant after adjusting for age and other factors.

A low IGF-I threshold was also observed during a 3-yr decline in information processing speed. In conclusion, this study suggested that IGF-I levels below 9.

Studies on centenarians showed increased prevalence of dementia in those with lowest serum IGF-I levels Ghrelin mimetics have been shown to normalize IGF-I levels in the elderly and to increase IGF binding protein 3; therefore, these compounds may prove beneficial as neuroprotective agents during aging 25 , The age-associated decline in GH and IGF-I is likely to cause deficits in functioning of the CNS because both hormones play an important role in vascular maintenance and remodeling. The cerebrovasculature is a source of IGF-I and nerve growth factor NGF , which are known to play an important role in memory , — During aging, cerebral blood flow decreases and, together with reduced production of sex steroids, correlates with the age-related decline in plasma GH and IGF-I levels.

In BN rats, arteriolar density and anastomoses decline markedly between the ages of 7 and 29 months. However, GH treatment produces increases in IGF-I, reverses the age-dependent changes, and increases the number of cortical arterioles These data suggest that preventing the decline in GH and IGF-I during aging would help prevent age-related reductions in vascular density.

The continued viability of adult neurones requires neurotropic factors to support plasticity and provide neuroprotection. A decline in production of such factors probably contributes to the age-related functional deficits that occur in the aging brain. Production of specific NMDA receptor subtypes in the hippocampus of rats and mice falls during aging and appears to be regulated by IGF-I , ; NMDA receptors have been implicated in memory and learning — The reduced expression of specific NMDA receptor subtypes in the hippocampus, which is reversible by IGF-I treatment, probably affects cognitive function.

By contrast, in a study of aging rhesus monkeys yr , the levels of NMDAR2b were unchanged in the hippocampus but reduced in the prefrontal cortex and caudate nucleus Hence, we must remain cognizant of the need for caution when extrapolating data from rodent models to humans. At this stage, spatial learning and reference memory were compared in the treated and control groups using the Morris water maze. The performances of the aged rats were also compared with 6-month-old rats. The results confirmed that spatial memory declined during aging and that chronic D-Ala 2 -GHRH treatment prevented this decline.

GHRH treatment also improved mental activity, psychomotor function, behavior, and humor in elderly human subjects SWS and secretion of GH decrease proportionality during aging The major peak of GH release associated with sleep is markedly reduced in elderly subjects, and the amplitude of the nighttime cortisol peak increases 68 , 87 , — The effect of fasting on the amplitude of GH release and on sleep patterns was investigated in a small group of elderly subjects Therefore, although age-associated hyposomatotropism was partially restored, fasting did not induce changes in SWS.

However, the beneficial effect of exogenous GHRH on sleep has been questioned because of poor reproducibility.

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A possible reason for the disparities might relate to the modes of GHRH administration used in different studies. Bolus iv injections and intranasal administration are more efficient at delivering molecules rapidly to the CNS than slow iv infusion. Because GH secretagogues like ghrelin and its synthetic mimetics stimulate the release of GHRH from hypothalamic neurons — , improvements in sleep quality elicited by the GH secretagogue MK are likely mediated by direct stimulation of hypothalamic GHRH neurons Increased somatostatin tone might cause the reduced amplitude of GH release observed in aging hypothalamus.

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